Tag Archive for: targeted therapies

Hope Unleashed: Advancing Therapies for Defiant Mutations in Lung Cancer

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Hope Unleashed: Advancing Therapies for Defiant Mutations in Lung Cancer from Patient Empowerment Network on Vimeo.

What promising studies in lung cancer mutations are there that patients should know about? Expert Dr. Joshua Sabari from NYU Langone discusses common lung cancer mutations, incidence rates, promising and potential studies, and proactive patient advice.

[ACT]IVATION TIP

“…no matter what your lung cancer type is, no matter any clinical characteristic, you need next generation sequencing done, biomarker testing done, to identify these mutations. And even when we identify the mutation, I think as a group, as an academic community, we need to do more to study novel therapeutics and to better understand the biology of these mutations so that we can get better treatments to our patients.”

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Transcript:

Lisa Hatfield:

Dr. Sabari, can you speak to some of the more defiant mutations in lung cancer, and what promising studies are we looking at right now?

Dr. Joshua Sabari:

Yeah, so I think in lung cancer the most common mutations that we see are EGFR and KRAS. EGFR mutations are a quite broad range of alterations. The most common are in exon 19 deletion and exon 21. These are the location of the mutations. They make up about 80 percent to 85 percent. We have phenomenal treatments in the frontline setting, but most patients only remain on therapy for about two years before there is progression. So, we need to better understand resistance mechanisms, and we need to better understand the next generation of therapies that are available.

In contrast to EGFR, KRAS is equally as common. We see this in about 25 percent to 30 percent of the patient population. Unlike EGFR, KRAS is almost exclusively seen in people who’ve smoked in the past. And there are many different KRAS mutations or alleles. There’s KRAS G12C where we have two FDA-approved match targeted therapies in the second-line setting.

But we need better options, better opportunities for our patients in the frontline setting. And for KRAS, we’re not doing as well as we should, right? KRAS mutations, most people have about a 30 percent to 40 percent chance of responding to therapy. And the median time on treatment is in that six to seven month range. So this is a defiant mutation. It’s a mutation where we need to do better and we need to really develop the next generation of inhibitors for our patients.

So I guess the activation tip here is, again, no matter what your lung cancer type is, no matter any clinical characteristic, you need next generation sequencing done, biomarker testing done, to identify these mutations. And even when we identify the mutation, I think as a group, as an academic community, we need to do more to study novel therapeutics and to better understand the biology of these mutations so that we can get better treatments to our patients.

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Advances in Small Cell Lung Cancer Research | Hope for the Future

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Advances in Small Cell Lung Cancer Research | Hope for the Future from Patient Empowerment Network on Vimeo.

What new treatments are being studied for small cell lung cancer (SCLC)? Dr. Triparna Sen, a leading researcher in the field, shares promising updates, including advances being made with LSD1 inhibitors, DDR (DNA Damage Response) inhibitors, and DLL-3 targeted therapies.

Dr. Triparna Sen is an associate professor in the department of oncological sciences and co-director of the Lung Cancer PDX Platform at the Icahn School of Medicine at Mount Sinai in New York. Learn more about Dr. Sen.

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Transcript:

Katherine:

Dr. Sen, you are a leading researcher in the field. What is the latest research news that you can share with us about small cell lung cancer?

Dr. Sen:

There’s a lot of great research going on in my lab and labs all across the world. I think for the first time in a very long time, we are really trying to dissect the biology of small cell.   

It has been a research in making for many years. I think we have now really come to a point where we are really trying to understand the disease. I’ll go into a little more about the questions you are trying to answer. So, one of the main questions or one  of the main things that kind of is a hurdle to getting durable treatment options is that the frontline chemotherapy and immunotherapy doesn’t work as well as they should even for the approved regimens, which is the chemotherapy and the immunotherapy.  

The patients often do not have durable benefits. Even if patients have durable benefits, it’s only in a very minority of patient population which means in only about 10 to 15 percent of the total patient population actually do have any benefit from the frontline treatment. So, the main question that we are trying to answer is that why do these patients not respond to immunotherapy and chemotherapy in the frontline.  

What are the mechanisms of resistance to chemotherapy and immunotherapy? Primary resistance, what I mean by primary resistance is that patients who never respond. The disease comes back even while they’re getting the frontline chemo. So, the primary resistance, the mechanisms. Of course, when they have acquired resistance after the maintenance regimen when they come back, why are these patients having this acquired resistance to chemotherapy and immunotherapy? Because only when we understand resistance mechanisms will we be able to then come to the combination strategies.

That’s the next area of research is that once we understand the mechanism of chemotherapy and immunotherapy resistance is then coming up with effective combination therapy. So, what should we combine with immunotherapy in order to make immunotherapy better? I’ll give you an example from the research that we did. 

So, our lab focus is, as I said, on making immunotherapy better. What we understood is that there are certain epigenetic modifiers like LSD1.  

Repressing these, repressing LSD1, with a small molecule inhibitor actually augments or benefits the response to immunotherapy. So now, we are looking at LSD1 inhibitors in combination with immunotherapy. That’s one area that we are focusing on. The second are that we published extensively on is DNA damage response inhibitors which really works in combination with immunotherapy and makes immunotherapy response better.  

Now, we are investigating that in the lab the combination strategies of combining these DNA damage response inhibitors with immunotherapy. So, combination strategies. I think always coming up with novel targets. I will mention there are many novel targets that are right now in the clinical trials actually showing really, really encouraging data.  

I’m talking about DLL3 targeted BiTEs or ADCs we have seen that are showing preliminary data. We have seen a really good really good response in patients. So, finding these targets that are very specific for small cell and that can work in these unique population of patients.  

So, DLL3 targeted agents. There are agents that target B7-H3. So, we are looking at these novel targets and where they could fit in the current therapeutic regimen. Finally, since small cell lung cancer is not a surgical disease, we have to look for other options to find biomarkers. So, liquid biopsy. Liquid biopsy, what I mean by that is understanding the disease not just from tissue but also from blood.  

There’s a lot of research that’s happening in understanding the biology of small cell from blood draws from these patients.  

So, the field of using liquid biopsy or understanding the disease from blood draws is one of the areas that many labs, including ours, are focusing on, and how we can utilize these blood samples to then monitor the disease and also understand the resistance mechanisms to various drugs. I think these are the areas that we are investigating and seems, to me, very important areas that we need to address in order to really manage small cell lung cancer.   

Katherine:

What do these advances mean for small cell lung cancer patients? Are you hopeful?  

Dr. Sen:

Oh, yes. Of course. We’re always hopeful. That’s the goal, right. The goal is to have effective therapies that work and that works for a long time. That also benefits the patients in terms of quality of life which means without very severe adverse effects.   

So, very hopeful. Because I think what was limiting us for all those years for the last 40 to 50 years is that we really did not understand the complexity of small cell lung cancer. It is a very complex disease. It is very different from non-small cell lung cancer which has these mutations that you can target drugs against. So, there are this EGFR mutations and KRAS mutations in non-small cell.  

But small cell, it’s not that. It is not a disease where we have these GATA function mutations that we can devise therapies against. It’s a very different disease. The disease is aggressive. The disease progresses fast, and it also changes its physiology very fast. So, I think for the first time, we really are trying to understand the biology. What that helps is then to come with very informed decisions about therapy.  

So, yeah, I’m very hopeful. Because I think we have now targets that we are actually seeing benefits in patients. I think the more and more we understand resistance mechanisms, we’ll also be able to manage that better.   

Katherine:

That’s very promising news. 

Exploring Renal Cell Carcinoma Research: Expert Insights on Immunotherapy and Targeted Therapy

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Exploring Renal Cell Carcinoma Research: Expert Insights on Immunotherapy and Targeted Therapy from Patient Empowerment Network on Vimeo.

What’s important in renal cell carcinoma research news? Expert Dr. Moshe Ornstein from Cleveland Clinic shares an overview of research updates on immunotherapy, targeted therapy, and combination therapies.

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Transcript: 

Lisa Hatfield:

Dr. Ornstein, can you speak to the latest news in renal cell carcinoma?

Dr. Moshe Ornstein:

So just by way of a 30,000 foot view, when it comes to renal cell carcinoma, approximately two-thirds of patients are diagnosed when the cancer is in a localized stage, where the cancer is treated with curative intent, generally with surgery. For patients who present with metastatic kidney cancer, in other words, kidney cancer that has spread beyond the kidney, or for patients who had their kidney removed and then developed a recurrence or the cancer had come back to the lungs or the bones or anywhere beyond the kidney, those patients are treated with what’s called systemic therapy. Those are medicines that really cover head to toe, not a specific area, but head to toe.

And when we think about treatment options in kidney cancer, there are two main treatment options. One is immunotherapy. Immunotherapy is generally what’s called checkpoint inhibitors. And these are therapies that “release the brakes” on the immune system, and allow the body’s immune system to be activated to target the cancer.

And the other type of medicine is called targeted therapies. And these for the most part, are vascular targeted therapies, and the way I describe it is they shrink the blood supply to the tumors. So again, you have those tumors that are diagnosed at a local stage. You have those tumors that are metastatic or advanced beyond the kidney. And the main treatment paradigms have to do with immunotherapy and targeted therapy.

So we just had the ASCO GU meeting, and I just want to describe the updates and how they fit into sort of the overall treatment paradigms across the different treatment sections, in other words, localized and metastatic. So for a patient who presents and comes in with just a kidney mass, that’s a kidney cancer, generally that patient’s going to be treated with surgery. In general, there’s no rule for therapy before surgery. For many years, for that patient who had their kidney cancer removed from the kidney, either part of the kidney or the whole kidney removed, we really didn’t know what to do with those patients, and the standard of care was just to watch those patients.

And we’ll get into a discussion about what watching the patient means. But one of the updates from the recent meetings has been that for patients who have their kidney removed because of kidney cancer, there is now a rule in some patients, this has to be a discussion with the doctor, to use immunotherapy to help prevent or delay the cancer from coming back. It’s a personal discussion.

We have a lot of data to support the use of a medicine called pembrolizumab (Keytruda), which is an immunotherapy that patients would get for a year after their kidney surgery. So that’s really the big recent update in the localized kidney cancer world, where the kidney cancer has been removed by surgery, and there’s now a treatment option, a year of immunotherapy after surgery for the right patient. So now, we move to the metastatic patient.

So again, the patient who has metastatic disease, either comes in with metastatic disease upfront, meaning the kidney’s there, the tumor’s in the kidney, and there’s advanced disease. And the other type is the patient who had their kidney removed a year ago, two years ago, sometimes five years ago, and now shows up with new spots in the lungs or the bones or elsewhere in the body. And that is metastatic or advanced kidney cancer.

So by and large, the overwhelming majority, and in my clinical practice, 95 percent of these patients are going to get an immunotherapy-based regimen as the first treatment for advanced kidney cancer. And there are different types of immunotherapy-based regimens. There’s an immunotherapy in combination with immunotherapy, and that’s called ipilimumab (Yervoy) and nivolumab (Opdivo), so double immunotherapy, or an immunotherapy plus a targeted therapy.

Lisa, we spoke about the targeted therapy, cutting the blood supply. So in addition to getting two immunotherapies, some patients won’t get two immunotherapies, they’ll get one immunotherapy in combination with a targeted therapy. And those combinations include axitinib (Inlyta) and pembrolizumab, lenvatinib (Lenvima) and pembrolizumab and cabozantinib (Cabometyx) and nivolumab as the primary combination treatments for the first line of therapy for metastatic kidney cancer.

And the real updates from the recent meetings in this setting is just that with additional follow-up, in other words, we’ve seen follow-up at two years after the trial started, three years, four years, now five years, we’re seeing that there’s a subset of patients that continue to benefit with this combination years down the road. So, encouraging for patients. Again, it’s not every patient, different patients need different things, but just the knowledge that we have long-term follow-up data for patients who have gotten an immunotherapy-based combination for the front-line treatment for their advanced kidney cancer.

And the last update I want to touch on is once we move beyond that first line of immunotherapy-based combinations, we really don’t know exactly what to do beyond that. Meaning, if somebody got an immunotherapy-based combination, and then the kidney cancer got worse, what do we give next? And generally, we’re giving more of these vascular inhibitors, these targeted therapies. And the latest advancement in this area, in the refractory setting, in other words post immunotherapy-based combination is the introduction of a new medicine called belzutifan (Welireg), which is not a classic vascular inhibitor, but is something called the HIF-2α inhibitor.

It’s a very well-tolerated therapy in many of the patients. And it does have activity in the right patient. And it’s now FDA-approved relatively recently for patients who have already had an immunotherapy-based combination. So that’s kind of the major update. The post-surgery treatment with immunotherapy, long-term data for immunotherapy-based combinations in the metastatic setting, and a novel therapy, a new mechanism of action with a pill with a therapy called belzutifan for patients whose kidney cancer is getting worse despite standard treatments upfront.

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Understanding Immune System Recovery Post Follicular Lymphoma Treatment

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Understanding Immune System Recovery Post Follicular Lymphoma Treatment from Patient Empowerment Network on Vimeo.

Follicular lymphoma treatment may impact the immune system in different ways. Expert Dr. Kami Maddocks from The Ohio State University Comprehensive Cancer Center discusses how immune function may be impacted and how recovery is monitored.

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Transcript:

Lisa Hatfield:

So another person is asking, “How long does it take for the immune system to really start bouncing back after follicular lymphoma treatment? And what blood test results indicate a weakening immune system?”

Dr. Kami Maddocks:

Yeah, so this is a great question. It also can be a complicated question with many different answers. So one, it can depend on the treatment that a patient receives. Two, it can actually depend on their different parts to the immune system. So different parts of the immune system can recover at different time periods from treatment. So acutely, our neutrophils are something that often gets…they’re bacteria infection fighting cells. Those are the cells that during chemotherapy, when that count gets low and patients are counseled on if you have a fever during your treatment, you need to be evaluated and be seen because if you have an infection and a fever during chemo or some of these treatments, your blood counts are low, you might need to be in the hospital on IV antibiotics.

So those neutrophil parts of it are usually quicker to recover, so they drop with treatment and then recover pretty quickly with each cycle, including after an ended treatment cycle. Sometimes when patients have been treated with several different therapies, it can be harder for those cells to recover. They can stay lower for longer. Then there’s a component of the immune system, so we are ripping out the lymphocytes, because that’s what the cancers have.

And so things targeted. Chemotherapy in general kills the lymphocytes, but there also are targeted therapies like rituximab (Rituxan) bispecific antibodies CAR-T cells, those are particularly wiping…targeted towards proteins on the lymphocytes and wiping them out. Those can be for a more prolonged time. In general, we usually think of about a six-month period so patients can be at increased risk for viral infections in that six-month period may not respond as well to vaccines in that period.

But for some patients it takes longer and some patients recover quicker. It also can depend on where patients are at in their journey because every therapy that they’ve had can take a little bit longer to recover. The last part I’ll add is just sometimes when the lymphocytes are wiped out for a long time people’s proteins, their immunoglobulins that help fight infection get low. And so sometimes we actually will end up giving patients replacement of IVIG to help if they’re having lots of infections.

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An Overview of Current Gastric Cancer Treatment Options

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An Overview of Current Gastric Cancer Treatment Options from Patient Empowerment Network on Vimeo.

Treatments for gastric cancer have expanded in recent years, providing new options for patients. Dr. Yelena Janjigian, a specialist and researcher, shares an overview of available gastric cancer therapies and outlines the different treatment classes.

Dr. Yelena Janjigian is Chief of Gastrointestinal Oncology Service at Memorial Sloan Kettering Cancer Center. 

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Transcript:

Katherine:

Okay. I’d like to move onto current gastric cancer treatment options. Can you provide an overview of what’s available now?  

Dr. Janjigian:

Right. So, in patients with intermediate or early-stage tumors, really surgery is the main way to cure patients. Occasionally when we have an amazing response to chemotherapy or chemotherapy with immunotherapy or just immunotherapy, we can avoid surgery. But in most patients, surgery in early-stage disease is a gold standard for cure. Of course, it can be a very jarring thing to say to someone. “We have to take out. your stomach.” But patients do live without either fully their stomach removed or partially removed. And that’s the gold standard. We do additionally other treatments to help maximize chances of cure, but surgery is the main state. As I mentioned earlier, most of our patients, however, present with later stages where surgery is not feasible.  

And when I say it’s not feasible, we would only attempt an operation if we thought there was a possibility of removing the cancer completely. Leaving some of the tumor behind, even if it’s only 1 percent of the cancer behind, makes patients unwell. They may not be able to tolerate additional chemo, so we do not recommend doing suboptimal surgery unless cancer can be completely removed. So, in those patients, we always explain the situation.

And the disease is not potentially as curable, but it’s absolutely always treatable. And since the development of our immunotherapy options, really, we’ve changed the trajectory and the course of those cancers. We won’t know the stage or the final response to therapy until we’ve start it. But in those patients, usually a form of long-term therapy. Chronic treatment is very important.  

And usually it involves a combination of chemotherapy and some targeted agents, biologic agents, meaning that they were designed in the lab to target the cancer specifically. And usually, they involve some sort of immunotherapy.   

Katherine:

Excuse me. Can you go into some detail about the targeted therapies and immunotherapies that you use?  

Dr. Janjigian:

Sure. So, conventional chemotherapy works on any rapidly dividing cell. And these are chemotherapies that have been tried and true in the clinic for decades, right? And they work still in gastric. And in  particular they’re very important. And then over the last 10 years or so, we’ve started developing target agents in the lab that target the specific biologic tumor biomarkers. And when you think about tumor biomarkers, I would think about them as almost ZIP codes, right? How do you direct the cancer cell to die? 

And how do you inhibit the cancer cell for the thing that is uniquely what’s making it grow as opposed to normal cells, right? So, that’s the difference between chemotherapy because chemotherapy can affect any rapidly dividing normal cell and cancer cell, while biologic agents ideally only affect the target, cancer, the cell. So, that’s why it’s very appealing to do both to help maximize response and survival on treatment. So, the biologic therapies that are available in and already approved in our disease for stomach cancer are something called HER2 directed treatments.

And that’s been my focus in the lab. And then in my group has really spearheaded a lot of this research for HER2-positive tumors. In gastric cancer it occurs in up to 20 to 30 percent of tumors, but we have drugs such as trastuzumab or Herceptin, T-DXd, trastuzumab deruxtecan-nxki (Enhertu) or in HER2 that target these agents.  

And furthermore, our work here at Memorial Sloan Kettering demonstrated the combination therapies really for HER2-positive disease has helped improve outcomes in those patients. So, that’s biologic therapy. Other biologic therapies that’s approved in gastric cancer is something called VEGFR-2 inhibitor. These are drugs that target blood vessel formation around the tumor to help the chemotherapy drugs work well and better. Those drugs are called ramucirumab or Cyramza. And that’s used in a combination of chemotherapy in second-line treatment. And there’s other drugs such as regorafenib (Stivarga) and other inhibitors that maybe have some targetable activity in our disease. And last but not the least is immunotherapy. So, immunotherapy’s a completely different class of drugs.  

We think about immunotherapies, really the fundamental problem with cancer, right? The cancer issues that it started as a normal cell. So, at some point, it was a normal cell that then became and went awry and went rogue. And the body did not recognize that there was a problem. And the immune system did not eliminate that cancer cell. Before it started to metastasize and give us problems in their body, right? So, the fundamental question is why is the body’s immune system, why did it not recognize it as a abnormal cell?

Well, because it really acts and looks like a normal cell from the immune perspective. Our immune system is trained not to hurt us, right? And that’s why in patients with rheumatoid arthritis or other autoimmune disorders, what happens is the immune system goes awry. So, what the immune checkpoint blockade or immunotherapy for cancer does, is it helps take some of those brakes off our immune system and help our immune system recognize the cancer and give it permission to say, “Hey, you know what?  

You thought it was a normal cell. It’s not. It’s a cancer cell. Please help us eliminate it.” And that’s worked well because I think in for some of our patients, the immune system actually knows how to target and suppress the cancer much better than any of the fancy drugs we can design in the lab.

And that’s why in some patients, immune checkpoint blockade immunotherapy has been such a game changer if you do respond, your duration and durability of response is so much more better than anything that would go to just done on our own in the lab or with other chemotherapies. So, it really is a nice way to think about it. And the patients feel like they’re part of the solutions. It’s always nice for them to have that.  

But it’s been a real game changer for both HER2-positive and HER2-negative disease in combination with chemotherapy. I’ve had the pleasure of leading some of these studies. And it’s nice to be able to update the three or the four or the five-year survival rate from these studies in a disease where in the past most patients died within a year.   

Accessing Financial Resources for Lung Cancer Care

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Accessing Financial Resources for Lung Cancer Care from Patient Empowerment Network on Vimeo.

Is there financial support for patients that need assistance with the cost of lung cancer care? Dr. Erin Schenk shares advice and resources available to help alleviate the financial burden that some patients and care partners may experience.

Dr. Erin Schenk is a medical oncologist, lung cancer researcher, and assistant professor in the division of medical oncology at the University of Colorado Anschutz Medical Center. Learn more about Dr. Schenk.

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Transcript:

Katherine Banwell:

You know, one thing patients are often concerned about is the financial aspect, the financial burden that is involved in their treatment care. How do they deal with that? Are there resources available for them? 

Dr. Erin Schenk:

There can be and this definitely can vary based on what treatment you’re being given and where you are, at what institution and what state you’re being treated at since resources are different. But for example, the targeted therapies or the TKIs I made reference to earlier, those can have some significant out-of-pocket costs and most of the,  if not all of the manufacturers of those various TKIs have patient assistance programs that help to reduce the out-of-pocket costs for those specific medicines.  

When I prescribe a TKI for a patient often what’s part of that is a prior authorization to try to understand what’s the out-of-pocket cost for the patient and then kind of get on top of whether or not we need to apply for patient assistance to help pay for the cost of that medication. So, that’s one way that we can help. 

I think, in again, this is specific to my institution and our clinical practice, but we often have – we work very closely with other cancer doctors in the community. So, if traveling to our site is a major burden we can usually have them visit with a oncologist who’s close to them so there’s less travel, there’s less costs in you know gas and staying somewhere. But they still can be connected with us. So, while they can get most of their care under a doctor that’s closer to them, every so often they come back and see me and just talk about how things are going and what you know might be worthwhile to consider down the road.  

And I would also recommend that if there are other costs or concerns you know, kind of above and beyond these things that we’ve touched on, connecting with a social worker through the cancer center can be helpful in dealing with paperwork for disability or retirement or sometimes connecting to resources if there’s a childcare need. 

Or you’re caring for a spouse and you need additional help at home. You know all of the different burdens that are present in life that just get magnified with a cancer diagnosis and you know, we can – there’s usually a really big attempt to try to find a way to help figure out navigating those so that you can get the care you need.

Small Cell Lung Cancer Care and Outcomes in Underrepresented Communities

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Small Cell Lung Cancer Care and Outcomes in Underrepresented Communities from Patient Empowerment Network on Vimeo.

How does small cell lung cancer (SCLC) care look in underrepresented communities? Dr. Rafael Santana-Davila with the University of Washington School of Medicine explains how health outcomes differ in some ZIP codes and shares advice for questions to ask your doctor to access optimal SCLC care.

[ACT]IVATION TIP

“…patients should ask their doctors, ‘What are the latest advances in this disease? Am I eligible for it to receive those advances? And where can I see a sub-specialist in this disease? And is it a worthwhile point?’”

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Transcript:

Lisa Hatfield:

Does treating small cell lung cancer patients in underrepresented communities look different than the general population? And are there specific considerations or recommendations SCLC patients from underrepresented communities when it comes to treatment options, including clinical trials or targeted therapies?

Rafael Santana-Davila:

In the majority of cases, patients treated in underrepresented communities do not look different than in the general population in small cell lung cancer. Why? It’s because community oncologists are very good. So they have a hard job, but they’re very good. So the majority of patients get the standard of treatment.

Although we know though that patients with underrepresented communities do fare worse.  And we do not know the reasons for that. A lot of that is because of poverty or many other things. I’ve seen people say that one of the main factors that will determine how long you live is what ZIP code you were born in. So underrepresented communities do do worse in general, not specifically for small cell, but in general.

I do think that what we..like we said before is what patients need to do is advocate for themselves and ask their doctors, “Am I eligible for a clinical trial? Am I eligible for what is the latest and greatest for the disease? Any new advances that you see coming?”And like we said before is seek a second opinion with a sub-specialist in the treating of this disease.

So as like we said before in terms of activation, is you need to…patients need to ask their doctors, “What are the latest advances in this disease? Am I eligible for it to receive those advances? And where can I see a sub-specialist in this disease? And is it a worthwhile point?” Many times it may not be an initial diagnosis, but when patients have recurring disease, that’s when clinical trials are really important because that’s where we’re making the most advances in the treatment of small cell lung cancers, when patients have disease that has recurred despite chemo-immunotherapy.

So my activation tip for this is that patients should ask their doctors, “What are the latest developments in the treatment of this lung cancer? And am I eligible to receive those treatments? And is this a time where I should seek a second opinion or be referred to a clinical trial and another center?”

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What Are Treatment Options for Endometrial Cancer?

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What Are Treatment Options for Endometrial Cancer? from Patient Empowerment Network on Vimeo. 

What endometrial cancer treatment options are currently available? Endometrial cancer expert Dr. Emily Ko shares an overview of options, including chemotherapy, surgery, radiation, targeted therapies, combination therapies, hormonal therapies, and discusses considerations for patients who are trying to preserve their fertility.

Dr. Emily Ko is a gynecologic oncologist and Associate Professor of Obstetrics and Gynecology at the University of Pennsylvania. Learn more about Dr. Ko.
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Transcript:

Katherine:

I’d like to talk about the treatments that are currently available. You mentioned chemotherapy, but what else is available for people? 

Dr. Ko:

Absolutely. So, treatment for endometrial cancer is usually some combination of surgery, and then it may be followed by possibly chemotherapy, as well as radiation, and sometimes, it may be a combination of all three treatments, or sometimes, it’s a combination of one or two of those, depending on the exact stage, depending on the exact cell type, and some of the other factors. 

Katherine:

Are hormonal therapies used as well, and targeted therapies? 

Dr. Ko:

Yes. 

Katherine:

I know they are in other cancers. 

Dr. Ko:

Yes. And so, I think the question is where do those come into play? So, I would say the usual algorithm most commonly would be that surgery is done first, as the most common first step, and then, based on the information obtained from surgery and the pathology report that comes from that, then there’s usually some type of a recommendation about should there be a second stepped treatment, and that frequently can be chemotherapy/radiation.  

Now, the areas where targeted therapy – for example, immunotherapy – where does that come in? So, that now has come into the – I would call it the second stage. We’re combining it with the classic chemotherapy drugs – Taxol-carboplatin, for example. That’s one example where it could come into play. Another example could come into play where a patient had gone through classic Taxol/paclitaxel and carboplatin, then had cancer come back, and so, that could be another instance where that pembrolizumab or pembro with lenvatinib (Lenvima) combination can be used in the setting of recurrence. 

Now, we could also say, hey, if your cancer type has those hormonal receptors present or is some type of what we call endometrioid histology, and we think that hormonal therapy may be more effective in that case, then that could also be used in a setting where the cancer has kind of grown again, the cancer has grown back, or actually, there are certain situations where patients, for example, may not undergo a hysterectomy. 

And, there are unique cases and those situations where patients are still trying to preserve their fertility, and therefore not wanting to undergo a hysterectomy, or they’re unable to undergo surgery safely. And so, in some unique situations, we may also use hormonal therapy as the mechanism to treat their cancer, and whether that is by way of a pill, whether that is by way of a progesterone intrauterine device, IUD, that is placed into the uterus, we also have situations where we tailor the therapy to the condition of the patient. 

Katherine:

When treating more advanced endometrial cancer disease in general, are the treatment options different than if you were treating somebody who had stage I or stage II, for instance? 

Dr. Ko:

Sure, great question. So, for some patients with, say, stage I, surgery alone is enough. 

For some other patients, subcategories of stage I, where we call them more high/intermediate-risk patients, they’re stage I, but there are a few features about their pathology that might make them slightly higher risk for recurrence – in those cases, we might consider a little bit of radiation after surgery, what we call adjuvant radiation or what we call radiation vaginal brachytherapy. Just three short treatments of a little bit of radiation to the top of the vagina has been shown to possibly decrease chance of recurrence in that area with very minimal side effects. 

So, that would be more commonly in line with stage I. There are some subtypes that can still be what we call high-risk, even in stage I/stage II uterine serous carcinoma, uterine carcinosarcoma. In those cases, we might also recommend chemotherapy along with some vaginal brachytherapy following their hysterectomy, so that’s the early stage. 

And then, with the advanced stage, yes. So, frequently, it’d be surgery first to secure the diagnosis, followed by some type of – it might be primarily chemotherapy, or it could be combination chemotherapy with radiation. And over time, I would say our paradigm for what we use for chemotherapy and radiation has changed a little bit.  

If you go back a couple decades, I think radiation was used a lot – whole pelvic radiation, even just without any chemotherapy. And then, we then had more data from research clinical trials, GOG-258 or PORTEC-3, that then had given us evidence that perhaps doing chemotherapy with some combination of radiation is going to be beneficial, or even moving towards primarily radiation could be a very good option in terms of long-term benefit/long-term survival. 

And, of course, that brings us to the present day, those two trials that I mentioned from ASCO, the GY018 and the RUBY, now bringing in the immunotherapy component to the chemotherapy, so there has definitely been an evolution to managing advanced stage. 

Recent Advances in Treating Breast Cancer

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Recent Advances in Treating Breast Cancer from Patient Empowerment Network on Vimeo.

What are the latest breast cancer treatment and research advances? Expert Dr. Bhuvaneswari Ramaswamy shares treatment updates for specific breast cancer types and discusses testing for circulating tumor DNA.

Dr. Bhuvaneswari Ramaswamy is the Section Chief of Breast Medical Oncology and the Director of the Medical Oncology Fellowship Program in Breast Cancer at The Ohio State College of Medicine. Learn more about this expert here.

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Transcript:

Katherine:

Are there emerging therapies that are showing promise?

Dr. Ramaswamy:  

Oh, my God. There’s just tremendous emerging therapies that are showing extraordinary progress. And I talk about this to my patients all the time. I mean, I tell them like two years ago say in a patient with – patient with metastatic disease, I’ll say, last year this drug wasn’t approved.

This drug is now approved for you to be given, and it shows extraordinary effect. So, every year we have new drugs getting approved, and we are also trying to get it used to be a little bit of a richness on the HER2-positive disease. And now we are seeing definitely a lot of richness on hormone receptor-positive disease. And I think we’re starting to see some new particular immunotherapy and other targeted therapies showing some response in triple-negative breast cancer.

Now, I know that’s a place that we still need to see more newer therapies, but overall, in the stage IV setting, we have really many options to keep them in good quality of life and longer. But people will ask, “Really, why do I even need to get to stage IV?” Really look at me and improve the curative setting. And that again, we are able to pick the higher risk patients, what me – what it means to have higher risk disease, how do we target them, newer drugs to target them. So, I think in so many ways we are doing better. And we are also getting to a place can we detect higher-risk patients, not just  by their initial diagnosis and response, but follow them sequentially by circulating tumor cells?

And we are getting to that place where we can actually do circulating tumor DNA, so just isolate the DNA, and we know what will belong to the tumor. And then circulating tumor cells seemingly even after your curative therapy. And so that is something that’s getting approved. And so we are not only seeing treatment, but we are also trying to see better detection of that reference. So, I think we are in so many ways, improving. And I am – I’ve been in this for 20 years, some of the things that thought was a dream is coming true. So, truly just keep living well and keep thriving. There are options.

Katherine:                     

Yeah. That’s, it’s positive.

Dr. Ramaswamy:          

Yes.

AML Targeted Therapy: How Molecular Test Results Impact Treatment Options

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AML Targeted Therapy: How Molecular Test Results Impact Treatment Options from Patient Empowerment Network on Vimeo.

How could the results of molecular testing affect your acute myeloid leukemia (AML) treatment choice? Dr. Sanam Loghavi explains how inhibitor therapy works to treat AML.

Dr. Sanam Loghavi is a hematopathologist and molecular pathologist at The University of Texas MD Anderson Cancer Center. Learn more about Dr. Loghavi.

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Transcript:

Katherine Banwell:

Dr. Loghavi, how do molecular test results impact the care plan and treatment choices? 

Dr. Sanam Loghavi:

Sure. So, again, associated with really two major factors in the care of the patient. One is the decision of how intensely to treat the patient and whether or not the patient is a candidate for a hematopoietic stem cell transplant. And then the other is the availability of targeted therapies to those patients.  

So, there are now several molecular alterations that make the disease amenable to treatment with targeted therapies, including mutations in FLT3, which is a name of a gene, mutations in IDH1, IDH1 or IDH2. And again, depending on the change, the patients may receive targeted therapy. 

Katherine Banwell:

Dr. Loghavi, you mentioned inhibitor therapy. What is this treatment, and how does it work? 

Dr. Sanam Loghavi:

Sure. So, again, it depends on the medication and it depends on the molecular change. 

But essentially what happens when you have a mutation in a gene the normal function of that gene is impaired and a lot of the times that’s why you develop leukemia is because of the impairment of that normal function. So, usually what targeted therapies do, if that mutation is causing an apparent activation of let’s say a signaling molecule, then those targeted therapies will block that signaling. Or if it’s a deregulation of an epigenetic – and epigenetic means beyond genetic, so epigenetic factor, then the goal of that targeted therapy is to maintain that normal function or restore that normal function. 

What Are the Noted Disparities in Lung Cancer Screening and Access?

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What Are the Noted Disparities in Lung Cancer Screening and Access? from Patient Empowerment Network on Vimeo.

What are some lung cancer disparities in the U.S.? Dr. Lecia Sequist shares insight about disparities in lung cancer screening and care, some causes of the disparities, and ways that advocacy groups are trying to decrease disparities. 

Dr. Sequist is program director of Cancer Early Detection & Diagnostics at Massachusetts General Hospital and also The Landry Family Professor of Medicine at Harvard Medical School.

[ACT]IVATION TIP:

“…be sure to ask your doctor if genetic testing has been performed on your cancer, and if not, can it be performed? It’s not always the right answer, depends on the type of cancer that you have and the stage, but if you have adenocarcinoma and an advanced cancer, like stage III or stage IV, it is the standard to get genetic testing and that should be something that can be done.”

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How Should Newly Diagnosed Lung Cancer Patients Deal with Disease Stigma

Transcript:

Lisa Hatfield:

Thank you. Dr. Sequist, with cancer care, there are some noted disparities, particularly with access to screening and care. What are some of those disparities with lung cancer screening and care?

Dr. Lecia Sequist:

Lung cancer, unfortunately, there are a lot of disparities around the globe, but even if we focus on the U.S., there’s a lot of regional disparities as far as who’s getting cancer, who’s getting lung cancer, where the cancer treatment centers are located, where the screening is available. Lung cancer screening is really effective as far as finding cancer in the earliest stages. It’s not equally available across the country. Some of it has to do with there are certain states that expanded their Medicaid coverage as part of the medical care reform that happened about seven, eight years ago, and there are some states that didn’t expand the Medicaid, and then that situation translated into whether lung cancer screening was easy to get started in hospitals in that state. So there are some regions of the country, and a lot of them are in the South as well as the Western U.S., where if you want to get lung cancer screening, you may have to travel more than 30 miles or even more than 50 miles in order to get lung cancer screening.

There’s lots of activists and patient advocacy groups that are working to try and fix that problem so that anyone could have access to lung cancer screening within a reasonable distance of where they live, but there’s a lot of barriers. Similarly, there are barriers to getting genetic testing performed. We know that doing genetic testing on a lung cancer, it can be really helpful, especially if you have adenocarcinoma, the most common type of lung cancer, getting genetic testing done to see if there are targeted therapies that can be used to treat the cancer is a really important step in the diagnosis, but not all patients are having that done. And as you might imagine, there’s disparities, racial disparities in who’s getting these tests ordered and who is not having that testing done. And so it is important. My activation tip for patients would be to be sure to ask your doctor if genetic testing has been performed on your cancer, and if not, can it be performed? It’s not always the right answer, depends on the type of cancer that you have and the stage, but if you have adenocarcinoma and an advanced cancer, like stage III or stage IV, it is the standard to get genetic testing and that should be something that can be done. 

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What Are Advanced Prostate Cancer Treatment Options?

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What Are Advanced Prostate Cancer Treatment Options? from Patient Empowerment Network on Vimeo.

What is advanced prostate cancer and how is it treated? Expert Dr. Tanya Dorff explains advanced prostate cancer and discusses available treatment approaches, including clinical trial considerations.

Dr. Tanya Dorff is Associate Professor in the Department of Medical Oncology & Therapeutics Research at City of Hope. Learn more about Dr. Dorff.

 

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Transcript:

Katherine:

First, what does it mean to have advanced disease? 

Dr. Dorff:

Advanced prostate cancer signals cancer that’s come back after curative intention or has presented de novo in a way that means we don’t currently have a tool to cure it. That’s at least how I view advanced prostate cancer. You could take a broader definition and consider some high-risk localized patients who need multimodal therapy, but to me, it’s really signaling a shift from something we’re aiming to cure versus something we’re aiming to manage, so that can manifest just as a PSA that’s rising, what we call biochemical recurrence, or it can manifest as visible metastatic disease. 

Katherine:

What does “locally advanced mean? 

Dr. Dorff:

So, “locally advanced” means that it hasn’t metastasized, but it might be involving the local structures, like the seminal vesicles or the bladder or some of the regional lymph nodes, the pelvic lymph nodes. 

Katherine:

How is advanced prostate cancer treated? 

Dr. Dorff:

The cornerstone of treatment for advanced prostate cancer has really been hormone therapy. I think there’s a lot of negative stuff out there on the internet about hormone therapy that I think does a disservice to patients because hormone therapy is truly very, very effective and, for many men, can be quite livable. 

I have patients who live more than a decade on hormone therapy, and they’re running their businesses and they’re raising their grandkids, they’re traveling, they’re running 10Ks, they’re doing all the things that they might want to be doing. That’s not to say there aren’t side effects, but hormone therapy is an effective cornerstone, and I really hope people won’t dismiss it offhand because of the negative things they’ve heard or read about it. 

Katherine:

What about other treatment classes?  

Dr. Dorff:

Most of our other treatments are really layered on top of hormone therapy. We may get to a point – 10 years from now, I don’t know, sometime in the future – when we don’t start with the hormone therapy, so a lot of patients come in asking about the new radiopharmaceutical, the Lutetium-177-PSMA that got approved last year, or about whether chemotherapy can be used. They can be, but they’re really layered on top of hormone therapy, so the hormone therapy is the first treatment, it’s the most effective right now, and then it’s continued as we swap out – we add a novel hormonal agent like abiraterone (Zytiga), or enzalutamide (Xtandi), or one of the others. 

When that is no longer effective, we swap that out, we might use chemotherapy or the radiopharmaceutical. There’s also an immunotherapy that’s been around for more than a decade called sipuleucel-T, and now there’s the targeted therapies – the PARP inhibitors – as well for select patients. 

Katherine:

Where do clinical trials fit into treatment?  

Dr. Dorff:

That’s a great question. I’m so glad you asked. Clinical trials some people mistakenly believe are your last choice, like you’ve gone through every single treatment we have, and then you go to a clinical trial. That’s not the case. Some of the biggest advances in prostate cancer have been when we’ve taken drugs that work in a more advanced resistance setting, like a second- or third-line, and when we move them right up front, first-line, we dramatically amplify their benefit. We dramatically improve survival. 

So, if we don’t think about a clinical trial in the first line, we’re going to miss the opportunity to not only develop those new treatment paradigms, but actually participate in them ahead of when they become the new standard of care down the road. 

Another misconception that people have often about clinical trials is that they are always randomized, there’s always a flipping of the coin in assignment of different treatments, and that they may include a placebo. So, most of our clinical trials at this point do not include placebo. Because we have so many effective treatment options, we’re more and more frequently comparing either two drugs against one, so everyone’s getting at least one effective drug, or we’re not comparing at all, but everyone’s getting some new treatment or some combination of treatments when we’re working out dosing in that scenario, like a Phase II. 

So, clinical trials are really an option at any stage of prostate cancer, even at diagnosis for localized disease all the way through, and truly, I hope people would consider looking at those as options because that’s where some of the most innovative treatment options are going to become available to them. 

Three Promising Areas of Lung Cancer Research

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What are three promising areas of lung cancer research? In the “Emerging Therapies| Hope for the Future of Lung Cancer Care” program, expert Dr. Jyoti Patel from Robert H. Lurie Comprehensive Cancer Center of Northwestern University shares updates about emerging research and insights about the future of lung cancer care. 

1. Identification of Oncogenes

Identification of oncogenes is an active area of lung cancer research efforts. HER2 mutations and EGFR Exon 20 mutations are a couple examples of oncogenes that are targeted in research to develop more effective treatments against them. The epidermal growth factor receptor (EGFR) gene mutation that adds the exon 20 mutation is rare, but when the mutation occurs it’s more likely to occur in those with a non-small cell lung cancer (NSCLC) type of adenocarcinoma, in women, in those of Asian descent, and young adults with NSCLC.

 2. Mitigate Resistance in Targeted Therapies

Drug resistance is also under study to mitigate issues for those who receive targeted therapies. Unfortunately, those who are treated with targeted therapies eventually develop resistance, so this is why this is another focus of current research efforts. There are three generations of EGFR treatments, and now fourth-generation tyrosine kinase inhibitor treatments are being researched to provide an additional line of treatments.

3. Understanding Tumor Microenvironment

The tumor microenvironment is under study to understand more about the different types of responses to immunotherapies. Though some patients have positive and vigorous responses to immunotherapies, other patients exhibit immunity to the impact of immunotherapies. Researchers are looking at the tumor microenvironment for potential ways to co-stimulate vigorous and durable immunotherapy responses for improved lung cancer care.

Lung cancer research is currently investigating many areas of research, and recent lung cancer treatment advances have increased patient survival rates and quality of life. Researchers are also investigating many areas for further screening and treatment advances, including potential blood tests for early detection. If you want to learn more about lung cancer care and treatments, check out our lung cancer information.

What Does Triplet Therapy in AML Mean for the Future?

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What Does Triplet Therapy in AML Mean for the Future? from Patient Empowerment Network on Vimeo.

What do acute myeloid leukemia (AML) patients need to know about triplet therapy? Dr. Naval Daver from the University of Texas MD Anderson Cancer Center shares his perspective. Learn about the meaning, progress, and outlook for triplet therapy. 

[ACT]IVATION TIP from Dr. Daver: “Some of the early data with the FLT3 inhibitor as well as the CD47 antibody triplets are showing very, very promising activity and are now moving into larger multi-center and randomized studies.”

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Transcript: 

Art:

Dr. Daver, what does triplet therapy in AML mean for the future?

Dr. Naval Daver:

So when we say triplet therapy, what we’re really thinking about is building on the existing FDA-approved combination of HMA venetoclax (Venclexta), so as a background venetoclax, showed a CR, CRI which is a complete remission rate of about 70 to 75 percent with the median survival in 15 months.

This was in older patients, about 75 years in age, those who were not considered fit for intensive chemotherapy, although this was a major step forward in comparison to what we have seen with traditional low intensities with azacitidine (Onureg or Vidaza), decitabine (Dacogen) alone, we do see the three-year survival is about 25 to 30 percent. 

So this is progress compared to 10 percent long-term survival, we used to get a decade ago, but, of course, we want to improve on that. Also, a molecular analysis of data has shown that there are certain molecular subsets that don’t respond as well to azacitidine, venetoclax or if they respond they relapse quickly these include FLT3 mutated and the TP53 mutated as well as potentially MLL rearranged.

And so here we have started incorporating the targeted therapies like inhibitors like the menin inhibitors like CD47 antibodies to target those specific high-risk or bad molecular cytogenetic groups, and we are seeing that with the combinations of these three drugs, especially for those particular molecular subsets.

So azacitidine and venetoclax for FLT3 inhibitor for FLT3 mutator, azacitidine, and venetoclax, magrolimab for TP53 mutated, the response rates that we’re getting, as well as the depth of response and the early trends towards survival are looking very, very promising compared to what we have seen with azacitidine venetoclax alone.

So we believe, and I personally believe that these three drug combinations, the so-called triplets will actually be eventually the way to go forward now, that means that one has to realize that when you add a third drug, there is a cumulative myelosuppression, azacitidine-venetoclax is already a myelosuppressive regimen. 

Yes, it’s manageable, but it is myelosuppressive. And the third drug, this can become more cumulative, so we have been working for the last three, four years and continue to work on those optimization because since we are seeing true synergy but pre-clinically and what we think in the clinic, we are not needing to give full doses and we’re doing reduced durations of venetoclax and those with FLT3 inhibitor, and now we feel that some of those triplets are actually giving very, very, very good efficacy.

There’s a lot of discussion in the community of whether we need to combine all two drugs up front or can be sequence these drugs or can we introduce a targeted therapy based on a molecular escape, and I think a lot of these will have to be evaluated and many of these are being looked at in various trials, but I do think the bottom line is that bringing in your targeted therapy or immunotherapies early on in the frontline setting and some way or the other is probably where you’re going to get the most bang for the buck and the most benefit in curing patients long-term rather than trying to reserve them for the salvage, because in salvage AML historically, nothing has really been able to improve the long-term cure rate significantly.

So the activation tip for this question is that now with the identification of certain molecular subsets that have poorer outcomes with the HMA venetoclax, we have started incorporating targeted and immunotherapies in the earlier settings, either up front in the three drug combination or an early sequential approach.

And we believe that with such combinations, we may be able to achieve deeper remission and longer responses. Some of the early data with the FLT3 inhibitor as well as the CD47 antibody triplets are showing very, very promising activity and are now moving into larger multi-center and randomized studies. 

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The Importance of the FLT3 Mutation in AML

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The Importance of the FLT3 Mutation In AML from Patient Empowerment Network on Vimeo.

What do acute myeloid leukemia (AML) patients need to  know about FLT3 mutation? Dr. Naval Daver from the University of Texas MD Anderson Cancer Center discusses considerations about the mutation. Learn about the incidence of the FLT3 mutation, risk of relapse, and treatment options.

[ACT]IVATION TIP from Dr. Daver: “ it is very important to know the status of the FLT3 the mutation, both in diagnosis to see if one would benefit by the addition of the FLT3 inhibitor to the frontline induction chemo as well as in relapse because this would open up the option for FLT3  inhibitor targeted therapies, which would probably have the best chance of response and long-term outcomes.“ 

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Transcript: 

Art:

Dr. Daver, for AML with a FLT3 mutation, what have we learned, and what is currently being investigated?

Dr. Naval Daver:

AML with the FLT3 mutation is very important from both prognostic and from therapy perspective, prognostically, this is considered to be one of the high-risk mutations, it’s also one of the most frequent mutations in AML in, seen in about 30 to 35 percent of younger and about 15 to 20 percent of older patients with AML, and these patients often have very prolific disease, elevated white count leukocytosis. And without the addition of FLT3 inhibitors, there is a high risk of relapse and a short overall survival. 

Over the last 15 years, a number of targeted therapies called the FLT3 inhibitors have emerged, these started with the first-generation FLT3 inhibitors drugs, such as lestaurtinib and sorafenib (Nexavar), now we have the second-generation FLT3 inhibitors, this includes drugs like gilteritinib (Xospata), quizartinib, and crenolanib which are more potent, specific, and better tolerated.

The first study that showed that the incorporation of FLT3 inhibitors improves outcome was a study called RATIFY Study, this is a frontline study looking at newly diagnosed FLT3 mutated younger patients where we added the FLT3 inhibitor midostaurin (Rydapt or Tauritmo), which is the first-generation FLT3 inhibitor to the standard induction chemo versus a placebo, added to standard induction chemo, induction chemo being standard of care to that time and this showed that in the addition of FLT3 inhibitor to induction chemo did improve remission rates and overall survival as compared to induction, and led to the approval of the FLT3 inhibitor midostaurin in the frontline setting. 

Since then, two other FLT3 inhibitors, second-generation potent FLT3 inhibitors drugs called gilteritinib, and lestaurtinib have also been evaluated. Gilteritinib, in a relapsed setting where single-agent gilteritinib, has given 50 to 60 percent response rates and has been extremely well-tolerated and much better than any other salvage treatment in the FLT3 space that we have ever seen, and in the frontline setting quizartinib and second-generation inhibitor also very recently, just a few months ago, there was data showing the combination of his art with intensive chemotherapy improved survival as compared to intensive chemotherapy alone. 

And so we think we are…they will be a third for the inhibitor to get approved, so there’s been a lot of progress overall in the three space, and there are other newer FLT3 inhibitors also in early clinical investigation that we think could eventually be as part or even better, the activation point related to this question is that, for the inhibitors have dramatically improved outcomes, both in the frontline setting when added to traditional backbone intensive chemotherapy as well as potentially lower intensity therapy, as well as in the relapsed refractory setting, and it is very important to know the status of the FLT3 the mutation, both in diagnosis to see if one would benefit by the addition of the FLT3 inhibitor to the frontline induction chemo as well as in relapse because this would open up the option for FLT3  inhibitor targeted therapies, which would probably have the best chance of response and long-term outcomes. 

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