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Patient Profiles: Breast Cancer Part I

Female breast cancer awareness, with it’s pink ribbons, and Save the Ta-tas t-shirts, and fundraising 5Ks, sweeps into October each year with the same prevalence as pumpkins. No other cancer has managed to garner as much support, attention, or money. But, even without the pink campaigns, the prevalence of breast cancer is not a secret. An estimated one in eight women is diagnosed in our country, and there are about 1.38 million new cases worldwide each year. You’d be hard-pressed to find someone who doesn’t know a breast cancer survivor. This month, in a three-part series, Patient Empowerment Network is taking a closer look at five survivor stories and one caregiver. These women represent the more than 3.1 million women in the United States who have a history of breast cancer. In today’s installment, you’ll be introduced to five of the six women, and you’ll learn that getting a breast cancer diagnosis wasn’t really a surprise to any of them.

Breast cancer survivors are interlaced through all of our lives, and there is something very endearing about how openly willing they are to share their stories. They freely talk about their diagnosis and treatment, but more than that, they talk about their darkest moments alone in the hospital, or their need for counseling after treatment. They discuss the lengths they will go to endure invasive treatment that may prolong their lives, and they share their prayers to live long enough to see their children grown. They are so deeply candid that it’s as if they are inviting you to be a guest for the day in their exclusive club.

Only it’s a club you don’t really want to be a part of, says Betty Abbott, who was diagnosed five years ago. She was 72 at the time, and her cancer was ductal and non-invasive. She says it’s the kind you want to get if you’re going to get it. But, is there really a kind of cancer any woman wants to get? While the death rates for breast cancer have been decreasing since 1989 thanks to increased awareness, early detection, and advances in treatment, breast cancer is still the second leading cause of cancer deaths in women in the United States, second only to lung cancer. In 2018, approximately 40,920 women are expected to die from breast cancer.

Cancer is cancer, no matter the stage, the type, or the form. “That’s the thing about breast cancer…it’s still cancer,” says Liz Abbott. She’s Betty’s daughter. The two are very close, and Liz was with Betty every step of the way through diagnosis and treatment. Liz hasn’t had breast cancer…yet, but she fully expects to get it. She knows the statistics. Even though less than 15 percent of people who get diagnosed with breast cancer have a relative diagnosed with it, a woman’s chance of getting breast cancer nearly doubles if a first degree relative (a mother, sister, daughter) has had it. So many women get breast cancer, so many families of women, that for some women it’s no longer if they will get it, It’s when. Since her mom’s diagnosis, “our new realities are very different,” says Liz, who can’t help but worry if breast cancer is her own daughter’s path as well.

It was the path for Shannon Knudsen, who was diagnosed three years ago, when she was 43. Like Liz, Shannon was very close with her mother and walked with her through diagnosis and treatment of breast cancer. Shannon’s grandmother and great grandmother had breast cancer as well. So, for Shannon, breast cancer was never an if. “I never thought I wasn’t going to get it,” she says. “It was always a matter of when.” So Shannon wasn’t surprised by the diagnosis, but she says she was angry. You see, while she was prepared and had a plan, cancer still managed to throw her what she calls “an interesting little twist”.

Since she watched what her mom went through, being diagnosed at 49 with recurrence as leukemia 16 years later that was ultimately terminal, Shannon was diligent about staying on top of cancer research, and as soon as she learned that genetic testing was available, she looked into having it done. She was absolutely positive that her family carried the BRCA gene mutation. The BRCA1 and BRCA2 genes produce proteins that help repair damaged DNA cells. When either of the genes has a mutation and the genes don’t produce the protein or function correctly, DNA cells are more likely to develop changes that can lead to cancer. There are specific mutations of the genes that increase the risk of female breast and ovarian cancers. People who have inherited the mutations, which can come from the mother or the father, are more likely to develop breast and ovarian cancers at younger ages.

As soon as Shannon’s insurance covered the testing, she had it done. Fully expecting a positive result, Shannon was prepared to have a preemptive double mastectomy with reconstruction. But, Shannon’s results were negative. She doesn’t carry the BRCA 1 or BRCA 2 mutations.“I was shocked,” says Shannon, and she feels like the results gave her a little false security. That’s where the anger came in, because in August 2015, when her mammogram and subsequent 3D testing showed a black and jagged spot of concern, she knew that meant she was bound for chemotherapy, and that was something she had always planned to avoid by having preventive surgery. “I was 100 percent prepared to do that, and it didn’t work out that way,” says Shannon. Cancer, as it often does, had other plans.

Cancer had other plans for Tina Donahue as well. “It was a really, really difficult time in our lives,” says Tina of her diagnosis in 1991. It’s not that Tina wasn’t expecting to get a diagnosis at some point. She also had a family history of the disease, her maternal aunt died from breast cancer, and Tina was a nurse so she had a keen understanding of her risk, but when she was diagnosed at 44, she had just been promoted to an executive vice president position at work, and she had three young sons. She was also in school to get her MBA. Cancer was not part of her plan, and she thought she was going to have to quit school when she was diagnosed. However, thanks to the support of the other women in her study group, Tina didn’t have to quit school. She says the women rallied around her, told her not to quit and helped her, encouraged her, and tutored her through.

When it came to treatment, Tina and Shannon, though diagnosed more than 20 years apart, had very similar methods. “I just wanted to hit it as aggressively as I could and give myself as much life as I could,” says Shannon. She told her surgical oncologist that hers would be the easiest consultation ever. She had done the research, she knew the risks, she knew exactly what treatment she wanted. Tina, who also wanted to treat her cancer aggressively says she told her doctors, “Give me everything you’ve got.” Both women had a double mastectomy and reconstruction with silicone implants. Tina says her implants lasted 23 years before she noticed they started getting folds in them, which was a sign that both implants, though contained, had burst, and she had to have them redone. Shannon’s implants are a newer technology called gummy bear implants and are designed so that they won’t burst. Tina says the silicone felt and looked more natural, and Shannon says that was important to her as well. Tina also says that if she hadn’t been a nurse who had seen a lot of recurrence in women who had had a single mastectomy, and if she hadn’t been witness to her aunt’s experience, she may not have opted for the double mastectomy.

Diana Geiser did not opt for the double mastectomy, but now says she wishes she had. Diagnosed at age 50, Diana says she struggled with the decision at the time and remembers feeling like she wanted to keep part of herself. “Now I wish I’d done both,” she says explaining that one of the draw backs is that her natural breast gets bigger or smaller with weight fluctuations, but her reconstructed breast does not.

Regardless, all three women had four rounds of chemotherapy. They all had clear lymph nodes, and were hormone-receptor-negative (HR negative), meaning that it was likely that hormonal therapies wouldn’t work for them. Tina, still wanting to treat her cancer aggressively, says she wanted to kill everything and had low dose chemotherapy. She lost some of her hair, but not all of it. For Shannon and Diana, the pathology reports came back showing their tumors were aggressive, Shannon’s highly so, making chemotherapy necessary. They both lost all of their hair, which is something that must be incredibly pertinent to breast cancer survivors, because whether they did or they didn’t lose it, they all tell you about their hair.

Next time, in Part II, meet Meredith.

 


Sources:

https://www.breastcancer.org/symptoms/understand_bc/statistics

https://www.breastcancer.org/symptoms/diagnosis/hormone_status

https://www.breastcancer.org/research-news/20080813

http://www.who.int/cancer/events/breast_cancer_month/en/

https://www.cancer.gov/types/breast

https://www.cancer.gov/about-cancer/causes-prevention/genetics/brca-fact-sheet#q2

Ask the MPN Expert – Dr. Naveen Pemmaraju

Ask the MPN Expert – Dr. Pemmaraju

“Ask the Expert” session with MPN specialist Dr. Naveen Pemmaraju from The University of Texas MD Anderson Cancer Center.


Transcript:

Andrew: And greetings from near San Diego, Carlsbad, California. I’m Andrew Schorr from Patient Power. Welcome to this patient empowerment network program, and thanks to Incyte Corporation for helping make it possible. They have no editorial control. I’m a myelofibrosis patient, have been for several years, so I’m vitally interested in this. Welcome to our MPN community, and welcome to one of our favorite experts joining us from MD Anderson Cancer Center in Houston. There’s Dr. Naveen Pemmaraju. You can see behind his desk there all the working on the cures of tomorrow, but Naveen, thank you so much for being with us.

Dr. Pemmaraju: Thanks for having me, Andrew. My pleasure.

Andrew: Okay. Let’s get right started. We’ve gotten all sorts of questions in. If you have a question, send it to MPN@patientpower.info, but we’ve gotten a lot already and I’ll start to buzz through them over the next 30 minutes. This question is from Cynthia and she says, “I was diagnosed with ET (Essential Thrombocythemia). I’m JAK2 positive,” so she has that JAK gene. “When I was 66 years old,” now she’s 68, I’m about to be 68 as well, “What markers on my blood work, asides platelets, are important for my doctor to watch? What indicates a need for another bone marrow biopsy?”

Dr. Pemmaraju: Well, thanks, Andrew. And thanks to the question from Cynthia out there. This is very important. This is what we talk about day-to-day, week-to-week in the clinic. There are a couple of perimeters outside of the platelets. One, I would say the most important for us to watch are the other of the big two. That’s your hemoglobin number, also known as anemia; if it’s too low, or polycythemia, if it’s too high, and then the white blood cell count is also very important. Again, if too high, or too low, it can tell us what’s going on.

With ET, the key thing is it can transform, or change into any of the other MPNs. For example, PV (polycythemia Vera), myelofibrosis, or – and I hate to mention it, but it does happen five, maybe seven percent of our patients, where the disease can go to Acute Myeloid Leukemia, AML. So, distinct blood count changes, either too high, or too low, can give us clues if the MPN is changing, or in fact, going to AML.

And so, the answer for a repeat bone marrow is based on that, which is, let’s look together, patient and provider to see if there are subtle or avert changes in the blood counts that are markedly different from the previous visit, rather than having a pre-prescribed, every three months, or every six months type of a deal.
Andrew: But, Naveen, with all you’re doing now with sophisticated testing, do you still have to poke us in the hip, or couldn’t they just do it from our arm?

Dr. Pemmaraju: I wish, Andrew. I think this is very important. I think with the juxtaposition, you have this sophisticated gene panel testing, JAK2 CALR, MPL, and yet we’re still sticking a needle in people’s backs in a very painful procedure. Nothing still has overmatched as the gold standard, the bone marrow aspiration biopsy. So, for now, we’re – pun intended, I guess – stuck with this procedure. But your point is a good one. For example, with bone marrow transplant, can you believe it nowadays, they’ve moved from not having to exclusively do it from bone marrow source to peripheral blood, so I think you’re on the right track and we need to work on different ways of accessing this important information.

Andrew: Okay. One thing about bone marrow biopsy, it doesn’t have to be painful. It’s uncomfortable, but it doesn’t have to be painful if you have somebody experienced doing it.

Dr. Pemmaraju: I wanna emphasize how right that is because at least here, at our center at MD Anderson, as you know, we have a team that is dedicated to doing it many, many people, many repetitions doing it, so there might be local discomfort, but a lot of our patients do not experience pain. I’m glad you brought that up.

Andrew: Right. And that’s been my experience both there, and at other major centers. Okay. Here’s a question from Denise. Denise says, “I have PV and I’m trying to improve my health by making smoothies containing large amounts of dark green vegetables, such as spinach, kale, and watercress. I’ve been warned by some members of our community that these foods will increase iron and raise the hematocrit, putting me at risk. Is that true? And should people with PV avoid these foods that are high in vitamin K?”

Dr. Pemmaraju: Well, this is an important question and I remember five to 10 years ago we would say things like, “Well, we don’t really know the answer,” or you know, “Diet doesn’t really have anything to do.” But now with more and more understanding of the total therapy for patients and approach to the whole body, I think this is an important question. So, yes, iron levels do matter. Too low, then you’re iron deficient. (That can definitely happen in our patients.) Too high, potentially may fuel the fire, if you will, for polycythemia Vera.

So, I think iron levels are important to watch and certainly can be increased by what our question is being asked about. But there’s another aspect, too, that some of the medications that we prescribe and take. One example is Coumadin, or Warfarin that a lot of our patients know, which is a high-level blood thinner. It’s an anticoagulant. And man, oh, man, that is exquisitely dependent on the vitamin K pathway. So sensitive, that in some patients in some cases even salad consumption, or spinach, so healthy foods because of the vitamin K level in them can alter this level. It’s called the INR. And so, it’s something we have to watch out for.

So, not only in terms of iron metabolites, but also drug-to-drug interactions. So, it is always best to mention these things when we’re going on new medications.

Andrew: Right. Talk to your doctor.

Dr. Pemmaraju: Talk to your doctor.

Andrew: What you’re doing –

Dr. Pemmaraju: Everything.

Andrew: – what you’re eating. Yeah. Okay. Here’s a question from Sally. Sally says, “I have ET with the MPL mutation. So, I have JAK, but there’s also MPL. I believe, not much is know about my mutation. Can you shed light on it, or me and our community here today?”

Dr. Pemmaraju: Yeah, great question. So, when I look at these mutations as the big three, I go back to the time of William Dameshek, who hypothesized in the ‘50s and ‘60s that MPNs would be a unified group of diseases; ET, PV, and MF. And now, 67 years later, we’ve proven that. So, JAK2, we’ve known about since 2005. The most common, most major recurring mutation, fifty to 60 percent of patients of myelofibrosis. Then in 2013, 2014 the CALR mutation was elucidated. Can you believe, that’s only been four, five years. That’s the second most common. But there’s a third of the big three. That’s the least common, the MPL; MPL mutation.

That’s a mutation in something called the thrombopoietin receptor (TPO), which is in charge of helping to stimulate and make platelets. So, in terms of MPN patients, it does make sense and it has something to do with platelets, and that axis. It is the least common; by far the less common of these three, so I would say maybe something to the point of three to seven percent of our patients will have it.
Up until recently, we didn’t know if it had any prognostic significance, but our Italian colleagues published a very nice paper in Blood a few years ago, independent of the IPSS risk, that I’m sure we’ll talk about later. That if you just take patients with myelofibrosis, not ET and PV, you can stratify our patients based on the mutation risk. And not everyone knows about this.

For example, in this scoring, CALR mutation alone is the best prognosis for our patients. JAK2, or MPL is what’s called an intermediate prognosis, and the so-called triple negative, if you don’t have any of these big three, the implication being that you likely have something else, like ASXL1, then those patients tend to have the worst prognosis. So, MPL helps us to diagnose and confirm an MF diagnosis, and it also may have prognostic significance in our modern era.

Andrew: Okay. I don’t want people to freak out because this is a moving target as they learn and say, “Oh, my god. I have triple negative…

Dr. Pemmaraju: That’s right.

Andrew: Right. Okay? Because there’s progress going on all the time.

Dr. Pemmaraju: Well said.

Andrew: This is what they’re learning now. Okay. Now. Here’s the big one and you mentioned it. You said, a small percentage of us with myelofibrosis have the risk of progressing to AML. I know there been a lot of new drugs now either approved, or in development for AML. And some that help people who have secondary AML.

Dr. Pemmaraju: Oh, yes.

Andrew: Right? But tell us about the risk of progression, and then what do you do about it?

Dr. Pemmaraju: Right. So, that’s a great topic, and as you know, you’ve been doing this for so long now. This has often been a very not great part of the conversation, but it’s an exciting time for our patients based on the research I’m about to share. So, the first part is progression to AML, which we touched on earlier. We do have an objective prognostics scoring system. Actually we have so many scoring systems now that many of our patients are starting to see them.

But the IPSS, or International Prognostics Scoring System, was first developed by our colleague, Cervantes et al, this is right before 2010, so ’07 to ’09. That one is supposed to be applied at diagnosis and based on five of these risk factors, we can prognosticate, or tell which of our patients are at a higher risk for AML. And so, a lot of our viewers ask that. So, it is true. Age – over a certain age, white count of 25,000, circulating blasts, constitutional symptoms, and anemia made up that original five.

Since that time, there are dynamic scoring systems, DIPSS, DIPSS+ and others that include, or modify as some of those risk factors. So, we can tell, at least based on a textbook impression, who has a higher likelihood of going to AML. Once our patients go to AML, there’s a lot of hope now. There have been four – count them – four new FDA approvals for AML in just the last 12-24 months. They apply to different segments of AMLs, two of them are targeted therapy, so one drug called Midostaurin hits the FLT3 inhibitor, one drug hits the IDH1 and 2. Actually those are two separate drugs.

The drug you were referring to had a code name CPX-351, or VYXEOS, and it does have an approved label for so-called secondary, or therapy-related AML. Although I will caution our viewers that – MPN patients, specifically, we’re not included in those early data sets. They were more geared towards patients with MDS leading to AML, but the principle is there for us.

And then finally there’s another drug called Gemtuzumab or Mylotarg. So, you have four FDA approvals, ongoing clinical trials with combination therapy, excitement and ongoing investigation for CAR-T cells, optimizing stem cell transplant, and then combining possibly MPN drugs with AML drugs in a clinical trial setting. So, I think this is actually a very, very important time to talk about AML in all of our MF and MPN sessions.

Andrew: Okay. Just one brief question, and – if someone like me, where I’m on Jakafi myself, but if that sort of poops out, or that, or another medicine is not working for me, and I’m developing AML, do you feel now it’s a more hopeful time than it’d had been previously?

Dr. Pemmaraju: I do, Andrew, and you know me. I used the word ‘hope’ very seriously and very carefully. Before with AML – and I mean, just five to seven years ago, it was not as hopeful of a time for us, as researchers, and for our patients. Not just because of the FDA approvals. That obviously is very encouraging and applies to a lot of our patients, but also because of the funding, the research, and the ideas for combination chemotherapies, and the emergence of these immune therapies. I think it’s a hopeful time for all of us involved with AML.

And specifically as you were mentioning this secondary, or post-MPN, or post-MDS AML, which is largely been an urgent unmet medical need.

Andrew: Okay. And just to everybody understands, AML, Acute Myeloid Leukemia, so it’s acute and as has been in the past a five alarm fire and now they’re developing medicines for that. All right. Let’s go on. Bonnie has a question. “I have myelofibrosis and my only symptom is that my spleen is enlarged. I’m on Hydroxyurea, but hesitant to switch to Jakafi or Ruxolitinib. Assuming no real discomfort and just moderate weight loss and stable blood counts, does an enlarging spleen itself cause problems?” And also, I guess the bigger question, Naveen is, is there a penalty for waiting if there is a treatment that might line up with what you got?

Dr. Pemmaraju: You’re right on. Yeah. This is very, very serious, important topic. So, for the first part of the question, the spleen itself being enlarged can in fact cause some really, really big problems for a lot of our patients. It is true, as the questioner’s asking, that one can have mild splenomegaly. So, a spleen that’s slightly enlarged, not yet causing physical symptoms of early satiety, which means getting full fast, or physical discomfort, but a lot of patients do have that. So, yes, a big spleen alone can cause not only local problems, but also systemic. Because again, it’s a disease of cytokines; messengers and proteins that are being scattered all throughout the body, causing the body to feel flu-like symptoms, or fatigue.

Now, the studies for Ruxolitinib are very specific. These are two Phase 3 studies, they are called Comfort 1 and 2, published in the New England Journal five six years ago now. And they did include patients with intermediate to, or high-risk disease. Or intermediate to high-risk disease, shall we say. And although the spleen itself doesn’t come out in the scoring system, some position is that it should be patients with more advanced, or higher scoring diseases than say someone with lower risk disease.

So, with the trial data that we have we know a couple of things. 1) The drug got approved in those more advanced patients. 2) There was early crossover that was allowed. So, one of the comfort studies, Andrew, was as you know, randomize to placebo. So, no active therapy, and one was best available therapy. Even with the early crossover allowed to the Ruxolitinib, both are not showing overall survival benefit. Translated into more layman’s terms, what that means is, it does appear, maybe, possibly, that if you got the drug at the beginning early on, there looks to have been some long-term benefit.

We won’t know that until further studies are done, and those studies are being planned. Those are called ‘early intervention’ studies, so people at a lower, earlier stage, low risk, Intermediate 1, and I think we’ll all be eager to see how that benefits our patients.

Andrew: Okay. Great. So, the penalty for waiting – right now it appears there could be a penalty. In other words, it could be better to get on it. Don’t wait. If you and your doctor agree, there’s a therapy for you.

Dr. Pemmaraju: I think that’s exactly the resource position to take, which is I think that – I believe that there are a subset of our patients who exactly fit what you said. They are symptomatic, out of proportion to the risk scores that are available. The spleen is highly enlarged, although they have lower intermediate risk by IPSS. And that’s exactly the are of investigation for myself, and our colleagues. And even in the clinic there might be some role to assessing patients as you said like that. So, it shows you the limitation of these text book scoring systems and how much research we have left to do.

Andrew: Okay. Well, you know more than you did before, so, I –

Dr. Pemmaraju: Well said.

Andrew: – I’m happy about that. Okay. So, here’s a question from Jane. She says, “I have myelofibrosis, but it’s not progressing, and I’m CALR negative.” So, that’s one. “I’m JAK negative.” That’s two. “And I’m waiting to hear if I’m actually triple negative, as you said, which would be JAK, CALR, and MPL. Are there medicines to slow progression for me?”

Dr. Pemmaraju: Well, that’s the ultimate question. Isn’t it? So, the first concept is this triple negative. And if our viewers have heard that before you have, that was borrowed from the breast cancer literature, which was a similar sentiment, which is having the top three markers negative. And just in that case, as in RMF, the supposition is the same, that that means that you have a higher risk disease.

But going from negative to positive, what it does mean now with the new sequencing and molecular studies that are coming out, is that it really looks like 90 percent, maybe even close to a 100 percent of patients, have some form of a molecular driver. And those other mutations you’re going to start to hear about are becoming common; ASXL1, TP53, EZH2, IDH, etc. etc. So, triple negative may mean that we don’t have those big three, but there might be something else that’s driving the MF, and it means that it’s a higher risk to progress to AML and for some patients to not do as well.

But this questioner brings up a very good point. What the textbook risk score says does not have to imply to each individual patients. So, just because the finding is that, okay. Triple negative patients as a population may do worse, it may not apply to that individual patient. So, in this person’s case, maybe they’ve been diagnosed very, very early. That’s a good thing. Maybe the driver mutations and the triple negative matter, which is what I think. So, ASXL1 mutation vs. some other ones.

And then finally, each patient is different. Everyone’s case is different. You have other co-morbidities, other underlying drivers of disease. So, I think that’s the good point. But, we do have to say, at least for right now, I like your phrase ‘of a moving target’. The understanding that if you are this triple negative disease in this classical sense, should mean that you are a higher risk at some point to progress, as compared to others in your group, and so, possibly closer monitoring and observation is necessary.

Andrew: Right. And see an MPN specialist. Because what if there’s a drug in development that’s an AS – What is it? AS –

Dr. Pemmaraju: ASXL1.

Andrew: Inhibitor. And that’s driving your bus. Right? Maybe you wanna be in that trial. [

Dr. Pemmaraju: Absolutely right. Clinical trials are important for all of our patients with any rare cancers, or any cancers in general.

Andrew: Right. Okay. Let’s go on. I just wanna take this question from Susan. It really rang true for me. Susan writes, “Is it common for an ET patient to experience numbness in the scalp, ears, and face? I’m currently on 1,500 milligrams of Hydrea daily.” And I wonder if you can broad this out because I was telling you before the program, I’m getting every once in a while – I wake up with a little prickliness. Not itchy, and I go back to sleep, but is that related to my MPN? So, she has scalp questions, is it the MPN, ET whatever? Is it the medicine?

Andrew: This is coming up in my clinic on a weekly basis. The short answer is, yes. It’s always due to the MPN. And I’m here to tell you why. This is an underappreciated part of what we do as healthcare providers in patients. For anyone who’s ever filled out the Myeloproliferative Neoplasm (MPN) Symptom Assessment Form Total Symptom Score:, developed by Ruben Mesa, his colleagues, now shortened down to a nice, nifty 10 ques – sheet. You know, actually, peripheral neuropathy is one of those 10 questions. Do you have numbness and tingling? So, even though we don’t talk about it, that’s our fault, peripheral neuropathy is a thing. It’s a common aspect of the MPN.

No. 2 is – and you brought this up to me nicely as well, is some of the mediations that we prescribe at the chemotherapeutic level can also cause nerve damage and neuropathy. JAK inhibitors either as a class, or some of these individual ones, both FDA approved in clinical trials have been associated with either a central, or peripheral neuropathy. So, I think that’s another big aspect.

And then finally, I hate to say it, but these drug-to-drug interactions of all of these medicines can cause that. When you factor that, plus vitamin deficiencies, thyroid deficiencies, iron abnormalities, restless leg syndrome, our patients have a host of reasons to have neuropathy. Usually this is an intermittent phenomenon, a come and go phenomenon. When it starts to become more of a permanent phenomenon and progressive, that’s a big concern, and that would really require a separate neurologic work up.

True, there are some chemotherapy drugs that can cause that, but I would say that would necessitate a multi-disciplinary approach; neurologists and all of this kind of thing.

Andrew: Okay. You used the name of a drug that people take. Is a blood thinner, Coumadin. Somebody may take diabetes medicines, I also have Chronic Lymphocytic Leukemia and take medicines for that. Okay. So, if we’re developing some of this and we have an MPN, which of the many doctors we have doo we go to first – do we go to you as our MPN specialist? Do we start there?

Dr. Pemmaraju: Yes. Absolutely. I think the phrase and the motto of every MPN expert that you’ll meet (and you and I know all of them now) is, ‘Tell us everything.’ Because I will tell you what. Now that we have more understanding – not full understanding yet, but more understanding of the biology of these diseases, it turns out that a lot of things that are happening are due to MPN.

One example I’ll give you, Andrew, our colleague and friend, Claire Harrison has pioneered this phrase called, ‘presenteeism’. Presenteeism. Not absenteeism, as we learned when we were younger. The concept that our patients with MPN are there, they’re here at work, with their loved ones, they’re at dinner, but they’re not really there. That’s also a question on the questionnaire; inability to concentrate. Subtle, subtle, subtle, but this is part of the MPN process. We’re not talking about it enough, but programs like this will get the message out there. So, tell your MPN doctor everything because more than likely they know it’s part of the MPN.

Andrew: I gotta tell my wife. I’ve been married 33 years.

Dr. Pemmaraju: This is all recorded, so you can tell her.

Andrew: All right. Esther, where are you? Okay. No. Let’s go on. So, Heather sent in this question. “My local hematologist, oncologist will only give me a phlebotomy after my hematocrit is over 51. What is the standard marker? I have PV and I’m really struggling with symptoms.”

Dr. Pemmaraju: I actually have data to share with you and your viewers. So, before four years ago, we did use to do it either based on convention, symptom burden, or a pre-designed abstract number. But now we have data. So, our Italian colleagues, Barbui and colleagues published in the New England Journal about four years ago a very nice paper that starts to answer this question. They randomize patients with P. Vera to two groups. They called it a liberal group, where you could get phlebotomies at any number essentially just like what’s being asked here, and then a more stringent group, which they came up with the hematocrit goal of 45 and below. Or below 45.

And the trial was actually stopped early because it showed a four-fold decrease in cardiovascular morbidity and mortality. That means, four times less chance of people having cardiac events or cardiac deaths in the stringent phlebotomy group. That is when you put the goal below 45. Yes, it’s only one study, but it’s with several hundred patients with P. Vera in a nice controlled situation. So, that has become a lot of us – for us, the de facto of standard of care.
So, I would advise, if you’re a higher risk patient with P. Vera, the so-called triple therapy approach, where you’re doing, you know, baby aspirin if you qualify. The phlebotomy goal of 45 and below, and then of course, cytoreductive therapy if you need it in the higher-risk situation. So, 45 and below, it should be validated, we should do more studies here in the States, but that’s something that I think we can use with high-level data.

Andrew: Okay, thanks. Here’s a question we got in from Kimberley. She says, “My daughter is 22, she was diagnosed in 2013 with ET, and she’s been on Hydroxyurea, but is decided she no longer wants to take the med. What should she be aware of, or cautious about, given that she’s no longer taking it?”

Dr. Pemmaraju: Ugh. Well, this is an area that’s very dear to me and very important to my research. With our group here, with Dr. Serge Verstovsek and my colleagues, we just published a paper on our experience with adolescents and young adults with MPN, or AYA. As its own separate field, AYA cancer has become a very important understanding that really didn’t exist, in my opinion, 20 years ago. But our patients are not always older patients. So, young patients can get MPN, too. Yes, patients in their teens and twenties can get them just like this questioner.

So, this is a type of patient that I’m seeing quite commonly in the clinic. Couple of points to say. One is, who can blame her? Who wants to take a life-long, indefinite oral chemotherapy that may or may not have short-term and long-term side effects? In our study what we found is, approximately 10 percent of our patients met this definition. The NCCN gives it, I think, age 16 to 39. So, younger than 40. And out of those patients, I was surprised to see that a good seven percent had a thrombotic event. That means a blood clot, either at the time of diagnosis just prior to, or just after. Well, that’s a pretty good clip, and that would be more than the general population than what you would expect.

The problem with the young patient with MPN has several issues. One is, what about at the time of fertility and pregnancy? Two, what about at the time of surgical procedures? I’m talking about routine things, such as dental and other care. And then three, as they start to transition into their older adult years. So, in this patient’s case, this is a very difficult thing. We don’t have many drugs. We have Hydroxyurea, we have Interferon, which possibly might be better for a younger patient. If someone has myelofibrosis, there’s no age requirements. So, if you qualify, then the JAK inhibitor, as a class.

But this is just one of those in-between, vulnerable populations, and we really don’t have great treatments for in general, an AYA cancer, and specifically here. And so, the main thing that we would say to this person is, really, really close follow-up early on with an MPN expert, as you always advocate. Two, is at the time of fertility planning, pregnancy in our family planning is to have high-risk maternal-fetal experts involved early on. (I think, this is something important.) And three, really cautious planning in and around surgical procedures, looking for bleeding and blood clots. I think those are some basic guidelines for anyone to follow.

Andrew: Well, great advice for mom and daughter. I wanted to post this, just a quick question from Caroline who lives in the United Kingdom is diagnosed with primary myelofibrosis four years ago at age 49. And she said, “I’ve tried to find others with myelofibrosis of a similar age, but so far no luck.” So, is being diagnosed at her age, age 49 with myelofibrosis, unusual?

Dr. Pemmaraju: There you go. That’s perfect. So, that also goes along with our “Young people get MNPs as well.” This was a disease – first of all a disease, now we recognize it as a cancer that was thought to be 60, 70, 80, 90 and older. And now we realize that there’s a significant subset of our populations diagnosed in their teens, twenties, thirties, and forties. So, we definitely want our question – our viewer to know, no, you’re not alone at all. Please, see our paper that we just put out there and several other of my colleagues, including Brady Stein and others.

Two is, my goodness. Not only you’re not alone, but I actually believe – and I know you know this too – that a lot of rare cancers are sometimes are under diagnosed and underappreciated. It does require expert bone marrow, expertise, someone to identify it, someone to do a bone marrow. And lastly, for this patient looking for other patients, I would refer them to sources, such as this one. Patient Power, support groups on Facebook, we have a Twitter feed, as you know, a grassroots Twitter, that’s investigators initiative called #MPNSM (myeloproliferative neoplasm on social media).

So, there are lots of different ways for this person to connect with not only younger patients with the disease, but also as a support group, virtually. And I think platforms, such as Patient Power, have frankly revolutionized the way people have obtained information, have communicated with each other, and specifically for a patient like this in the UK, who is not able to connect with me. And when there are people all over the world waiting to talk to her.

Andrew: Right. I wanna call at our friends in the United Kingdom, MPN Voice.

Dr. Pemmaraju: Oh, yes.

Andrew: It’s Claire Harrison, who you mentioned, wonderful, devoted.

Dr. Pemmaraju: Outstanding.

Andrew: She’s an expert, out of London, helps run it. So, please, connect with them. Okay, here is a question from Erin, as we’re getting near the end of our program. “Can ET ever cause systemic inflammation? And is that what causes symptoms? The inflammation.”

Dr. Pemmaraju: Yes, yes, and yes. So, inflammation, I think, used to be a word that may have been potentially, if I may say, a wastebasket term, but now is a very specific term. So, now we know that a lot of our hematologic disorders and malignancies lead to a high level of inflammation. That means tissue damage. Tissue injury. That’s what inflammation means. There are some conditions that the patient does not even have a blood cancer diagnosis, but has a molecular mutation, that’s called CHIP (clonal hematopoiesis of indeterminate potential), and those patients appear to have a higher likelihood of cardiovascular disease and death. That’s New England Journal of Medicine. The likely pathway is inflammation.

In our patients with MPN, even the quote on quote, earlier stages, such as ET and PV. This is a disease of cytokines and inflammation. So, high levels of abnormal messengers and signals. So, yes, inflammation is part of the disease, patients have a higher rate of cardiovascular events and death. That’s inflammation. And then of course, the bone marrow milieu itself, as it progresses to myelofibrosis has an up ramp, if you will, of cytokines and inflammation. Last part of it is the therapies that we’re working on are trying to either target inflammation itself, or to bring down that level.

Andrew: Okay. I wanna see if – Here’s a – one that just popped in as we get near the end of our program. Roger says, “Are there any drugs being studied that improve anemia in patients with a low hemoglobin?” What’s the easiest way to find out about clinical trials if you live out of the state, or out of the country where this trial may be –?

Dr. Pemmaraju: Yes. Your best resource to look that up is run by the Federal Government, the NH, it’s called clinicaltrials.gov, that’s dot G-O-V. This is an outstanding website, well curated, updated as quickly as they can, and it has a nice search function. You can search by investigator, disease type, condition, and there’s even a box for ‘other’ where you can type in something like ‘myelofibrosis’.

There are several drugs in development. These drugs are known as Luspatercept and Sotatercept, for example. And they’re a class of drugs that are anemia targeting in myelofibrosis and myelodisplastic syndrome. So, the answer is, yes. And you can find out these types of clinical trials either online at this website, or at other websites. But this is an important, urgent, unmet medical need that we are working on, and there are active clinical trials for patients to enroll on.

Andrew: Well, okay. And the last thing I would ask you about – and this always comes up, Naveen, but I wanna hear what you have to say is somebody we have people with ET, we have people with PD, MF, and we talked at one end about acute myeloid leukemia. What do we know about progression now? So, if I’m sitting there with ET, am I necessarily going to go onto PV, or MF? Or anywhere along the line, and how do we know?

Dr. Pemmaraju: We do know a little bit more. So, the answer is no. So, a lot of our patients do stay in the chronic phase, as you’re asking. So, if you’re ET, or PV – and our European colleagues have really done these nice population studies, where the majority – the vast majority of patients with ET and PV are expected in the modern era to have normal life expectancies as long as you’re mitigating in some bleeds, clots, and these type of events.

But for the minority, who don’t have a normal life expectancy, you’re talking about progression to AML, which is a minority of all these. Right? Maybe 5-7 percent of cases at the most. There are some things we have identified. One is that there are some dynamic acquisition of molecular mutations that are happening at the time of progression. And what I mean by that is, there are new injuries to the DNA that people appear to be picking up. So, two important studies our colleague, Raajit Rampal showed that the acquisition of TP53 mutation, which is the guardian of the genome present in 50 (five, zero) percent of human cancers. That looks like it’s more common when ET and PV are trying to take off to AML.

Another study by our Mayo colleagues just published in Blood Advances showed that other mutations, such as PTPN11, or RUNX1, just to name some particular ones, and then we’ve known about ASXL-1 now for a while. So, rapidly change in blood counts in concert with new molecular mutations, and then a baseline if you have high-risk mutations. That seems to be a way for us to predict who might transform faster than others.

Now, that’s an addition to the traditional risk factors that you and I have already discussed, the IPSS risk, or etc. So, there are some ways that we can monitor. A lot of these may be in the research setting. Some are ready for the clinic, but there are some ways now.

Andrew: Okay. So, ladies and gentlemen, I hope this program is been worthwhile for you. Remember that the big meeting of Dr. Pemmaraju and his colleagues from around the world with thousands of hematologists is this the American Society of Hematology meeting, which once again, will be, yay, near me, in San Diego.

Dr. Pemmaraju: Very good.

Andrew: Esther and I’ll just drive over. And the Patient Power team will be there, the Patient Empowerment Network team will be there. So, we’re there for you. So, look for more programs as we go through the fall, and certainly in December, when this meeting happens. And that’s where a lot of the research that Dr. Pemmaraju talks about is presented.

Dr. Pemmaraju: Right.

Andrew: And then we’ll have more news. So, we’re living with these long-term conditions, thank god for most all of us, and it’s a moving target, as I’ve described. I wanna thank you for joining the Patient Empowerment Network program, for sponsoring this program. We thank Incyte Corporation for its support, and Dr. Naveen Pemmaraju from M.D. Anderson, and the Leukemia Department there, thank you for being a partner in this, and just explaining things, and your passion. And Naveen, again, back to your whiteboard back there. Figure it out.

Dr. Pemmaraju: It’s all there. Yes, sir, Andrew.

Andrew: It’s all there. Figure it out. Okay? All right. Thank you so much for being with us from around the world. We love it. We’ve got a community. This is what it’s all about and we’ll have future ask the expert programs. I’m Andrew Schorr near San Diego. Thanks to the Patient Empowerment Network for making all this happen. Remember, knowledge can be the best medicine of all.

Fact or Fiction: 10 Common Breast Cancer Myths Busted

October is Breast Cancer Awareness Month, and while many of us may think there is already plenty of awareness of breast cancer these days, it’s quite surprising how many myths exist alongside the facts.  Some breast cancer myths still continue despite a lack of evidence. A survey found that agreement with the phrase: “It seems like everything causes cancer” is on the increase. The danger is that when people believe this, confusion and misinformation about risk factors also increase. This can lead to unnecessary worry and can even hinder good prevention and treatment decisions.  So let’s untangle the facts from the fiction by busting ten of the most common myths which persist about breast cancer.

 

Myth #1: Finding a lump in your breast means you have breast cancer

Fact: Most breast lumps are caused by benign (noncancerous) changes, cysts, or other conditions.

Breast tissue is changing all the time because of fluctuating hormone levels, especially during times of menstruation and breastfeeding. It’s important to be aware of how your breasts normally look and feel, and know what changes to look for.

Take Action: While most breast lumps will not turn out to be cancer, lumps that feel harder or different from the rest of the breast (or the other breast), or change over time, should always be checked by your doctor.

 

Myth #2: Feeling pain in your breast is a symptom of breast cancer

Fact: Most breast cancers do not cause pain in the breast (although some do).

Many women experience breast pain or discomfort in the week leading up to their period. The pain usually goes away after menstruation.  Other breast conditions, such as mastitis (an infection of the tissue of the breast that occurs most frequently during breastfeeding), may cause a more sudden pain.

Take Action: If you have breast pain that is severe or persists and is not related to the menstrual cycle, you should be checked by your doctor.

 

Myth #3: Breast cancer is a hereditary disease

Fact: Only 5% to 10% of breast cancers are thought to be hereditary. The other 90% are largely due lifestyle and environmental factors. 

The risk in a person believing this myth is that they might think there is nothing they can do to prevent breast cancer if it is already in their family. Genetic testing can help you understand your inherited risk and allow you to make choices about your future care.
Some high-risk women also choose to have a prophylactic mastectomy to decrease their risk.

Take Action:  Cancer is a complex group of diseases with many possible causes, including lifestyle factors such as smoking, diet, and physical activity. Lower your risk of developing breast cancer by maintaining a healthy weight, exercising regularly, and limiting the amount of alcohol you drink.

 

Myth #4: Only women get breast cancer

Fact: While the incidence of breast cancer in women is significantly higher than in men, men can get breast cancer.

Many people don’t think of men as having breasts. In fact both men and women have breast tissue, although men have much smaller amounts than women. According to the National Breast Cancer Foundation, men carry a higher mortality than women do, primarily because awareness among men is less and they are less likely to assume a lump is breast cancer, which can cause a delay in seeking treatment.

Take Action:  Know the signs of male breast cancer. Symptoms include a hard lump underneath the nipple and areola and color change in the surrounding area.

 

Myth #5: Breast cancer only occurs in post-menopausal women

Fact: While it is true that the older a woman is, the higher her breast cancer risk becomes, breast cancer does occur in younger women.

Although breast cancer in young women is rare, more than 250,000 women living in the United States today were diagnosed with it under age 40[1]. In young women, breast cancer tends to be diagnosed in its later stages and be more aggressive. Young women also have a higher mortality rate and higher risk of metastatic recurrence (return of breast cancer in areas beyond the breast).

There is no effective breast cancer screening tool yet for women under 40, most of whom have dense breast tissue that prevents routine mammograms from being a useful screening tool.

Take Action:  Being breast aware is very important. Become familiar with how your  breasts normally look and feel and, if you notice a change, you should see your doctor as soon as possible.

 

Myth #6: Wearing an underwire bra causes breast cancer  

Fact: Claims that underwire bras cause breast cancer have been widely debunked as unscientific.

According to the myth, wearing your bra every night or for too long daily prevents your pores from being able to breathe. Sweat accumulates and toxins build up which are believed to cause breast cancer. Another version of this myth is that wearing a bra which is too tight or sleeping in your bra can cause breast cancer. The American Cancer Society (ACS) states “we do not know of any epidemiologic studies published in scientific journals that suggest bras directly contribute to breast cancer.”

 

Myth #7: Deodorants can cause breast cancer

Fact: There is no evidence to back the claims that deodorants and antiperspirants cause cancer.

People sometimes worry about whether chemicals in common products such as cosmetics or toiletries could cause cancer, but there is no good scientific evidence to show that these products affect the risk of cancer. According to Breastcancer.org, even the strongest antiperspirant doesn’t block all perspiration in the armpit. Most cancer-causing substances are removed by the kidneys and released through urine or processed by the liver. Toxins are cleared by lymph nodes and not by the sweat glands.

Take Action: If you still have concerns about the link between antiperspirants and breast cancer, see the NCI fact sheet on Antiperspirants/Deodorants and Breast Cancer for more information.

 

Myth #8: Breast cancer is a single disease

Fact: Breast cancer is not one disease, but a complex group of different types of tumours.

Until quite recently, breast cancer was thought of as one disease, so everybody got much the same treatment, which led to overtreatment for some patients.  We now know that at a molecular level tumors act and respond to treatments differently.  Researchers have to date classified breast cancer into 10 different subtypes.  Having a more detailed system of tumor categories can help tailor treatment to individual patients and predict women’s survival more accurately.

 

Myth #9:  Stress causes cancer

Fact:  The scientific evidence that stress causes cancer is not conclusive.

Despite studies which show weak evidence of an association between stressful events and a diagnosis of cancer, many people still hold the belief that stress is a factor in causing cancer. It’s unrealistic to think we can avoid stress completely. Everyone feels stressed at some point in their lives. But long periods of stress can cause mental health problems such as anxiety and depression and can contribute to physical health problems such as high blood pressure, heart disease, and ulcers. It makes sense then to get our stress levels under control.

Take Action: Adopt healthier coping mechanisms, such as learning stress-management techniques, taking the time to eat healthily and exercising more.

 

Myth #10:  Mammograms cause breast cancer

Fact: While mammograms do involve radiation exposure, the dose used is extremely low.

A mammogram (an x-ray of the breast) currently remains the gold standard for the early detection of breast cancer. Mammograms can detect lumps well before they can be felt, and the earlier that lumps are caught, the better one’s chances for survival. While it’s true that radiation is used in mammography, the amount is so small that any associated risks are tiny when compared to the benefits.

Take Action: According to the National Cancer Institute, the standard recommendation is an annual mammographic screening for women beginning at age 40. Base your decision on your physician’s recommendation and be sure to discuss any remaining questions or concerns you may have with your physician.

To wrap up, certain myths about breast cancer, though inaccurate, can nevertheless seem to make sense when we hear them repeated often enough.  While some risk factors for breast cancer are out of our control, knowing and understanding our risks will help us make the best choices possible for ourselves and our loved ones.

[1] Young Survival Coalition statistics on breast cancer in younger women.

 


For information on galactocele, please check out the blog What is a Galactocele, and What Can I Do About It? and 12 Breast Cancer Myths And Facts You Should Be Aware Of

Six Lessons Learned From Breast Cancer

“The period of greatest gain in knowledge and experience is the most difficult period in one’s life.”  — Dalai Lama

Writing in Oncology Times, radiation oncologist, Matthew Katz MD, described cancer as an illness of transformation. “Biologically” he wrote, “it represents a change in growth and homeostasis. Metaphorically, a cancer diagnosis can transform how you see yourself and the way you experience life afterward.” When the dust settles after the cancer storm has passed, it is not uncommon for patients to reappraise their lives. Cancer forces us to slow down and look at what really matters. Caught up in the routines of daily living, it is easy to avoid doing this; but cancer stops us in our tracks and pushes us to the edge of what is familiar. With cancer there is no hiding place; its sharp glare strips away pretence and artifice, revealing the true nature of our lives and relationships.

Cancer is an invitation to take stock and re-examine your life, to discover ways of leading a more meaningful and fulfilling life. Richard G. Tedeschi, PhD, professor of psychology at the University of North Carolina Charlotte, reports five common growth outcomes from interviews he conducted with trauma survivors.

  • A deepened appreciation of life.
  • Enhanced relationships with others.
  • An appreciation for personal strength and endurance.
  • Setting out on new pathways or pursuing new interests and opportunities.
  • Spiritual growth and development.

As part of breast cancer awareness month, I extended an invitation to six women to share what they have learned from their personal experience of breast cancer. Their answers to the question, “what did cancer teach you?” reflect the themes identified by Dr Tedeschi. The women’s experiences span a trajectory of breast cancer from recent diagnosis and active treatment, to several years’ post-treatment.

Elizabeth McKenzie, a licensed psychologist who lives in Seattle, WA, was diagnosed with breast cancer in 2012. She learned to appreciate the value of stillness and find healing in solitary pursuits.

“When I was diagnosed with cancer in 2012, I knew that I had just been enrolled in a crash course with countless learning objectives. Some of the lessons, however, have been unexpected.

I learned to appreciate stillness, the silence in life. I am an extroverted person. I work as a child/adolescent psychologist. I am married. I am a mother. I am a daughter and a sister. I have many friends. Before cancer, I thought that the foundation of my life was largely my connection with others. The time I was forced to be alone to heal from many surgeries for my own health, led to my pursuing other solitary pursuits, mindfulness meditation, nature photography, personal writing, and exercise.

Over time, I have learned that my individual experience was also part of that foundation; to have time alone to live in mindful stillness is a basic need for my mental and physical health, one that I had long neglected. In working on this solitary foundation, I have also strengthened my connection with others. I am now giving serious consideration to attending a residential mindfulness retreat, one that would require that I be silent, except for counseling with teachers, for 3-7 days. That is something that in the past, I would have considered myself neither able to do nor willing to give myself that kind of time. Today, I feel emotionally and physically ready for the experience of being by myself, with myself, surrounded by nature, for days on end. This gives me sense of peaceful willingness, a gentle hopefulness, in a life full of uncertainty.”

Becky Hogue, a PhD Candidate (Education) at the University of Ottawa, was diagnosed with breast cancer in 2014. Becky wanted to share a cautionary tale so others could learn from her hard-earned experience.

“When I think back about one thing that I’ve learned, it is that treatments change over time but advice is full of ‘old wives tales’ which are often based upon older treatments. This was never more poignant than during my last round of AC chemotherapy. Throughout AC chemo, I had been suffering from nausea. I knew from support group that people who tolerated it well only had nausea for three to five days. I had nausea for at least eight days. Given I was on a 13-day cycle, this meant more days with nausea then without. Now, my nausea was never really bad. When I complained to my oncologist, he asked me “when was the last time you threw up?” Never. My nausea was never that bad, it just lingered.

The folks at support group (especially those a year or so ahead of me) would talk about different nausea meds. The meds I was on were not the meds that everyone was talking about. I found myself wondering if I should be on different meds? In my mind, a change of meds would mean less nausea. I would tolerate the chemotherapy side effects so much better.

What I didn’t realize was that these different nausea meds were the old school meds. The meds my oncologist had me on were the new ones. People in support groups, and some of the older chemo nurses, were not familiar with the new meds. The recommendations I was getting about ‘what works’ were ‘old wives tales’, and I bought into them instead of trusting my oncologist.

For my last bout of AC chemo, I tried a different combination of anti-nausea meds. My oncologist was away, so his nurse practitioner changed my meds (in part because I asked for it). I’m sure that if my oncologist was there, he would have explained that I was on the new meds, but also that they were doing their job. I didn’t know the other option was the older option. I didn’t realize that the folk lore about the effectiveness was in part just because it was the older meds. The new meds had not been around long enough to be part of the lore. With the change my nausea was no better, but the side effects of the meds were much worse. I ended up with terrible mouth sores (so bad I needed liquid morphine to manage the pain). One of my biggest regrets regarding my treatment was that I changed anti-nausea meds for the last cycle of AC chemo.  I had forgotten my own advice. I had forgotten who I had decided to trust (my oncologist), and let the ‘lore’ effect my treatment.

This tale is meant to be a cautionary one. Not so much about seeking advice, but about remembering that people who have followed this path before you did so at a different time. The treatment options (and side effect management options) available to you today may not be the same ones that were available for someone else a year ago. Although older treatments may work, chances are the newer ones are better. Before changing treatment plans based upon what you are hearing on the net or in support groups, ask yourself ‘is this an old tale’? And finally, decide who you are going to trust, and trust them.”

Audrey Birt, a two-time breast cancer survivor, focussed on lessons of courage, connection and resilience.

“Cancer taught me I’m more resilient than I would have believed, it helped make me braver. It also taught me that life cannot be controlled. This made me more able to live in the moment and for the moment and that’s probably not so good for my bank balance but it’s great for my life balance in a way. It taught me to reengage with writing through my blog and in a funny way it changed my life and connection to others. But it also taught me my fragility and that’s a lesson I’m still learning, one day at a time!”

Author of From Zero to Mastectomy, Jackie Fox, has written of how breast cancer “gave me part of myself back”.

“One of the obvious benefits of cancer is reconnecting with friends and family, but old loves like art and music may reappear in your life as well. In my case, I started writing poetry again. I hadn’t written or published anything for nearly 20 years and I really thought that part of my life was over. I’m so grateful to have it back and I hope I never lose it again.”

Liz O’Riordan was diagnosed with breast cancer in July 2015. From her unique perspective as a consultant breast surgeon, she is learning what it’s like to be a patient from the other side.

“Being a patient in my own speciality has opened my eyes to a lot of little things that could be changed to improve patient care. I learned that the language of cancer is completely different for a patient compared to a doctor. I have been made acutely aware that some of the phrases I’ve used in clinic when breaking bad news, that I’ve heard others say, or come up with myself, now make me cringe. A lot of women get recalled from screening with tiny low grade cancers (<1cm), and I’ve said “If you’re going to get breast cancer, this is a good one to have”, or “You’re lucky that we caught it early”. All of these phrases were said with good intentions, to try and reassure the women that they were unlikely to die of their cancer, and would not need chemo. And most women are still in shock, so I never see them truly react to what I have just said. But no cancer is a good one to have, and no-one is lucky to get cancer. I will pay close attention to what I say to patients in the future.”

The final lesson is one of authenticity and integrity, something Eileen Rosenbloom who was diagnosed with breast cancer in June 2010, believes cancer cannot take away.

“Although I often felt like cancer was a thief that had taken everything from me, being so ill also created an opportunity to see what it could never take — the very essence that is me. Sometimes I’d look at my eyes in the mirror and think: There I am, right there. I’m still me. It felt empowering to realize no matter how dark things got, I still had control over some part of myself. My very essence remained intact, even if stripped down to a raw version without any frills.”

Whatever place you are at with a diagnosis of breast cancer, there are lessons to be learned. These will be unique to you; but you can also learn from those who have walked this path before you. Reach out to them, and lean on their experience to help make the way a little smoother for your own journey.

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