How Healthcare May Be Improved With Artificial Intelligence

If you have not been up to date with healthcare news, or do not work in any healthcare related field, you may be unaware of the gradual increase how reliant the sector is on technology. Every facet of society has been on an upward climb with how digitized it is, and healthcare is no exception. From breakthroughs as interesting as robotic surgery to standardizing electronic patient notes, both primary and secondary care have grown accustomed to the benefits of how artificial intelligence can benefit them.

In healthcare, introducing new treatment whether based in technology or pharmaceuticals is highly expensive, though great efforts are being taken to increase efficiency, reduce human errors and improve healthcare overall. In the long running of things, this would save the healthcare economy billions in coming decades.

Genomics

There has been a public declaration made by IBM Watson Health to incorporate artificial intelligence to the ongoing battle against cancer. The focus currently lies with later stage cancer patients who are at their most critical points. This is because it is likely current treatments have failed for them, or aren’t strong enough. New treatments could offer them the best chances when facing their life or death situations.

Specific genetic factors involved in cancer can be identified and targeted with idealized therapies. This offers hope to many Veterans in the US, and cancer patients worldwide.

Drug Discovery

It has been about three whole decades since a new effective antibiotic has been discovered. This has led to a seemingly losing battle with the emergence of more superbugs (antibiotic resistant pathogens) significantly often. The journey to discovering new drugs is very expensive, meaning many drug companies have slowed down the process of discovery. However, Pfizer’s use of IBM Watson (technology that utilizes machine-based learning) is pioneering the path to finding new drugs that are active for cancer and immune therapies.

Other drug companies such as Sanofi are using artificial intelligence to find new therapies for metabolic disease; Genentech are also leading the way in cancer research with artificial intelligence from Cambridge, Massachusetts.

Robotic Surgery

The correct term for this is robot-assisted surgery, because though it looks like a robot is handling the surgery from the operating theatre, there is actually a surgeon (or multiple surgeons) that are controlling the robotic tools remotely. This has been rolled out successfully in multiple countries so far. These include the United Kingdom and Dubai. The major benefits of robot-assisted surgery is increased precision and accuracy. There is less room for human error, and more room for improved patient care.

Secondary Prevention

One of three or sometimes four main branches of prevention, secondary prevention relates mostly to medical imaging. There has been a huge surge of technological advances in this area in the past century. The simple ultrasound has become 3D imaging and the simple radiograph has become detailed computerised tomography. New approaches can now be taken, that reveals more information about patients. This leads to clearer imaging, faster diagnosing and better results.

Personalized Medicine

Genetic screening has been more incorporated into healthcare since the sequencing of the human genome in recent decades. With genetic information and associations readily available, more accessible means of accessing patient DNA have been developed. There are now easy methods of reaching a patient’s genetic code and assessing their risk for certain health issues that carry genetic risks.

“Polygenic scoring weighs the linear combination of multiple small genetic variations and are used in predisposition assessment,” says Mary Crawford, tech blogger at Australia2Write and Write Myx.

Visual Assisting

Nursing is investing in the development of virtual assistants, which can take over the role of healthcare assistants and push the healthcare staff population to higher fields of work. Healthcare providers will then be able to maintain continuous contact with patients.

Better Data Security

A major leap in healthcare is digitizing patient records, and rolling out a singular way of standardizing them across the country. Though this is extremely useful for transferring patients from healthcare provider to healthcare provider, it creates room for a cyber-attacks that will steal sensitive data.

“As artificial intelligence increases with patient data storage, it also increases with cybersecurity. Extra security is essential to patient protection,” says Erick Schmid, data analyst for Brit Student and Next Course Work.

Discussing how healthcare may become revolutionized by artificial intelligence may conjure up images of the 1985 movie Daryl. However, the movements are very much real and non-fictional. Productivity is on the rise and medicine has become more business-minded.

Due to its benefits, artificial intelligence is certainly gaining popularity in the healthcare industry and there are developments every year. There are predictions that the involvement of artificial intelligence will grow by 1000% by 2015, pushing it to become a 13 billion dollar industry.

Michael Dehoyos is a medical Blogger at Phd Kingdom and Academic brits. He assists companies in their marketing strategy concepts, and contributes to numerous sites and publications. Also, he is a writer at Case Study Help, academic service.

Patientchat Etiquette & Guidelines

Chat etiquette & guidelines:

  • Patient Chat is appropriate for patients, doctors, nurses, caregivers, mental health professionals, complementary care providers,  loved ones of patients, basically anyone and everyone that cares about improving the healthcare system and a patient’s journey through it.
  • Please try to stay on topic.
  • No problem if you jump in late, just say hello and join in.
  • Please don’t pop in and promote a business or product. If it is relevant to the discussion, feel free to share. We have had some companies not participate but just tweet out links. Please participate in the chat instead. Chatters will click through to your profile if they’re interested in you.
  • Please say hello even if you’re just following along. It helps us gage if the chats are reaching people.
  • Please share the chats with other people and Retweet as much as you can to help spread the word.
  • Discussion topics and questions are asked with a T1, T2, T3, etc. Be sure to include the appropriate number in your answer, T1, T2, T3. For example: We ask, “T1. What is your favorite color? #patientchat” You respond, “T1. Blue. #patientchat”
  • Be sure to include the hashtag in your tweets and responses. If you use a tool like tchat.io, it will automatically append the #patientchat hashtag to your tweets.
  • Feel free to challenge the status quo with your responses and be creative! However, be mindful and polite at the same time.
  • Be respectful, even if you disagree with someone. Focus on dialogue and solutions.
  • Please don’t discount other people’s stories and experiences. You may disagree & think your way is better. Honor others’ experiences that are different from your own.
  • As #patientchat has grown in its reach, we regularly become a trending topic on Twitter. When this happens, you may see unrelated posts in the Patient Chat feed. This happens because other people try to abuse trending topics on Twitter and promote unrelated causes and spam. It is still safe to participate in Patient Chats. If this happens, you can BLOCK or REPORT the abusive tweet directly in Twitter. See Twitter’s abuse report guidelines. 

Office Visit Planner – Myeloma

Appointments with your physician can be overwhelming. To optimize your visit, it’s best to arrive organized and prepared to take notes. Our Office Visit Planner can help. Guides for your first office visit as well as your follow-up office visit, tailored for patients and caregivers, are available below. Download, print and bring along with you to the appointment.

For Patients:

First Office Visit Planner
Follow Up Visit Planner

For Care Partners:

First Office Visit Planner
Follow Up Visit Planner

 

Jennifer Lessinger

Jennifer Lessinger is a professional writer and editor who learned the value of patient empowerment during her struggle with a hard-to-diagnose and complex endocrine disorder.

5 Ways to Have a Productive Day with a Chronic Illness

“Having a productive day is very subjective; what is productive for one person is not for another”.

Some days, I find waking up, washing and eating productive. Others assess,  I am being productive when I  do University work.  What I have noticed though – is we all have tasks that need to be completed and this can send us into panic mode. The vicious cycle, of where to start and where to finish has a ripple effect – like a child who got denied candy at the fun fair.

If you are someone sat there reading this with a chronic illness, I am sure you have an inkling of the cycle I am talking about. If you don’t well… I sit here, in envy.  What I am going to call the ‘ torrential storm cycle’ makes you question which direction to go in first.   Anxiety and stress are no strangers, crawling around your body, taking its toll , physically and mentally.  This post is designed to stop you in your tracks, so you aren’t continuously interrogating yourself about ability and self-worth.

“I spend 90% of my time in bed, but a chronic illness does not mean accomplishing your goals are not possible”.

Achieving those goals may just take comprise, planning and longer than you anticipated.


5 Ways to have a Productive Day with a Chronic Illness

1. Evaluate tasks ft. the spoon theory

If you haven’t heard of Christine Miserandino’s Spoon theory , it is a great place to start to help you have a productive day.  The theory in a nutshell, is that anyone who is chronically ill has 12 spoons each day (each one resembling energy) and spoons are exchanged for tasks.  The amount of spoons exchanged will depend on factors such as the length of the task and how strenuous. The point here, is spoon must be used wisely so you don’t burn out. By ordering tasks by importance you can identify what needs to be done on what day and start to put a plan in motion.

spoon-theory-e1510325926400.jpg

In reality, you may find executing a plan is not always possible. However, the spoon theory gives you a general consensus of how much you can get done in a day.

You may find – once you start having a productive day you are at the opposite end of the spectrum. At Uni, I get told a theory is just that a theory. I am taught to challenge theorists view. So it may not be a surprise to hear I wasn’t a firm believer of the Spoon theory at first.  I was so productive one day I felt on top of the world. I couldn’t believe my eyes. I had completed an exam, handed in an assignment, found a job, booked a flight, travelled home from Uni and packed for a holiday and cuddled my little bunny.

Shortly, after this semester came to a close – I realised I used the reserve of spoons for months. I had to fly home 3 weeks early from working abroad, quit the job I found and was  behind in every subject at Uni. Barely, attending lectures and hospital appointments.  What I am trying to emphasise, is pushing yourself one day really can have a detrimental effect on your health.

“You need to work out what is realistic to get done in a day for YOU”.

 Which takes me to by next point…


 2. Break down tasks

 Breaking down tasks makes things more manageable.  Something,  I am training myself in like a disobedient dog. I am one of those people who seeks to think holistically to even do a task.  However, breaking down tasks can relieve stress, because you know you are achieving something – which has got to be better than nothing, right?

goal

I have found people have been more understanding about my illness when they can see that I am trying rather than wallowing in self-pity.  The amount you need to break-down a task will depend on its complexity. It may be a case of trial and error, but you know your body better than anyone in time you will have this down to a tee.

If it’s something academic, you could try and break things down with titles and research areas and tie the ideas together later.  You may not get the best grades you are used to due to time constraints.  However, at least you will pass and can try and work harder when you are feeling a bit brighter on future work. If the task is practical, like cooking, you could do prep at a certain time and then cook later in the day.  Or if you’re a little bit cheeky – ask someone to help you to make the task manageable.


3. Follow your Body Clock

Most people would say, sort out your body clock first and foremost. It may work, but it is something I have been trying to do for over 10 years. My body just likes to be up during the night. The fatigue and pain is more manageable after I have digested by one meal per day.

“To have a productive day you must follow your natural body clock”.

You don’t want to set yourself up for failure by taking a U-turn and trying to achieve tasks when your energy levels and pain threshold is low.

body clock

“Remember you can always move tasks to another day as long as you’re motivated to accomplish them”.


4. Relax… just not too much

Whether you have a chronic illness or not, everyone should take time to wind down.  If you’re fortunate enough TAKE a bath, or go and visit someone who does! Watch a comedy, listen to music or sit in silence, do what works for YOU. I am not saying you are not going to wake up still feeling fatigued because you probably will BUT subconsciously your body and mind is still getting a valuable break and you get a hint of happiness.  I find relaxing whilst doing a task slowly usually gives me the right balance. However, this may not work for everyone.

“Just remember, don’t relax too much or you won’t get anything done”.

bath.jpg


5. Relieve stress with a pet

Patting pets are proven to having a calming effect on humans (Rodriguez2012), which may help you to think more clearly and be more productive! It is ideal if you own a pet and go and give them love when you are stressed and they are in a good mood. If your pet is moody, trust me try hugging your friends’ pet or the other four tips AND come back to this one later.  When my pets are hungry they treats me like food and it makes me feel rejected and has the opposite effect.  If you cannot keep an animal, I suggest you look out for the nearest dog on your walks or go visit an animal shelter. That way you can have your rare day out, killing two birds with one stone.


This blog was written by Morgan Shaw and originally posted on her blog, Brains & Bodies, here.

Applying Patient Advocacy Initiatives to Your Patient Journey #patientchat Highlights

Last week, we hosted an Empowered #patientchat on applying patient advocacy initiatives to the patient journey with special guest Seth Rotberg (@Srotberg15). Seth is a rare disease advocate and motivational speaker who is passionate about bringing his personal experience to better support the health community. The #patientchat community came together and shared their best advice and tips.

Top Tweets and Advice

 

You Have Power

 

 

 

 

Be Confident

 

 

 

 

Patient Advocacy Has Benefits

 

 


Full Chat

 

Spotlight On: World Cancer Day 2019

Today is World Cancer Day, which is a day to unite people worldwide in the fight against cancer. World Cancer Day is an initiative of the Union for International Cancer Control (UICC).

2019 marks the launch of the 3-year ‘I Am and I Will’ campaign. ‘I Am and I Will’ is an empowering call-to-action urging for personal commitment and represents the power of individual action taken now to impact the future. You can follow along with all of today’s happenings with the official hashtags #WorldCancerDay and #IAmAndIWill. Head on over to worldcancerday.org to learn more about:

  • Why cancer matters
  • How to take action
  • Find activities taking part around the world

For more information take a look at this infographic provided by worldcancerday.org.

WCD19_Infographic_FA

The Importance of Clean Air for Recovering Cancer Patients

Air quality is an important part of living a healthy life, and studies show that patients with certain forms of cancer can face more difficult odds during recovery if they live in areas with heavy air pollution. Patients who live in wide open, green spaces can also be affected, however, as homes have been known to contain, sometimes, even more pollutants than the air outside. And, you don’t even have to be diagnosed with lung cancer in order to feel affected by mold spores and other pollutants that are circulating throughout the air in a home or recovery facility. Learning how to combat at-home air pollutants and keep other bacteria at bay will help ensure a quicker, easier recovery.

Special Attention on Avoiding Infection

When recovering from cancer treatment, it’s especially important for patients to avoid contact with other people or any sort of allergen that could cause infection. This is why hospital rooms are kept so clean, in order to allow your immune system to build itself back up over time. Most recovery facilities and rooms will feature a HEPA air purifier that has the ability to catch and destroy any virus, bacteria or mold in the air. Air filters, therefore, are a great tool when to facilitate quick recovery, especially for patients diagnosed with upper respiratory types of cancer. High-quality filters can clean the average-sized hospital time up to 12 times per hour. If you’re going to invest in an air filter or purifier for your home, it’s important to look for one with a HEPA filter as it will help capture microscopic dust and allergens that can cause harm even after your treatment and recovery are over.

Keeping Home Clean During Recovery

Once you’ve been discharged from a hospital or care facility, it’s extremely important to keep your home very clean, for much of the same reasons of avoiding infection or viruses. While this includes washing bedding and clothing in hot water nearly daily and cleaning all hard surfaces with disinfectants, it also means managing the humidity and mold in your home. Seeing as humidity is the cause of a lot of home health problems, it’s a good idea to first invest in a portable humidity meter to stay on top of the levels. Then, you’ll want to ensure that the humidity levels never rise above about 60%. Doing so can permit mold, which can cause autoimmunity, fatigue, nausea, and even asthma, all of which are things you’ll want to avoid especially if you’re recovering from cancer treatment.

Clean Air Equals Peace of Mind

The great news is that there’s currently no scientific evidence to back the idea that exposure to mold spores can lead to cancer. The real issue at hand is purifying and dehumidifying the air to ensure that no other types of bacteria or virus can enter into your lungs and compromise your immune system during such a delicate recovery period. Clean air will ensure you can breath easily and relax as you embark on the journey that is recovery, and that peace of mind will mean everything once you’re back at home and ready to just rest.

Starting the Year Empowered #patientchat Highlights

On Friday, January 11th, we hosted an Empowered #patientchat on starting the new year off empowered. This time of year is a good time to reflect on the past year and set goals for the new year – including being empowered in your health.

Being an empowered patient can have many different definitions, but most include patients taking an active role in their health by furthering their education on disease and treatment options, participating in shared decision-making with healthcare professionals, and advocating for themselves to get the best care they deserve.

The Top Tweet Takeaways…

 

You Are the Expert of YOU

Inspire by Example

Organization is Key


Full Conversation

ASH 2018 – Tools for Staying Up-to-Date on CLL Research

CLL patient advocate, Lee Swanson, interviews Dr. Anthony Mato, Director of the CLL Program at Memorial Sloan Kettering Cancer Center about the exciting news for CLL patients at the ASH 2018 meeting.


Transcript: 

Lee Swanson:

Hello.  I’m Lee Swanson at the American Society of Hematology conference in San Diego joined right now by Dr. Anthony Mato from Memorial Sloan‑Kettering in New York.  And, Doctor, CLL, what’s come out now at this conference about CLL that patients want to know about?

Dr. Mato:

This has been a very exciting ASH meeting for patients with CLL.  There’s been a couple of big themes, but probably the largest is the comparisons of novel agents to chemoimmunotherapy combinations.  We saw two presentations looking at ibrutinib and rituximab as compared to the chemo combo FCR, which is a standard of care for patients who are young and fit, and we also saw a comparison of ibrutinib with or without rituximab, the antibody, compared to bendamustine Rituxan.

The overlying theme of the two presentations is that the patients who received ibrutinib tended to do better, certainly in terms of progression‑free survival and even in terms of overall survival with regards to the FCR comparison.  So a big theme is that there are fewer and fewer patients who are the right candidates for chemoimmunotherapy, and it appears that BTK inhibitors, at least as of this moment, will be the standard of care frontline for patients with CLL.

Dr. Mato:

So the good news and the bad news:  You don’t have to do chemotherapy.  On the other hand, chemotherapy is a defined six‑, seven‑month regimen.  Does this mean you’re taking a pill forever?

Dr. Mato:

Based on the current way that ibrutinib has been studied and labeled that means you’re on a long‑term‑‑it’s a long‑term commitment to ibrutinib.  There have been updates at the meeting of ibrutinib‑based and venetoclax‑based combination therapies where there is the hope that giving ibrutinib with a partner, for example, or venetoclax with a partner will allow us to treat to a fixed duration and then stop for patients, and that duration would either be based on some predetermined time point or on depth of response based on response criteria or minimal residual disease criteria.

So right now it’s a long‑term commitment, especially frontline.  In the long‑term I think we’re headed toward the direction where we can define which patients may stop sooner and then be retreated.

Lee Swanson:

If you stop, can you be retreated with the same?

Dr. Mato:

That’s a great question.  There’s not a lot of information about that, but there’s no reason biologically to think that that wouldn’t be a problem.  Specifically, if you stop in the setting of responding disease it’s not likely you’ve required resistance to that drug, and so retreatment should be a reasonable strategy.  We’re at Memorial Sloan Kettering now designing many trials that will try to answer those questions and allow us to stop either monotherapies by themselves or combinations to treat to a depth of response and then stop, so that’s something we’re really interested in.

Lee Swanson:

So if a patient gets a diagnosis now from‑‑sometimes from a primary care physician, of CLL what’s the conversation they should have?

Dr. Mato:

From the primary care physician?  Well, I think the primaries are great at identifying an elevated white blood cell count and the signs and symptoms of CLL even making the diagnosis.  Flow cytometry is readily available now to anyone who wants to order it.  I think the conversation with a primary care physician should be who should that patient see as a CLL expert to help guide the observation period which is important, as many patients are not treated initially, and also to help them to be informed as to how the field is changing.  Because the progress is so rapid you really need to have someone who is focused in on this area to help guide that particular management strategy long term.

Lee Swanson:

It’s important to get to a specialist, at least get a communication with a specialist.

Dr. Mato:

Exactly.  And of course the local oncologist and the internist are very important in terms of patient management, but ultimately there could be somebody who could help drive that‑‑some of the more important decisions based on the newest standards.

Lee Swanson:

So all of these things coming out, how does a patient keep up on what’s going on?

Dr. Mato:

That’s a really great and difficult question to answer because there’s so many different sources of information, some more reputable than others on advances in the field.  I think that probably the best source is having a physician, a trusted provider who is up to date, who can help interpret some of the more complicated findings from the research studies.  But in addition there are patient organizations and professional societies who are reputable, who provide up‑to‑date, very reasonable recommendations, either through their websites or through the literature that they provide for patients.

I think trying to avoid just general Google searches for advice on management of CLL is a good idea to not do.  I find that oftentimes things that get posted online can be just one‑off examples where somebody’s either extremely happy with care or very unhappy with an event, and it may not necessarily be representative for all patients.  So I would say professional societies, CLL focus, patient organizations, and then of course having a care team that’s very focused and very specialized in the area so that they can interpret what can be complicated.

Lee Swanson:

Okay.  Thank you very much, Doctor.  Appreciate your time.

Dr. Mato:

Thank you very much.  Yep.

Lee Swanson:

This is Lee Swanson.  I’m at the American Society of Hematology conference in San Diego.

ASH 2018 – Multiple Myeloma Highlights

A Multitude of Options in Myeloma

Dr. Robert Orlowski, Director of Myeloma and Professor in the Departments of Lymphoma/Myeloma and Experimental Therapeutics at The University of Texas MD Anderson discusses the multiple myeloma highlights and what patients can be excited about from the ASH 2018 meeting.


Transcript:

Esther Schorr: Hi there. This is Esther Schorr from Patient Power coming to you from ASH 2018 in San Diego, and I have with me today Dr. Bob Orlowski who has joined us at Patient Power before. He’s the Director of Myeloma and Professor in the Departments of Lymphoma and Myeloma and Experimental Therapeutics—that’s a very long title—at the University of MD Anderson—University of Texas MD Anderson. Sorry.

Dr. Orlowski: Thanks very much for having me.

Esther Schorr: I’m glad you’re here again.

Dr. Orlowski: It’s a pleasure to be back on Patient Power.

Esther Schorr: Thank you, sir. So what’s going on in myeloma now at ASH? What are the highlights? What are patients going to be excited about, and what are you excited about?

Dr. Orlowski: One of the exciting areas is definitely talking about the different therapies that are targeting what’s called BCMA or B-cell maturation antigen. This is a protein on the surface of myeloma cells, and the excitement about it is it’s a target which is almost only on myeloma or normal plasma cells, not on other kinds of tissues. And that’s important because if you want to target for immunotherapy, you don’t want that target to be on too many normal cells, or the immune therapy will kill those cells and cause side effects.

So there are really three categories of drugs now that are looking very attractive. One is what’s called an antibody-drug conjugate. So this is a plain old antibody that has another chemical attached to it, and it’s given usually IV right now, attaches to the myeloma cell. It then gets inside the cell and the drug is released. So the antibody is essentially like a carrier molecule.

Esther Schorr: Kind of like a cruise missile?

Dr. Orlowski: Sort of like that. I like that analogy, yes. And then it blows up, using that analogy, the cancer cell once it’s inside.

So one of the first of these drugs that already is in the clinic is showing a 60 percent response rate in very heavily pretreated patients. The registration study, meaning the trial that hopefully will get it approved by the FDA, has already finished enrolling, so we’re hopeful that maybe by the end of 2019 this drug as a single agent will be available. And it’s really easy to give. It’s IV once every three weeks, which is pretty darn good.

Esther Schorr: And what’s the drug called? I’m sorry I missed that.

Dr. Orlowski: Well, it’s a good question. Actually, it doesn’t have a name yet, which is why I didn’t tell you what it’s called, but the abbreviation for it is GSK 916.

Esther Schorr: Okay.

Dr. Orlowski: And the reason for that is it’s actually quite expensive to come up with a name, because they have to find a name that, first of all, is not confused with other drugs so that it minimizing errors and also one that us poor feeble-minded doctors will remember so that we prescribe it often.

Esther Schorr: We’re not sure how you can remember all the letters anyway. Okay. So that’s one. Is there something else going on that you got to share?

Dr. Orlowski: So a second category of drugs that target the same protein, BCMA, the first formal presentation of those data were shown here at ASH, and this is what’s called BiTE or Bi-specific T-cell engager. And it’s sort of is a molecule, if you want to use the cruise missile analogy, that has two war heads. One end binds to the cancer cell. The other end binds to the patient’s own T cell, brings them together and the T-cell attacks the cancer cell. So it’s a way to use immune therapy with the patient’s own immune cells, and there are reports here of the first one of these which is called AMG 420. Again, doesn’t have a name yet, but it’s showing in very heavily pretreated patients complete responses with MRD, or minimal residual disease, negativity, which is really exciting.

Esther Schorr: So and that’s different than—and we’ll probably talk about it in a minute—that’s different than CAR-T.

Dr. Orlowski: Exactly.

Esther Schorr: Okay. So we can talk about that in a minute.

Dr. Orlowski: Yeah, that would be great. So the next topic is the CAR-T, also against B-cell maturation antigen, or BCMA. It’s a little more complicated though because what you have to do is you take out the patient’s own T cells and then in a laboratory you infect them with a virus. The virus has a gene in it that expresses a receptor on the T cells so that they can better recognize the cancer cells.

Esther Schorr: An invitation.

Dr. Orlowski: Exactly. Kind of. I like that.

Esther Schorr: Okay.

Dr. Orlowski: And then you infuse the cells back into the patient. They find the cancer cell, they attack it, and they kill it. So it’s great, because it’s personalized. It uses the patient’s own T cells. The problem is that it takes two to four weeks to manufacture the cells after they’ve been taken out of the patients, and so in the meantime the myeloma can sometimes be creeping up. So that’s one problem.

And also there are activities with the disease or with the T cell against myeloma, but there are also some side effects like cytokine release syndrome. But the response rates with some of the more advanced molecules are in the 90 to 100 percent range, and the durability of that is at least a year to 18 months, depending on what patient population you look at. And those are the most mature data of the three categories of immune therapies that we’ve talked about.

Esther Schorr: So of those three are any of them being looked at for first-line therapy, or these are at the moment still for people who have relapsed or are more difficult cases?

Dr. Orlowski: Right now it’s more for very advanced disease, but there are already trials planned with all three of these technologists in earlier patients and some in newly diagnosed patients, especially those with high-risk disease, because they still don’t do as well with standard therapies that we have. So it’s really an exciting time because these are some of the best results we’ve had in very difficult to treat patients, which means they should work even better when we give them earlier.

Esther Schorr: So one other question then. What’s happened to stem cell transplants for multiple myeloma patients? With all of these new combinations of treatment s, where is that in the mix of consideration for treatment?

Dr. Orlowski: Stem cell transplant is still considered part of the standard of care for patients with newly diagnosed myeloma, and in some cases it can be used for relapsed disease, especially if the patient had a really good durable benefit with a first transplant. The advantage of the stem cell transplant right now is that it with works very well, the toxicity profile is very well defined, and compared to a CAR-T cell it’s actually relatively cheap. But as the technology hopefully becomes cheaper and more available there would be great interest in comparing outcomes of people getting chemo plus a transplant, for example, versus chemo plus a CAR-T cell.

Esther Schorr: So it sounds like there’s a lot more options that are coming up for multiple myeloma patients. Is there anything else that patients that are listening would want to know about, that they should feel good about?

Dr. Orlowski: Well, there’s a lot more data with other immune therapies including earlier use of daratumumab (Darzalex), which is an anti-CD38 antibody. One of the presentations, which is still to come on Tuesday, shows the data of that drug with lenalidomide and dexamethasone in previously untreated patients, and the results really look excellent. So that will probably be one of the new standards of care for transplant ineligible patients. And there are studies ongoing with daratumumab in transplant eligible patients as well.

Esther Schorr: That’s a lot.

Dr. Orlowski: And that’s not all of it, but I think that may be all we have time for.

Esther Schorr: Thank you so much, Dr. Orlowski, for being with us again and making this a little more comprehensible for us normal mortals.

Dr. Orlowski: Thank you very much.

Esther Schorr: This is Esther Schorr coming to you from ASH. And remember, knowledge can be the best medicine of all.


Please remember the opinions expressed on Patient Empowerment Network (PEN) are not necessarily the views of our sponsors, contributors, partners or PEN. Our discussions are not a substitute for seeking medical advice or care from your own doctor. That’s how you’ll get care that’s most appropriate for you.

5 Ways to Detect Cancer Before It’s Malignant

Cancer are diseases in which abnormal cells divide without control and can invade nearby tissues. Cancer cells can also spread to other parts of the body through the blood and lymph systems. In 2018 statistics, Cancer appears to be the second leading cause of death worldwide. It is responsible for an estimated more than 9 million death in 2018. About 1 in 6 deaths globally are caused by Cancer. There are several main types of cancer. There are several causes of cancer, however the main cause of cancer is the change or mutation in the Deoxyribonucleic acid (DNA) of cells. There are some factors that would lead to cell mutation. Usually cancer cells are genetics and that means it is hereditary. Other factors also are, individual’s lifestyle, diet, smoking, environment such as exposure to radiations and exposure to viruses and other infections.

There are several types of cancer nowadays, however according to statistics the following are the most spread types of cancer:

  1. Lung (2.09 million cases)
  2. Breast (2.09 million cases)
  3. Colorectal (1.80 million cases)
  4. Prostate (1.28 million cases)
  5. Skin cancer (non-melanoma) (1.04 million cases)
  6. Stomach (1.03 million cases)

Symptoms of cancer may vary depending on the type of cancer an individual has. However common symptoms of cancer are already established according to studies. The C-A-U-T-I-O-N U-S mnemonics is already an established common symptom of cancer according to studies, viz:

C- Changes in bowel or bladder habits;

A- A sore that does not heal;

U- Unusual bleeding or discharge;

T- Thickening or lump in the breast or any other part of the body;

I- Indigestion or difficulty swallowing;

O- Obvious change in a wart or mole;

N- Nagging cough or hoarseness;

U- Unexplained Anemia;

S- Sudden Weight loss.

Like in most diseases early detection plays an important part in the prevention and intervention of diseases. The same concept is very important also in cancer. It would help a lot in determining what type of cancer a person has and correspondingly its proper management. Once cancer is early detected, it can be prevented from spreading more damages to the person’s body by providing adequate and proper remedies. In most cases, cancer can be detected by the individual upon experiencing the above stated signs and symptoms. Some cancer may cause severe pain in the affected body parts, while some may cause unusual bleedings, sores and other unusual tissue growth that are visible and palpable to the infected individuals. According to studies, there are established cancer self-assessment methods applicable to men and women. In women, the breast self-examination (BSE) is applicable. It can be done regularly by women usually upon taking a bath and every month for purposes of detecting any lump in the breast. In men, the Testicular self-examination (TSE) is applicable also with the same duration in women. However, there are some cancer cases that are asymptomatic. In these cases, diagnostic tests may be conducted by the proper medical experts.

The following are the 5 common ways or methods to detect cancer:

  1. Biopsy– In most cancer cases, biopsy is the main method to determine whether cells are cancerous. In this method, the doctor will get a tissue sample for examination to be used in diagnosing cancer. The method of getting tissue samples can be made possible either through an image-guided biopsy, ultrasound, x-ray, computed tomography scan (CT scan), fluoroscopy and magnetic resonance imaging (MRI). Depending on what method used by the doctor the purpose is just to aid in guiding a specific organ or body part where the tissue samples can be obtained.
  2. Barium Enema – In this method an enema is required to clear the colon for purposes taking images through X-Ray by a radiology technician. This is used to detect colon cancer.
  3. Ultrasound– This is a method of taking images on the body part where cancer is suspected. It uses high-frequency sound waves to create images of internal body organs. The sound waves hit the organs and bounce back to a device called a transducer. The transducer turns the sound waves into images that are shown on a computer. There are two individuals that will conduct this method. The first individual is the sonographer or the specialist that operates ultrasound machine. 12 hours before the test, the patient is required to be in a “nothing per orem” (NPO) status, which means that the patient will not be allowed to eat or to drink 12 hours prior to the test. However, 1 hour before the test the patient is required to drink a quart of water to keep full bladder. During the test, the patient is required to remove his clothes and any metal object and is required to lie down on the examination table. The sonographer will then apply the echo gel to the skin of the patient in order to block the air pockets for better imaging quality. The Sonographer will then press the transducer firmly against the gel and move it back and forth. After the images are taken, the second individual, the radiologist, which is a medical doctor will then interpret the images for purposes of diagnosing cancer.
  1. Bone Scan– This method uses a small amount of radiation to detect cancer cells that start to propagate in the bones and bone tissues.
  2. Endoscopy– This method uses a thin scope that has camera on its tip connected to the monitor in order to determine any lumps or unusual tissue growths in the patient’s Gastro-intestinal tract.

In most cancer cases globally, early detection is the key to prevent extensive damages that are caused by cancer cell proliferation. It is also very important for proper cancer management.

Ask the CLL Expert – Dr. Richard Furman

Ask the CLL Expert – Dr. Richard Furman

CLL specialist Dr. Richard Furman, Director of the CLL Research Center at Weill Cornell Medicine, answered patients burning questions live in this installment of Ask The Expert.


Transcript

 

Andrew Schorr:

And hello.  Greetings.  I’m Andrew Schorr in southern California, San Diego area, and I’ve been living with CLL for 22 years, so I’m vitally interested in today’s Ask the Expert session, this Patient Empowerment Network program.  We want to thank PEN, as we call it, and also the financial supporters of this program, AbbVie Incorporated and Pharmacyclics, although reminding you that they have no editorial control.  You’ll be hearing from our leading expert in CLL in just a minute.

Over the next 30 minutes or so we’ll get to as many questions as we can.  Remember not to make it too personal.  Let it help everybody in the community.  And also discuss what you learn with your own CLL provider so you get the treatment that’s right for you.  Okay.

Let’s meet our expert joining us from New York City and Weill Cornell medicine, and that’s Dr. Richard Furman, who is the director of the CLL research center in New York City at Weill Cornell.  Dr. Furman, welcome back.  Thanks for being with us.

 

Dr. Furman:

Thank you.  It’s my pleasure.  Thank you for having me.

 

Andrew Schorr:

Okay.  We have lots of questions.  One of them that somebody wants to know about is, first of all, if they’ve been‑‑maybe this is an easy one.  If they’ve been diagnosed with SLL, small lymphocytic lymphoma, is that the same as CLL and what we’re talking about with CLL applies to them?

 

Dr. Furman:

So that’s a very important question, and this is one that I actually think is very indicative of how little we used to know.  So in 1993 we actually had a diagnosis of CLL, chronic lymphocytic leukemia, and a diagnosis of small lymphocytic lymphoma.  And we had patients that were diagnosed with SLL if they had a lymph node sent to the pathologist, or they were diagnosed with CLL if they had a bone marrow biopsy sent to the pathologist.

Clearly, we knew that patients could only have one diagnosis and not two, so in 1994 with the new lymphoma classification system the term was actually changed to be CLL/SLL.  So they really are exactly the same entity.  We don’t actually refer to differences anymore, and the whole, the whole individual‑‑the whole disease should be called CLL/SLL.

Now, an important thing is sometimes people require having a lymphocytosis to meet the definition of CLL, but the truth is both conditions are exactly the same.  Both should be treated exactly the same, and there should be no difference based upon having a lymphocytosis.

 

Andrew Schorr:

Okay.

 

Dr. Furman:

Why this is most important, let me just add, is that there are sometimes people will be diagnosed with stage IV SLL and it’s very important to recognize that these stage IV SLL patients unless they have thrombocytopenia below 100,000 like the Rai stage would indicate really are not stage IV.  So the lymphoma staging system would automatically make them stage IV, and that’s certainly not correct.

 

Andrew Schorr:

Okay.  Good point.  All right.  Here’s a question we got in from Julia and Betty and Shelly and Mark.  They all asked a similar question.  They’ve been on Imbruvica for five years now with success.

Is it working for most people, and what are some reasons why it doesn’t work for everyone?  And then what treatment options do you recommend if they relapse on Imbruvica?

 

Dr. Furman:

So right now I think the most important, there are a lot of prognostic markers available for CLL.  At last count we’re probably up to 115.  What’s most important is in 2018 what are those prognostic markers that really are relevant to the patient, and really as long as you stay as CLL you’re going to be able to have your disease very nicely controlled with our current agents and our novel agents.

So there are certain things that do indicate patients are likely to progress on ibrutinib, not likely progress must but who may progress, and people who might need something more, and that’s where a lot of our current clinical are research is focused.  So patients who have a risk of developing a Richter’s transformation or patients who have a likelihood of developing a BTK mutation that might generate resistance to ibrutinib are the two groups of people that we worry about most.

17p deletion is probably the most important predictor for predicting those patient outcomes.  There are other things that are predictive as well like having a NOTCH mutation.  Those are all readily obtainable prognostic markers that allow us to determine who’s at risk and who’s not at risk for progressing on ibrutinib.  If you don’t have 17p deletion or NOTCH1 mutation you have almost a 99 percent chance of being free from progression at five years on ibrutinib.  And it looks like most of the people who are going to progress will progress within five years.  So I think making it to that five‑year mark is really very‑‑is the most important thing.

 

Andrew Schorr:

Okay.  So if you do progress, what then?

 

Dr. Furman:

So fortunately we have a lot of great agents.

Venetoclax works very effectively in patients who progress on ibrutinib, generates some very, very deep responses and very long‑lasting responses.  So that’s certainly one option.  Another option is to be treated with a PI3‑kinase inhibitor.  So we have idelalisib and duvelisib now approved.  We will shortly have umbralisib approved as well as a novel agent.  We also have a whole array of other agents coming down the pipeline looking specifically at means for progression on venetoclax.  So we have an MCL1 inhibitor which targets the protein that’s likely responsible for resistance to venetoclax.  So all these things are actually currently in clinical trials and certainly will hold a great deal of promise.

 

Andrew Schorr:

Okay.  Here’s a question we got in from Jeff.  He says, for young and fit patients with relapsed disease what are the best combos now and coming.  And I suspect maybe Jeff had received FCR, so if he relapses after FCR, what about that?

 

Dr. Furman:

So my belief is that these novel agents should always be used up front, or if you’ve gotten chemotherapy up front they should be used immediately at relapse.  A lot of patients and physicians have the idea that there’s a benefit to holding back until you really need something, but I believe putting our best foot forward first is always the best approach.  So I always recommend going forward first with BTK inhibitor therapy, followed by venetoclax or venetoclax followed by BTK inhibitor therapy.  And I think so in a patient who has relapsed after FCR it will be ibrutinib or acalabrutinib.  In a patient who has relapsed after acalabrutinib and ibrutinib would then move on to venetoclax.

Now, what I’m really very excited about is the possibility of the combination of either BTK inhibitor therapy plus venetoclax or PI3 kinase inhibitor therapy with venetoclax.

You know, both of these combinations really take advantage of the synergy that happens when you take a BCR antagonist like ibrutinib, acalabrutinib or idelalisib and duvelisib and combine it with a Bcl‑2 inhibitor.  And it really sort of enables us to get very, very deep remissions with actually as short as just 12 months of treatment.  And so those are what we’re currently testing in patients right now and what I hope will be the frontline treatment for patients in the not‑too‑distant future.

 

Andrew Schorr:

Now, one of the things people wonder about is if you take these big guns and put them together could you, like you’ve been able to do with FCR, stop treatment or take a break from treatment at some time.

 

Dr. Furman:

So I’m a big believer in that if something’s working and you’re tolerating it well that we shouldn’t mess with it, but we are currently studying two different processes with relationship to the ibrutinib plus venetoclax combination.  So we’re taking patients who become MRD negative on the combination after 12 months and randomizing them to either just get ibrutinib or to get placebo.  And so that’s going to give us information as to whether or not it’s safe to stop patients on the combination and treat them with nothing long term.  We’ll see, one, how many patients relapse, and hopefully none, and, two, if they do relapse whether or not we can then restart ibrutinib and control their disease.  So this will provide us that important question as to whether or not we’re giving up something by discontinuing the therapy.

We’ll have as our comparative those patients who got ibrutinib plus venetoclax for 12 months and then just remained on the ibrutinib.

And so that will sort of be the patients who will continue on with their therapy, and then the other half will be patients who have discontinued all their therapy.

My belief for going to venetoclax is that you’re going to get almost all of the bang for your buck out of the first 12 to 24 months, so continuing it is unlikely to yield an additional benefit, so I think stopping it is safe.  But, once again, these are the studies that will provide us with those data.

 

Andrew Schorr:

Okay.  Now Maureen sent in a question where they responded to venetoclax and rituximab and they wondered what about testing for minimal residual disease?  They don’t have any lymph nodes or anything, but is that then appropriate to do a MRD test to see how deep the remission is?

 

Dr. Furman:

So the real important question should be whether or not that’s going to impact upon clinical management.

So MRD testing is easy, it’s noninvasive, it’s a peripheral blood test or a bone marrow biopsy, which I guess is only relatively noninvasive, and the information though is really not going to be of use.  So if you’re taking a patient who’s on ibrutinib and you’re going to continue the ibrutinib knowing the MRD status won’t change anything.  Likewise, if you have a patient who’s on venetoclax, who’s going to get a year of venetoclax on trial and then stop, knowing the MRD status won’t change anything as well.  So currently there’s no real reason for doing MRD assessments in patients except for just the ability to know.

Now, one day there’s some modeling that suggests that the time it takes you to reach MRD negativity is half the time you need to be on a substance, an agent, before you can actually claim to have a deep enough remission that you won’t relapse.  So we may one day say if you’ve been on ibrutinib for five years and became MRD negative, then 10 years of ibrutinib is enough and you can stop.  But that’s currently just theoretical and based on mathematical models.

 

Andrew Schorr:

Theresa wrote in, she said, my husband is being treated with acalabrutinib for five months.  He’s doing well, but should he have some sort of testing to know whether he will develop some sort of resistance in the future?

 

Dr. Furman:

So that’s a very important question, and the answer really is, you know, testing for it now isn’t going to be able to change anything.  Right now we would still continue the acalabrutinib until we see signs of clinical progression.  There’s some early data emerging from Ohio State where they’re doing PCR testing on all the peripheral blood of patients, on the peripheral blood of all patients to see whether or not they can detect any of these mutations that lead to resistance.  The problem is you’re still going to continue the treatment until you see the clinical relapse.

And, two, is you really‑‑you know, in essence when you look at the data that suggests that 92 percent of patients who get ibrutinib as a first‑line therapy will remain in remission at five years you’re talking about treating‑‑or testing a lot of people for very, very few people that will likely benefit.

 

Andrew Schorr:

Okay.  So if you have a question now, send it in, cll@patientpower.info, and we’ll do our best to pose it to Dr. Furman.  Okay.

So Beth with wrote in and wanted to know is there work going on on a CLL vaccine?

 

Dr. Furman:

So we’ve been playing with CLL vaccines for at least the past 25 years, and a lot of these vaccines were originally designed to be what we call antiidiotype, meaning they were directed against the antibody made by the cell itself.  Unfortunately, a lot of those vaccines have not proven effective, and we’ve gone through a lot of different iterations.  We’re still trying, and hopefully one day we will have better success.

Right now a lot of our current research is focused on not so much the target that the vaccine should be against but ways to make the vaccine more effective.  Things like using PD‑1 inhibitors, which can actually make the tumors more apparent to the immune system.  Or using things that can actually enhance the presentation of the actual vaccine to the immune system, and that includes everything from idelalisib and ibrutinib to other different molecules that may actually make it more readily apparent.

Now, we do also have some new targets like ROR1, which may prove to be very exciting and interesting, but this is still all very far away from anything that will be approvable.

 

Andrew Schorr:

Okay.  Now, here’s a question we got in from Cerisa, said, my understanding is that most drugs aim at destroying the CD20 protein like rituximab or obinutuzumab, etc.

Well, what about, CD9, CD15, CD23?  Are they not as bad as CD20 in CLL?

 

Dr. Furman:

So the thing that’s really important to keep in mind is only our monoclonal antibodies attack one protein in particular, and so we have obinutuzumab, rituximab, and ofatumumab all of which address or target CD20.  CD20 was the first protein targeted for two reasons.  One is it’s ubiquitously expressed on all B‑cell lymphomas, and so it’s a way to identify a target that we can actually generate one treatment for that will work in a large number of people.

The second is it’s a protein that doesn’t seem to actually get endocytosed or down modulated so that it remains positive in the cases most of the time.  One of the problems with some of the other proteins you mentioned is that they’re not expressed on the CLL cell.

So CD3, CD15, those are not present on CLL cells, but they’re also present on a lot of other cells as well.  The key about CD19 and 20 is that they’re only on B‑cells, and we really can actually do okay without our B‑cells.  And so that way the down side to knocking an out all our B‑cells is actually relatively minor.  And the CAR‑T cells, which are T‑cells taken out and reprogrammed, they’re reprogrammed to be directed against CD19 and 20, so in a way they work like the monoclonal antibodies.

 

Andrew Schorr:

Okay.  Lynn wrote in and asked about transplant in CLL, and I’ve met people who have had transplant, so where does transplant fit in now, and does CAR‑T cell experimental therapy maybe supersede that?

 

Dr. Furman:

One well, one of the things that’s important to keep in mind is that CAR‑T cells are still very novel, and the long‑term efficacy is not yet there, so we still need to do a lot of work to help that.

My belief is allogeneic transplants are very effective but they’re also very toxic and dangerous, and I do believe that they should be avoided if at all possible.  So I am very, very selective in who I refer for allogeneic transplant.

With our novel agents like ibrutinib, idelalisib, duvelisib, umbralisib, acalabrutinib, vecabrutinib, zenabrutinib, the list is just rapidly growing, I almost believe that the patient who really needs an allogeneic transplant will only be those patients who have developed or are at high risk of developing Richter’s transformations.  So I really do believe there’s a very limited role for allogeneic transplant at this point in time.

 

Andrew Schorr:

Okay.  And CAR‑T, you’re watching it.

 

Dr. Furman:

I am.

 

Andrew Schorr:

Okay.  Here’s a question that came in from Mike, and this is the bottom line for a lot of people when they’re diagnosed, and he says, what is the current state of treating CLL for those of us watch‑‑he says wait and see patients or watch and wait.  In other words, is it curable?

 

Dr. Furman:

So right now CLL is not curable.  The way that I would love everyone to start approaching CLL is very analogous to high blood pressure.  So we don’t cure high blood pressure, but if you take a pill a day it’s not going to have an impact on your longevity.  And I believe we’re there for about 75 to 80 percent of CLL patients, where they will be able to get a BTK inhibitor or a Bcl‑2 inhibitor or a combination and they will be able to not have to worry about their CLL for the rest of their lives.

There’s still the 20 percent who are going to develop either a Richter’s transformation or a progression on ibrutinib, and those are people we’ve got to figure out what to do differently for.  But all the others, even though it’s not curable, we can definitely I think keep it from having an impact on longevity.

People on watch and wait who are high risk of progressing and developing a Richter’s or progressing onto developing resistance to ibrutinib, we do have a couple of trials that are very interesting right now where we’re treating people at diagnosis with BTK inhibitors with the hope, because they’re so well tolerated and because they’re so effective, we might be able to have an impact and prevent those patients from developing resistance or developing a Richter’s transformation.

 

Andrew Schorr:

Wait a minute.  So are we looking at what has been the traditional watch and wait period differently now and some people will be treated much earlier?

 

Dr. Furman:

Well, we’re just starting to look at that right now in clinical trials.  So this is very early.  It’s for a very select group of people.

We know from the data‑‑so we have seven‑year data coming out at ASH this year where we’re going to have a group of people who were watched and waited and only when they had evidence of disease progression and needed treatment and got ibrutinib, 92 percent of them were still doing well and free from progression at seven years.  So for those 92 percent of patients we couldn’t do any better.  So it’s really just a very small group of patients who need something extra.

So, yes, we’ve proven I think in a large number of patients that BTK inhibitor therapy might be all that’s necessary, but in everyone else, in those 8 percent we do have studies going on to try to answer how to treat them differently.

 

Andrew Schorr:

Okay.  So we got a question early on about somebody who was asking about should he be taking a statin along with his oral therapy for CLL.  So people have other conditions.  So what about that?

 

Dr. Furman:

So if you have hyperlipidemia you should definitely be on a statin, otherwise, no, you don’t need a statin.  I think it’s important to keep in mind that there was a lot of data generated at one point about statins perhaps changing the CD20 expression on the surface of the CLL cells or making rituximab or other anti‑CD20 antibody therapy more efficacious.  I’m not aware of any data that suggests there’s an impact to statins on non‑anti‑CD20 therapy efficacy, and I think the impact on anti‑CD20 antibody efficacy is actually really quite small and unlikely to generate a significant difference.  So I really don’t believe there’s a need to do anything outside of just treating your lipids.

 

Andrew Schorr:

I promised our audience weeks ago that I’d ask you about this.  So should we have flu shots?  Should we have the shingles vaccine?

 

Dr. Furman:

So, absolutely.  Everyone should definitely get a flu shot each year.  And it’s important to get the flu shot each year because the immunity doesn’t persist.  So I actually recommend people get vaccinated either October or early November.  All right?  So any earlier than that I worry that you’re going to have your immunity peak before the height of the season, and later than that you may not actually have sufficient time to respond.

Regarding the shingles vaccine, so there’s a new shingles vaccine called Shingrix which is a recombinant vaccine, so it’s not a live vaccine, and that’s how it’s different than the previous shingles vaccine.  The previous shingles vaccine was an attenuated or live virus vaccine, and CLL patients really shouldn’t have taken it because it really theoretically could have caused shingles.

Now, the old shingles vaccine was also not very effective, so even though the risk was low with low efficacy there’s really no risk/benefit assessment that puts it in favor of doing.

But the new shingles vaccine actually has been tested in patients post autologous bone marrow transplants, so it’s very effective in patients who are very immunosuppressed, and because it’s not a live vaccine it is safe.  So I do recommend it for everyone.

 

Andrew Schorr:

Okay.  Dr. Furman, so you mentioned it earlier and we’ve heard about a lot of programs, the 17p deletion and I almost think of it as the dreaded 17p deletion, but is that necessarily true?  Pam wrote in, she said, I have the 17p deletion.  What are my options?  So first of all, are all 17ps alike, and then what are the options?

 

Dr. Furman:

So the thing that’s most important to keep in mind when we talk about prognostic markers is they’re really just surrogates for clinical behavior.  And so the answer always is going to be if you have historical data that’s always going to trump the prognostic marker.

So someone who is 17p deleted and their disease has remained stable for the last five years, their disease is stable, and the 17p deletion is not going to be what drives the prognosis.  I think that’s very important because when you look at a curve you’re going to see some people doing well and coming off the curve late and some people doing poorly coming off the curve early.  You know, where they are on the curve we have no idea how to predict.  All we know is that they’re on a particular curve.  So prognostic markers tell us about the population, never about the individual.

Now, with that being said, we do know 17p deletion a lot of it, the percentage of the deletion if you’re above 20 or below 20 does have an impact on how you do overall.  So 20 percent and below, they‑‑patients seem to have a better prognostic outcome than the patients who have 20 percent and above.

With that being said, I do have patients who have 17p deletion in 70 percent of their cells and they’re just hanging out doing quite nicely.  So clinical behavior does trump everything else.

 

Andrew Schorr:

Okay.  So, obviously, most CLL patients are older.  I’m 68 now, but I was diagnosed at 45, which is pretty young, but here’s Matthew who writes in he was diagnosed at age 31 and he wonders, he knows a lot of the statistics but he knows it’s mostly older people.  He’s trying to figure out, well, what’s his life going to be like.  So what do you say to younger patients with CLL today?

 

Dr. Furman:

So, remember, we’ve only had these novel agents since 2010, and so what I really do believe is that we really don’t know how good things are going to be yet.  I think things are going to be a lot better than we ever envisioned, so I am quite optimistic about the future.

We don’t know whether or not a 31‑year‑old could enjoy a normal long life expectancy but if they don’t have evidence of or suggestions that they’re going to have particularly aggressive disease and develop resistance to a BTK or a Richter’s transformation, they could theoretically have 40 years on a BTK inhibitor.  And so that’s certainly what my hope is for the future.

You know, all the survival curves that people talk about and all the survival curves that people show really don’t take into account any of the novel agents, and that’s always very important to keep in mind.  So we do some have data.  As I mentioned, the seven‑year data is coming out from‑‑will be out at ASH, and the seven‑year ibrutinib data really suggests almost a nearly flat curve for patients with CLL who get ibrutinib as a front‑line treatment.

 

Andrew Schorr:

So you mentioned over the years the Rai staging system, and Dr. Rai, the grand old man of CLL.

So how does that apply now?  You know, somebody’s diagnosed with CLL, they come across this Rai staging system, but is that meaningful for them today, or are there new ways of looking at it?

 

Dr. Furman:

So the Rai stage really still drives when we’re going to treat patients.  So patients are still treated based on meeting, you know, the classic indications for initiation of therapy.  So Rai stage 3 and 4, namely hemoglobin less than 11 or a platelet count less than 100,000, really are the two primary reasons why people initiate therapy.  We know that if you watch and wait someone until they meet classic criteria and they have disease that doesn’t harbor one of these high‑risk changes we know that they’re going to do extremely well.  So that’s good news.  Whether or not patients who have these other markers should be treated before they have aggressive disease is on open question.

Now, what I really do think that’s also important to keep in mind is, you know, the watch and wait ideology really came about when we had therapies that were not very effective and also were quite toxic.  Now that we have these novel therapies that are far less toxic and highly effective, maybe the bar should move towards initiation of therapy sooner, but that’s still on open research question and not one that we know the answer to yet.

 

Andrew Schorr:

Okay.  And Bob has had the same treatment I’ve had.  He had Gazyva or obinutuzumab with high‑dose methylprednisolone, and now that was, gee, about two years ago, and now his CLL has started to show up in his spleen and his lymph nodes.  He said, well, can he be treated with the same combination again, or might he move to something else?

 

Dr. Furman:

Well, that’s going to depend on a lot of factors.  Most importantly is whether or not there was, you know, he had received the full dose in which case the likelihood is that with just a two‑year remission I would expect that retreatment would generate a shorter remission this time, and the risks associated with high‑dose methyl prednisolone plus obinutuzumab probably don’t outweigh, or aren’t going to be‑‑the risks are going to outweigh the benefits that would be gained if we’re talking about a response that’s going to last less than two years.  So it would probably be better to move on to additional agents.  And, fortunately, we have so many others that I think it would be a way to avoid resistance and also develop‑‑avoid, actually, the toxicities associated with high‑ dose methylprednisolone.

 

Andrew Schorr:

Okay.  We’ll take just a few more questions, and thank you, Dr. Furman, for sticking with us.  And I relate to this one.  So I did have the obinutuzumab and rituximab years ago, and I developed sort of a history of sinus infections for a while and even some chest congestion and I’ve seen other people write in about it.

Do we have the sinus or the respiratory issues from the CD20 antibody or is it something else?

 

Dr. Furman:

So it’s important to recognize that CLL patients, 75 percent of CLL patients will develop hypogammaglobulinemia, and that hypogammaglobulinemia is probably most of the cause of the chronic sinusitis, chronic bronchitis, sort of that‑‑those issues with having the constant drainage.  So I do believe that CLL in and of itself is certainly the first factor that impacts upon that.

The anti‑CD20 by itself will also cause a lot of those problems as well, so the two together are just a double hit.  But we do know that CLL patients, totally regardless of their prior‑‑regardless of their prior treatments will run into those issues.

Now, with that being said, what people often forget is the most common cause of a chronic sinusitis in anyone, even a CLL patient who’s gotten obinutuzumab, is still going to be a deviated septum,  or it’s going to be a blocked sinus channel, so I always recommend and I always insist on all my patients being evaluated by an ear, nose and throat doctor first just to make sure there isn’t something anatomical that could be fixed.

 

Andrew Schorr:

I went to an ENT the other day, and also I’ve been doing‑‑and I know my Dr. Kipps here is urging me, I’m doing the nasal wash and all that stuff, just trying to have sinus hygiene, if you will, working on that.

Okay.  Couple more questions.  Aukie wanted to know, and we’ve talked about this in the CLL world forever, should he be taking a green tea extract?  Is there any validity for that?  What do we know?

 

Dr. Furman:

So my belief is no.  I think it’s important that we have a lot of alternative medicines, medicines that have been studied, and until they show evidence clinically I do believe that it’s important to actually stay clear of them, and there are a couple of reasons why.

So a lot of things work in the laboratory, but that doesn’t mean they’re going to translate into working clinically.  And a lot of the medications that are sold as alternative medications or homeopathic medicines are unregulated and can make claims that aren’t substantiated, but they also don’t have their products necessarily vetted.  So we’ve had a number of examples of people who have been taking a root or have been taking some leaf that’s turned out to be laced with amphetamines.  So a leaf that claims to enhance your energy output, absolutely, if it’s laced with amphetamine will certainly be able to accomplish that.

So it’s important to keep in mind that anything that’s made naturally or that occurs naturally doesn’t actually get regulated the same way as pharmaceuticals.  There was also a change in the laws in the 1990s where anything that was natural didn’t have to be tested and approved by the FDA, so the claims that they make‑‑like Tony the Tiger can say that Frosted Flakes are great without proving that in a randomized controlled clinical trial.  Because it’s a naturally occurring substance it can make claims that aren’t necessarily substantiated.  I do worry about that.  And there are some definite cases of patients coming to harm from taking medication‑‑from taking supplements that weren’t well regulated.

 

Andrew Schorr:

So, as you know, so many of us complain about fatigue with CLL.  What can we do about that?  Is there any medication or something you feel comfortable about as a supplement that could help with that?  Certainly, we’ve been telling people exercise is a good thing and can give you more energy, but what do you tell your patients when they talk about fatigue?

 

Dr. Furman:

So this is actually a very common question, and I really do believe it’s very important to remember that having CLL doesn’t protect you from the things that befuddle the rest of us.  So the most common cause of fatigue in a CLL patient is not going to be the CLL but it’s going to be the same thing that befuddles the rest of us.  So it’s poor sleep hygiene.  It’s not sleeping long enough.  It’s all those things that really should be addressed first and foremost.  So we see a lot of sleep apnea that’s undiagnosed.  We see a lot of people who are just not sleeping long enough.

If we’ve ruled out everything else and a patient seems to have progressive disease, yes, there are definitely patients with CLL whose fatigue is related to the CLL, but I’m a big believer that fatigue related to CLL should only be present in a patient who really has active signs of CLL.  So if someone is on watch and wait and their lymphocyte count is not changing and their lymph nodes are not enlarged, their fatigue is not going to be related to their CLL.

But if someone’s lymphocyte count’s climbing and their lymph nodes are growing then certainly their fatigue might in part be related to their CLL.

 

Andrew Schorr:

Okay.  This has been like being on a game show.  I keep throwing things at you.  I want to thank you for all your time.

Folks, we’re going to let Dr. Furman go, but we will be doing other Ask the Expert sessions and doing some live broadcasts in from ASH.  ASH, you alluded to, Dr. Furman, always has more coming out, more longer range studies, combination information.  So just to wrap up with, for those of us living with CLL, and, thank god, so many of us long term, me, 22 years, are you very hopeful that you have more options for us now no matter what our CLL situation is?

 

Dr. Furman:

I really do.  I think we have some amazing options now.  We have also the data that our current crop of novel agents really can be safe and effective long term, and that’s what I really think is so important to be cheerful about.

And in those patients who do progress we have a whole crop of other agents that will prove to be hopefully effective in those situations.  But I think it’s going to be the‑‑you know, the home run though is going to be the combination of BTK and Bcl‑2 inhibitor therapy or PI3 kinase and Bcl‑2 inhibitor therapy because in those situations I really do see patients getting very, very deep remissions that I hope will be extremely long lasting.

 

Andrew Schorr:

Think about it, folks.  I mean, I got FCR, a three‑drug combination, in 2000, 18 years ago, and it worked for a long time.  So the idea of combination therapy has worked well in cancer therapy hitting those cancer cells in multiple ways.  Dr. Furman, thank you so much for being with us today.

 

Dr. Furman:

My pleasure.

 

Andrew Schorr:

Okay.  From Weill Cornell.

And I just want to mention for our audience, remember we’ve got a lot coming up.  On Wednesday, November 28, we’re going to understand the ins and outs of watch and wait for those of you who are in that situation.  From the big ASH meeting in San Diego‑‑yay, I don’t have to get on a plane to go anywhere‑‑we’ll be also doing live broadcasting so be sure to be signed up for that.

And then on December 5th we’re going to talk about the financial issues because, as Dr. Furman talks about, combining these oral therapies, these are expensive, and so what support is there for you so you get the combination should you need it and it’s affordable.  So keep an eye on that.  Go to the Patient Empowerment Network’s website, powerfulpatients.org, and take a look at what we have on Patient Power as well.  Thank you so much, Dr. Furman.  Thanks to our audience and stay tuned for what comes out of the ASH meeting.  I’m Andrew Schorr.  Remember, knowledge can be the best medicine of all.

Please remember the opinions expressed on Patient Empowerment Network (PEN) are not necessarily the views of our sponsors, contributors, partners or PEN. Our discussions are not a substitute for seeking medical advice or care from your own doctor. That’s how you’ll get care that’s most appropriate for you.

Notable News: November 2018

November is National Lung Cancer Awareness Month, and if ever there were a cancer that needed an awareness month, it’s lung cancer. Sometimes referred to as the invisible cancer, lung cancer is a disease caught up in a smoke cloud of misconceptions, and those misconceptions can prevent patients from early detection, treatment, and support. Several of the myths and misconceptions about lung cancer are addressed and dispelled in a recent article at fredhutch.org. One of the main myths is that you only need to worry about lung cancer if you are or ever were a smoker. That’s simply not true. In fact, people who have never smoked can get lung cancer, and it can be a genetic disease. Other myths include the belief that there are no early detection screening processes and that there has been no progress in lung cancer research. While it’s true that other cancers seem to have more screening options and better prognosis, advancements are being made in lung cancer. Organizations such as Patient Empowerment Network are making progress in building awareness and reducing the stigmas about lung cancer. See the rest of the myths and misconceptions and how they are dispelled here.

There is nothing sweet about having lung cancer, but there may be a sugary clue that could lead to earlier detection, reports forbes.com. Researchers have discovered that early-stage, non-small cell lung cancer (NSCLC) tumors and precancerous lesions produce high levels of a molecule that they use to consume sugar to help fuel their growth. The molecule, called SGLT2, could be used to detect early stage NSCLC. Researchers also found that a diabetes drug, which blocks SGLT2, also prevented tumor progression in mice, which shows promise for possible future treatment of NSCLC. Further studies of SGLT2 could hinder the development of malignant NSCLC, and more information about this hopeful development can be found here.

Another hopeful lung cancer development comes in the form of a hot needle, reports dailymail.co.uk. The treatment, called radio frequency ablation, is being used to diagnose and treat difficult-to-reach tumors. In addition to being able to destroy the tumor by heating it up with radio frequency energy, doctors are able to use the needle to remove part of the tumor for biopsy. The needle works in place of attempting to access the tumors through invasive surgery. The hot-needle treatment is considered safe for repeated use, and a report showed that half of the patients treated with the hot needle survived at least five years. More information about this hot new treatment can be found here.

We would be remiss if we didn’t note that November is also National Family Caregiver’s Month. There are approximately 43.5 million unpaid caregivers in the United States and they are a critical component of a cancer patient’s journey. It is important for caregivers to make sure they are practicing self-care as well, and there are a number of resources available to them to help ensure caregivers have the information they need to care for their loved ones and themselves. The PEN Path to Patient Empowerment guide provides resources for care partners, including links to the Family Caregiver Alliance website and the American Cancer Society Caregiver Resource Guide. Chock full of information for caregivers about caregivers and the patients they care for, these resources are a must have for any caregiver and can be found here and here.

Oh, and November is also the month where we give thanks. Happy Thanksgiving from the PEN Family to your Family. We are thankful for you!

Molecular Profiling, Cancer, and You

When you get a cancer diagnosis, your doctor might, or might not, bring up the topic of molecular profiling. If s/he doesn’t, you definitely want to bring it up yourself, and here’s why: the results of that molecular profiling can significantly impact your cancer treatment options.

The conversations about this topic that I have been privy to, in both patient and clinical communities, tell me that not every doctor is aware of the full array of genetic testing options for every type of cancer. This means that patients need to fully participate in conversations about tools that put precision medicine on the table, which start with conversations about molecular profiling of your specific cancer cells. If your clinical team doesn’t bring it up, you need to bring it up.

Another conversation gets opened when you bring up molecular profiling for your cancer: the one about insurance coverage. Genetic testing is less expensive now than it was ten years ago, but it still carries a pretty hefty price tag.  There isn’t a lot of hard data on the cost of specific tests – like much of healthcare, it seems to be a case of “if we tell you, we’ll have to kill you” when it comes to price tags before purchase – but commercial tests like Caris Molecular Intelligence (formerly Target Now) (priced at $5,500) and OncInsights (priced at $4,000) are pretty steep, particularly if you have a high deductible plan. If your health plan covers testing you’re, well, covered. If not, you’ll have to pony up some serious coin to get your cancer’s molecular profile.

Here’s where the power of community in cancer comes into play. If we, as people dedicated to transforming cancer treatment – patient, clinician, policy wonk, family caregiver, or all of the above – work together to push for full coverage of molecular profiling as both a standard of care for cancer treatment, and a 100% covered service to cancer patients, we’ll start seeing some “cancer moonshot” promised become reality.

Since medicine is a science, and scientists want proven data, here are some tools to use to advocate for making molecular profiling standard, and covered. From the Journal of the National Cancer Institute in 2011, Ready or Not: Personal Tumor Profiling Tests Take Off; from the Journal of Clinical Medicine & Research in 2004, The Promise of Molecular Profiling for Cancer Identification and Treatment; from Medscape in 2014, Can Molecular Profiling Lower Cancer Costs?

If you’re dealing with a cancer diagnosis right now, and want to bring up molecular profiling with your clinical team, here are the key questions to ask:

  • What are the benefits of molecular profiling for my specific type of cancer?
  • Is my cancer tissue a good candidate for molecular profiling?
  • Will molecular profiling improve my treatment options?
  • When should my cells be tested?
  • How much will testing cost, and will my insurance cover it?
  • What if I’ve already had treatment — does molecular profiling give me any options?
  • What are the risks of testing?

The answer to your cancer lies in its DNA. Don’t miss a chance to survive, and thrive – put your DNA to work in your cancer treatment.