David Henry's JCSO Podcast

In this interview, Dr David Henry, the Editor-in-Chief of The Journal of Community and Supportive Oncology, and Dr Ken Anderson, the Kraft Family Professor of Medicine at Harvard Medical School and an international thought leader and investigator in myeloma, discuss three cases of patients with myeloma that are indicative of the remarkable therapeutic advances in oncology in general, and in myeloma in particular. 

Listen to the podcast below

In this interview, Dr David Henry, the Editor-in-Chief of The Journal of Community and Supportive Oncology, and Dr Ken Anderson, the Kraft Family Professor of Medicine at Harvard Medical School and an international thought leader and investigator in myeloma, discuss three cases of patients with myeloma that are indicative of the remarkable therapeutic advances in oncology in general, and in myeloma in particular. 

Listen to the podcast below

In this interview, Dr David Henry, the Editor-in-Chief of The Journal of Community and Supportive Oncology, and Dr Ken Anderson, the Kraft Family Professor of Medicine at Harvard Medical School and an international thought leader and investigator in myeloma, discuss three cases of patients with myeloma that are indicative of the remarkable therapeutic advances in oncology in general, and in myeloma in particular. 

Listen to the podcast below

DR HENRY I thought we might discuss some cases of patients with myeloma, starting with a relatively simple case and ending with one that is a little more complicated. For the first case, we have a 56-year-old healthy man with IgG kappa myeloma whose work-up shows he has multiple lytic bone lesions. He has normal renal function, normal calcium, and he’s transplant-eligible by other health issues. I’ll leave the cytogenetics up to you if that changes your approach. How would you develop or pose some options for this man’s treatment to begin with?

DR ANDERSON It’s important to start out by saying that we, in myeloma, have many new classes of drugs and many new opportunities to choose from to treat this patient.¹ As you know, we have proteasome inhibitors, the first-generation bortezomib, then carfilzomib and ixazomib. We have the immunomodulatory drugs (IMiDs), thalidomide, and now lenalidomide and pomalidomide. We have a histone deacetylase (HDAC) inhibitor approved called panobinostat, and we have 2 monoclonal antibodies approved, elotuzumab and daratumumab. These classes of medicine have made it possible for 20 different Food and Drug Administration (FDA) approvals in the last 10-15 years. These agents, having been tested in advanced myeloma, have moved toward initial management.

This person is 50 years old. He has adequate liver, heart, lung, and kidney function, so he would be eligible for high-dose therapy and stem-cell transplantation. In terms of initial management, there are many options (Figure 1). We strongly recommend that triplet therapy be used initially. The most common triplets would be lenalidomide, bortezomib, and dexamethasone (RVD)^2,3 or cyclophosphamide, bortezomib, and dexamethasone (CyBorD).⁴ If this man had neuropathy, perhaps carfilzomib, the second-generation proteasome inhibitor, with lenalidomide and dexamethasone could have been used. Why do we use these? The extent and frequency of response with these triplets is nearly universal overall response rate, with three-quarters very good partial and half-complete responses, including minimal residual disease negative responses. In this patient, we would therefore recommend treatment with either RVD or CyBorD for several cycles to maximal response.

DR HENRY In summary then, this would be, in 2017, off-protocol while the data is pending: it’s reasonable to get a deep induction response, collect stem cells, have a discussion with the patient, and then consider high-dose therapy or not.

DR ANDERSON Yes. I think it’s reasonable to discuss it. We need to be open and honest with patients that the standard of care remains transplant, that you incorporate novel treatments before the transplant and novel treatments as maintenance after the transplant. The happy news is that the outcome, especially for patients who have standard-risk myeloma, is at least a decade or longer progression-free survival. It’s an optimistic picture. The data in terms of transplant being needed or not, will come within the next several years.

For now, it is a standard of care to use 1 high-dose melphalan and stem-cell transplant in this setting. I will add into our discussion with patients – besides the opportunity to harvest stem cells and think about whether one needs to do a transplant early on or not – is the issue of toxicity. High-dose melphalan by itself has a small but real secondary incidence of cancer, myelodysplasia, or leukemia. If one uses lenalidomide maintenance after melphalan transplantation treatment, that risk of secondary cancer is slightly increased.

In my experience, if patients have achieved a complete response with induction therapy only, it’s not unreasonable to offer early transplant and be clear that’s the standard of care. The alternative is maintenance with lenalidomide, knowing once the stem cells have been harvested, that transplantation can be an option to treat relapsed myeloma. We have many other options available as well. Time will tell in terms of the ongoing randomized trials as to whether transplant remains central to our treatment paradigm.

DR HENRY This leads us to our second patient. Here we have an older man of 74 years. He’s a professional piano player, so we want to try to avoid peripheral neuropathy in him. He has some mild renal insufficiency and some coronary artery disease, so he’s deemed transplant-ineligible. He has IgG kappa myeloma, and he’s brand new. What would you consider to be options for him for treatment?

DR ANDERSON This brings up the issue of a transplant-ineligible patient. He has significant comorbidity that would make transplantation an increased risk. What we would recommend in such a patient is still triplet induction therapy incorporating novel agents (Figure 1). Lenalidomide, the immunomodulatory drug, can safely be given in the context of neuropathy because it does not cause significant neuropathy. It would need to be dose modified, depending on the degree of renal insufficiency. We would recommend also including proteasome inhibitors. Bortezomib, the first-generation proteasome inhibitor, would be contraindicated because it does have a small but real attendant neuropathy. If, however, it is given weekly and subcutaneously, the risk of attendant neuropathy is quite low. In this patient, therefore, one could start with lenalidomide and bortezomib weekly and subcutaneously,^1,2 with a very early and vigilant follow-up for the earliest signs of neuropathy, so as not to allow it to develop and compromise his career.

Alternatively, one could use a proteasome inhibitor that does not have attendant neuropathy. Carfilzomib, the second-generation proteasome inhibitor, does not have neuropathy.⁹ But we would need to have caution here, because this patient has a history of coronary artery disease, and carfilzomib has a very small, but real, incidence of cardiac toxicity so would need to be used judiciously in this setting. The third proteasome inhibitor, ixazomib, is the next-generation bortezomib-class proteasome inhibitor, and it’s oral.¹⁰ It has less neuropathy than does bortezomib, so in my view is a very realistic option for him together with lenalidomide. It does have a small incidence of neuropathy, so close monitoring for neuropathy would be indicated. We could use lenalidomide–dexamethasone as a doublet and avoid neuropathy,¹¹ but usually doublets are reserved only for frail patients.

My recommendation, therefore, would be RVD with the bortezomib weekly or subcutaneously, or alternatively, lenalidomide, ixazomib, dexamethasone as an all-oral regimen as induction therapy. In my view, this 74-year-old patient with comorbidity is not a transplant candidate. However, one can be very optimistic with this patient. The likelihood that he could have myeloma as a chronic illness and die from something else is quite high. Initial induction triplet therapy would achieve a very high response extent and frequency. The durability would be long, especially with lenalidomide maintenance if it’s standard-risk myeloma or lenalidomide and a proteasome inhibitor, probably ixazomib in this setting, if he were to have high-risk myeloma.

If myeloma relapses, then there are many options that could be used in this patient and achieve years of progression-free and overall survival. Indeed, he is 74 years old and will respond very well to induction triplet therapy, with many years’ duration of response due to continuous lenalidomide or lenalidomide and proteasome inhibitor maintenance. Then there are many effective options to treat relapsed therapy using triplet novel agents. Therefore, his lifespan is unlikely to be shortened by multiple myeloma.

DR HENRY It’s so incredible compared with what it was when I trained. The next patient, a 45-year-old woman with IgG lambda myeloma, has had RVD induction and responded. She had lenalidomide maintenance, but then she progressed, and she got her stem-cell transplant, and she’s progressing after that. I guess we’re looking here to fold in some of the newer agents. How you would you do that in this patient?DR ANDERSON Yes. I think one of the most remarkable and exciting developments with myeloma is the rapid approval of the novel classes of agents that I mentioned earlier – the proteasome inhibitors, the immunomodulatory drugs, the HDAC inhibitor, and the monoclonal antibodies.¹ They’re particularly relevant in a patient such as this one, whose myeloma has relapsed after what would be considered standard therapy for a young person with standard-risk myeloma. This patient had RVD and maintenance therapy, and then progressed. The transplant was given for relapsed myeloma. The opportunity to use stem-cell transplant in patients when myeloma becomes active after maintenance should not be forgotten as it can be very effective. In all the trials done to date in which early versus late transplant are compared, there have been similar outcomes. Therefore, if the transplant isn’t done early, don’t forget that it’s an option at the time the myeloma progresses. I do want to mention, that there are lots of options for relapsed myeloma (Figures 3 and 4). I mentioned RVD or CyBorD as initial triplet therapies.^2-4 In North America, those are the 2 most common regimens. If myeloma then relapses and is resistant to RVD or to CyBorD, then we need to identify alternatives.

We also need to think about the comorbidities in the patient – issues such as age, neuropathy, presence of renal dysfunction, and other clinical factors. And we need to think about what treatment they’ve had in the past. This patient has had RVD, maintenance with lenalidomide, and a stem-cell transplant. We can offer patients a variety of therapies, but in the context of resistance to the first-generation proteasome inhibitor bortezomib and the first-generation immunomodulatory drug lenalidomide, we would strongly recommend the second-generation immunomodulatory drug pomalidomide¹² together with a second-generation proteasome inhibitor, be that carfilzomib¹³ or ixazomib.¹⁴ When one uses the second-generation IMiDs and proteasome inhibitors together, there’s a very high frequency of response in the order of 70%-80%, which lasts years.

Besides carfilzomib and ixazomib proteasome inhibitors, we also have elotuzumab and daratumumab, the monoclonal antibodies.^15-17 These agents have been FDA approved to treat patients such as this one who has had 1-3 previous therapies for their myeloma. All of them have been approved in randomized phase 3 trials compared with lenalidomide-dexamethasone in the control arm.^13-15,17 They’ve all been found to be superior. Although lenalidomide-dexamethasone combined with daratumumab, ixazomib, elotuzumab, or carfilzomib is superior to lenalidomide in relapsed myeloma, the situation in North America, as in this patient, is usually that patients have had lenalidomide-dexamethasone as part of their initial treatment and their myeloma is refractory to lenalidomide.

Hence, we recommend, that we go to the second-generation pomalidomide and second-generation proteasome inhibitors, either carfilzomib or ixazomib. Having said that, the treatment paradigm is evolving. For example, the monoclonal antibody daratumumab was initially approved by the FDA in multiply relapsed disease as a single agent because it achieves a 30% response rate.¹⁶ It now has been moved earlier into the first relapse of multiple myeloma, where it achieves much higher response rates when combined with lenalidomide–dexamethasone or combined with bortezomib–dexamethasone.^17,18 Response rates of 70%-80% can be achieved, including minimal residual disease negative complete responses.

Today, in a patient who has had RVD transplant and myeloma has returned, we would recommend second-generation IMiDs, pomalidomide, and second-generation proteasome inhibitors, either carfilzomib or ixazomib. Data for daratumumab combined with lenalidomide-dexamethasone or with bortezomib-dexamethasone, look very promising. We need, however, to see more experience of daratumumab together with lenalidomide-dexamethasone or daratumumab together with bortezomib-dexamethasone in patients whose myeloma is refractory to RVD, that is, patients whose myeloma has returned after RVD induction treatment. Of note, pomalidomide, dexamethasone, and daratumumab have just been approved by the FDA and may also be active even in myeloma recurring after RVD treatment.¹⁹

Daratumumab in combination will be moving earlier and earlier and may be appropriate to treat the first relapse. I do want to stress, however, that at present I save daratumumab for the second or greater relapse. Daratumumab is active even when relapse occurs after treatment with second-generation IMiDs and proteasome inhibitors.

DR HENRY Before we close, I have a couple practical questions with these antibodies. Daratumumab has the track record of first-treatment severe reactions and long infusion times. How long are you anticipating the first daratumumab treatment takes? There has been some talk that maybe splitting it in half and going over 2 days is easier on the patient and the infusion center. Have you done that?

DR ANDERSON Yes, I think that’s a very important point. We need to be thinking – first and foremost – about efficacy of our therapy. Equally important, however, are the safety profile and the user-friendliness for the patient. Daratumumab infusions are quite long – on the order of 8 hours or longer on day 1 of infusion. And to date, all the clinical trials have used daratumumab infusions weekly for 8 treatments, followed by 8 treatments given every 2 weeks. Then monthly daratumumab is given as a maintenance therapy. Thus, there is a requirement for multiple outpatient clinic visits that can be prolonged.

One of the opportunities that’s being tested is to give daratumumab subcutaneously. While this is being evaluated in protocols now, the results that have been reported at our national meetings look to be quite promising in terms of efficacy, similar to results with the intravenous administration. Obviously, this would allow for a much more convenient clinic visit and shorter time for the patients being treated.

I should mention that the other antibody, elotuzumab, has been approved in combination with lenalidomide and dexamethasone.¹⁵ The infusions with lenalidomide, dexamethasone, and the antibody elotuzumab are much shorter, on the order of 2- or 3-hour visits. The place for elotuzumab in the management of relapsed myeloma is yet to be totally defined. We tend to use it now in the setting of more indolent relapses, where patients might have a slowly rising monoclonal protein. Elotuzumab-lenalidomide-dexamethasone has maintained an overall survival advantage at 4 years compared with lenalidomide-dexamethasone when used in relapsed myeloma.

We are quite excited about both antibodies. Daratumumab tends to get most of the activity, as it achieves responses as a single agent,¹⁶ and the depth of the responses are markedly increased when it’s combined with lenalidomide-dexamethasone or bortezomib-dexamethasone.^17,18 However, one shouldn’t forget elotuzumab¹⁵ based on its tolerability and the survival advantage I mentioned at 4 years.

The final point is that we think about myeloma genetically at the time of diagnosis and relapse in terms of standard or high-risk disease. One of the hallmarks of high-risk disease has been 17P deletion or P53 dysfunction. One of the most exciting outcomes of the development of monoclonal antibodies has been the responses observed even in the context of P53 deletion. Clearly, antibody-mediated cellular cytotoxicity, complement-mediated cytotoxicity, and other mechanisms of action of these antibodies do not require normal P53 function. The important point, therefore, is that what has previously been thought of as high-risk disease can nowadays be effectively treated with these new immune treatments, correlating with the marked improvement in survival and overall outcome.

DR HENRY We have outlined 3 kinds of myeloma patients we see, and especially interesting is the last patient, who has relapsed and then progressed, and in whom newer drugs have a role. Thank you for such a complete and thorough discussion, Dr Anderson.

DR HENRY I thought we might discuss some cases of patients with myeloma, starting with a relatively simple case and ending with one that is a little more complicated. For the first case, we have a 56-year-old healthy man with IgG kappa myeloma whose work-up shows he has multiple lytic bone lesions. He has normal renal function, normal calcium, and he’s transplant-eligible by other health issues. I’ll leave the cytogenetics up to you if that changes your approach. How would you develop or pose some options for this man’s treatment to begin with?

DR ANDERSON It’s important to start out by saying that we, in myeloma, have many new classes of drugs and many new opportunities to choose from to treat this patient.¹ As you know, we have proteasome inhibitors, the first-generation bortezomib, then carfilzomib and ixazomib. We have the immunomodulatory drugs (IMiDs), thalidomide, and now lenalidomide and pomalidomide. We have a histone deacetylase (HDAC) inhibitor approved called panobinostat, and we have 2 monoclonal antibodies approved, elotuzumab and daratumumab. These classes of medicine have made it possible for 20 different Food and Drug Administration (FDA) approvals in the last 10-15 years. These agents, having been tested in advanced myeloma, have moved toward initial management.

This person is 50 years old. He has adequate liver, heart, lung, and kidney function, so he would be eligible for high-dose therapy and stem-cell transplantation. In terms of initial management, there are many options (Figure 1). We strongly recommend that triplet therapy be used initially. The most common triplets would be lenalidomide, bortezomib, and dexamethasone (RVD)^2,3 or cyclophosphamide, bortezomib, and dexamethasone (CyBorD).⁴ If this man had neuropathy, perhaps carfilzomib, the second-generation proteasome inhibitor, with lenalidomide and dexamethasone could have been used. Why do we use these? The extent and frequency of response with these triplets is nearly universal overall response rate, with three-quarters very good partial and half-complete responses, including minimal residual disease negative responses. In this patient, we would therefore recommend treatment with either RVD or CyBorD for several cycles to maximal response.

DR HENRY In summary then, this would be, in 2017, off-protocol while the data is pending: it’s reasonable to get a deep induction response, collect stem cells, have a discussion with the patient, and then consider high-dose therapy or not.

DR ANDERSON Yes. I think it’s reasonable to discuss it. We need to be open and honest with patients that the standard of care remains transplant, that you incorporate novel treatments before the transplant and novel treatments as maintenance after the transplant. The happy news is that the outcome, especially for patients who have standard-risk myeloma, is at least a decade or longer progression-free survival. It’s an optimistic picture. The data in terms of transplant being needed or not, will come within the next several years.

For now, it is a standard of care to use 1 high-dose melphalan and stem-cell transplant in this setting. I will add into our discussion with patients – besides the opportunity to harvest stem cells and think about whether one needs to do a transplant early on or not – is the issue of toxicity. High-dose melphalan by itself has a small but real secondary incidence of cancer, myelodysplasia, or leukemia. If one uses lenalidomide maintenance after melphalan transplantation treatment, that risk of secondary cancer is slightly increased.

In my experience, if patients have achieved a complete response with induction therapy only, it’s not unreasonable to offer early transplant and be clear that’s the standard of care. The alternative is maintenance with lenalidomide, knowing once the stem cells have been harvested, that transplantation can be an option to treat relapsed myeloma. We have many other options available as well. Time will tell in terms of the ongoing randomized trials as to whether transplant remains central to our treatment paradigm.

DR HENRY This leads us to our second patient. Here we have an older man of 74 years. He’s a professional piano player, so we want to try to avoid peripheral neuropathy in him. He has some mild renal insufficiency and some coronary artery disease, so he’s deemed transplant-ineligible. He has IgG kappa myeloma, and he’s brand new. What would you consider to be options for him for treatment?

DR ANDERSON This brings up the issue of a transplant-ineligible patient. He has significant comorbidity that would make transplantation an increased risk. What we would recommend in such a patient is still triplet induction therapy incorporating novel agents (Figure 1). Lenalidomide, the immunomodulatory drug, can safely be given in the context of neuropathy because it does not cause significant neuropathy. It would need to be dose modified, depending on the degree of renal insufficiency. We would recommend also including proteasome inhibitors. Bortezomib, the first-generation proteasome inhibitor, would be contraindicated because it does have a small but real attendant neuropathy. If, however, it is given weekly and subcutaneously, the risk of attendant neuropathy is quite low. In this patient, therefore, one could start with lenalidomide and bortezomib weekly and subcutaneously,^1,2 with a very early and vigilant follow-up for the earliest signs of neuropathy, so as not to allow it to develop and compromise his career.

Alternatively, one could use a proteasome inhibitor that does not have attendant neuropathy. Carfilzomib, the second-generation proteasome inhibitor, does not have neuropathy.⁹ But we would need to have caution here, because this patient has a history of coronary artery disease, and carfilzomib has a very small, but real, incidence of cardiac toxicity so would need to be used judiciously in this setting. The third proteasome inhibitor, ixazomib, is the next-generation bortezomib-class proteasome inhibitor, and it’s oral.¹⁰ It has less neuropathy than does bortezomib, so in my view is a very realistic option for him together with lenalidomide. It does have a small incidence of neuropathy, so close monitoring for neuropathy would be indicated. We could use lenalidomide–dexamethasone as a doublet and avoid neuropathy,¹¹ but usually doublets are reserved only for frail patients.

My recommendation, therefore, would be RVD with the bortezomib weekly or subcutaneously, or alternatively, lenalidomide, ixazomib, dexamethasone as an all-oral regimen as induction therapy. In my view, this 74-year-old patient with comorbidity is not a transplant candidate. However, one can be very optimistic with this patient. The likelihood that he could have myeloma as a chronic illness and die from something else is quite high. Initial induction triplet therapy would achieve a very high response extent and frequency. The durability would be long, especially with lenalidomide maintenance if it’s standard-risk myeloma or lenalidomide and a proteasome inhibitor, probably ixazomib in this setting, if he were to have high-risk myeloma.

If myeloma relapses, then there are many options that could be used in this patient and achieve years of progression-free and overall survival. Indeed, he is 74 years old and will respond very well to induction triplet therapy, with many years’ duration of response due to continuous lenalidomide or lenalidomide and proteasome inhibitor maintenance. Then there are many effective options to treat relapsed therapy using triplet novel agents. Therefore, his lifespan is unlikely to be shortened by multiple myeloma.

DR HENRY It’s so incredible compared with what it was when I trained. The next patient, a 45-year-old woman with IgG lambda myeloma, has had RVD induction and responded. She had lenalidomide maintenance, but then she progressed, and she got her stem-cell transplant, and she’s progressing after that. I guess we’re looking here to fold in some of the newer agents. How you would you do that in this patient?DR ANDERSON Yes. I think one of the most remarkable and exciting developments with myeloma is the rapid approval of the novel classes of agents that I mentioned earlier – the proteasome inhibitors, the immunomodulatory drugs, the HDAC inhibitor, and the monoclonal antibodies.¹ They’re particularly relevant in a patient such as this one, whose myeloma has relapsed after what would be considered standard therapy for a young person with standard-risk myeloma. This patient had RVD and maintenance therapy, and then progressed. The transplant was given for relapsed myeloma. The opportunity to use stem-cell transplant in patients when myeloma becomes active after maintenance should not be forgotten as it can be very effective. In all the trials done to date in which early versus late transplant are compared, there have been similar outcomes. Therefore, if the transplant isn’t done early, don’t forget that it’s an option at the time the myeloma progresses. I do want to mention, that there are lots of options for relapsed myeloma (Figures 3 and 4). I mentioned RVD or CyBorD as initial triplet therapies.^2-4 In North America, those are the 2 most common regimens. If myeloma then relapses and is resistant to RVD or to CyBorD, then we need to identify alternatives.

We also need to think about the comorbidities in the patient – issues such as age, neuropathy, presence of renal dysfunction, and other clinical factors. And we need to think about what treatment they’ve had in the past. This patient has had RVD, maintenance with lenalidomide, and a stem-cell transplant. We can offer patients a variety of therapies, but in the context of resistance to the first-generation proteasome inhibitor bortezomib and the first-generation immunomodulatory drug lenalidomide, we would strongly recommend the second-generation immunomodulatory drug pomalidomide¹² together with a second-generation proteasome inhibitor, be that carfilzomib¹³ or ixazomib.¹⁴ When one uses the second-generation IMiDs and proteasome inhibitors together, there’s a very high frequency of response in the order of 70%-80%, which lasts years.

Besides carfilzomib and ixazomib proteasome inhibitors, we also have elotuzumab and daratumumab, the monoclonal antibodies.^15-17 These agents have been FDA approved to treat patients such as this one who has had 1-3 previous therapies for their myeloma. All of them have been approved in randomized phase 3 trials compared with lenalidomide-dexamethasone in the control arm.^13-15,17 They’ve all been found to be superior. Although lenalidomide-dexamethasone combined with daratumumab, ixazomib, elotuzumab, or carfilzomib is superior to lenalidomide in relapsed myeloma, the situation in North America, as in this patient, is usually that patients have had lenalidomide-dexamethasone as part of their initial treatment and their myeloma is refractory to lenalidomide.

Hence, we recommend, that we go to the second-generation pomalidomide and second-generation proteasome inhibitors, either carfilzomib or ixazomib. Having said that, the treatment paradigm is evolving. For example, the monoclonal antibody daratumumab was initially approved by the FDA in multiply relapsed disease as a single agent because it achieves a 30% response rate.¹⁶ It now has been moved earlier into the first relapse of multiple myeloma, where it achieves much higher response rates when combined with lenalidomide–dexamethasone or combined with bortezomib–dexamethasone.^17,18 Response rates of 70%-80% can be achieved, including minimal residual disease negative complete responses.

Today, in a patient who has had RVD transplant and myeloma has returned, we would recommend second-generation IMiDs, pomalidomide, and second-generation proteasome inhibitors, either carfilzomib or ixazomib. Data for daratumumab combined with lenalidomide-dexamethasone or with bortezomib-dexamethasone, look very promising. We need, however, to see more experience of daratumumab together with lenalidomide-dexamethasone or daratumumab together with bortezomib-dexamethasone in patients whose myeloma is refractory to RVD, that is, patients whose myeloma has returned after RVD induction treatment. Of note, pomalidomide, dexamethasone, and daratumumab have just been approved by the FDA and may also be active even in myeloma recurring after RVD treatment.¹⁹

Daratumumab in combination will be moving earlier and earlier and may be appropriate to treat the first relapse. I do want to stress, however, that at present I save daratumumab for the second or greater relapse. Daratumumab is active even when relapse occurs after treatment with second-generation IMiDs and proteasome inhibitors.

DR HENRY Before we close, I have a couple practical questions with these antibodies. Daratumumab has the track record of first-treatment severe reactions and long infusion times. How long are you anticipating the first daratumumab treatment takes? There has been some talk that maybe splitting it in half and going over 2 days is easier on the patient and the infusion center. Have you done that?

DR ANDERSON Yes, I think that’s a very important point. We need to be thinking – first and foremost – about efficacy of our therapy. Equally important, however, are the safety profile and the user-friendliness for the patient. Daratumumab infusions are quite long – on the order of 8 hours or longer on day 1 of infusion. And to date, all the clinical trials have used daratumumab infusions weekly for 8 treatments, followed by 8 treatments given every 2 weeks. Then monthly daratumumab is given as a maintenance therapy. Thus, there is a requirement for multiple outpatient clinic visits that can be prolonged.

One of the opportunities that’s being tested is to give daratumumab subcutaneously. While this is being evaluated in protocols now, the results that have been reported at our national meetings look to be quite promising in terms of efficacy, similar to results with the intravenous administration. Obviously, this would allow for a much more convenient clinic visit and shorter time for the patients being treated.

I should mention that the other antibody, elotuzumab, has been approved in combination with lenalidomide and dexamethasone.¹⁵ The infusions with lenalidomide, dexamethasone, and the antibody elotuzumab are much shorter, on the order of 2- or 3-hour visits. The place for elotuzumab in the management of relapsed myeloma is yet to be totally defined. We tend to use it now in the setting of more indolent relapses, where patients might have a slowly rising monoclonal protein. Elotuzumab-lenalidomide-dexamethasone has maintained an overall survival advantage at 4 years compared with lenalidomide-dexamethasone when used in relapsed myeloma.

We are quite excited about both antibodies. Daratumumab tends to get most of the activity, as it achieves responses as a single agent,¹⁶ and the depth of the responses are markedly increased when it’s combined with lenalidomide-dexamethasone or bortezomib-dexamethasone.^17,18 However, one shouldn’t forget elotuzumab¹⁵ based on its tolerability and the survival advantage I mentioned at 4 years.

The final point is that we think about myeloma genetically at the time of diagnosis and relapse in terms of standard or high-risk disease. One of the hallmarks of high-risk disease has been 17P deletion or P53 dysfunction. One of the most exciting outcomes of the development of monoclonal antibodies has been the responses observed even in the context of P53 deletion. Clearly, antibody-mediated cellular cytotoxicity, complement-mediated cytotoxicity, and other mechanisms of action of these antibodies do not require normal P53 function. The important point, therefore, is that what has previously been thought of as high-risk disease can nowadays be effectively treated with these new immune treatments, correlating with the marked improvement in survival and overall outcome.

DR HENRY We have outlined 3 kinds of myeloma patients we see, and especially interesting is the last patient, who has relapsed and then progressed, and in whom newer drugs have a role. Thank you for such a complete and thorough discussion, Dr Anderson.

DR HENRY I thought we might discuss some cases of patients with myeloma, starting with a relatively simple case and ending with one that is a little more complicated. For the first case, we have a 56-year-old healthy man with IgG kappa myeloma whose work-up shows he has multiple lytic bone lesions. He has normal renal function, normal calcium, and he’s transplant-eligible by other health issues. I’ll leave the cytogenetics up to you if that changes your approach. How would you develop or pose some options for this man’s treatment to begin with?

DR ANDERSON It’s important to start out by saying that we, in myeloma, have many new classes of drugs and many new opportunities to choose from to treat this patient.¹ As you know, we have proteasome inhibitors, the first-generation bortezomib, then carfilzomib and ixazomib. We have the immunomodulatory drugs (IMiDs), thalidomide, and now lenalidomide and pomalidomide. We have a histone deacetylase (HDAC) inhibitor approved called panobinostat, and we have 2 monoclonal antibodies approved, elotuzumab and daratumumab. These classes of medicine have made it possible for 20 different Food and Drug Administration (FDA) approvals in the last 10-15 years. These agents, having been tested in advanced myeloma, have moved toward initial management.

This person is 50 years old. He has adequate liver, heart, lung, and kidney function, so he would be eligible for high-dose therapy and stem-cell transplantation. In terms of initial management, there are many options (Figure 1). We strongly recommend that triplet therapy be used initially. The most common triplets would be lenalidomide, bortezomib, and dexamethasone (RVD)^2,3 or cyclophosphamide, bortezomib, and dexamethasone (CyBorD).⁴ If this man had neuropathy, perhaps carfilzomib, the second-generation proteasome inhibitor, with lenalidomide and dexamethasone could have been used. Why do we use these? The extent and frequency of response with these triplets is nearly universal overall response rate, with three-quarters very good partial and half-complete responses, including minimal residual disease negative responses. In this patient, we would therefore recommend treatment with either RVD or CyBorD for several cycles to maximal response.

DR HENRY In summary then, this would be, in 2017, off-protocol while the data is pending: it’s reasonable to get a deep induction response, collect stem cells, have a discussion with the patient, and then consider high-dose therapy or not.

DR ANDERSON Yes. I think it’s reasonable to discuss it. We need to be open and honest with patients that the standard of care remains transplant, that you incorporate novel treatments before the transplant and novel treatments as maintenance after the transplant. The happy news is that the outcome, especially for patients who have standard-risk myeloma, is at least a decade or longer progression-free survival. It’s an optimistic picture. The data in terms of transplant being needed or not, will come within the next several years.

For now, it is a standard of care to use 1 high-dose melphalan and stem-cell transplant in this setting. I will add into our discussion with patients – besides the opportunity to harvest stem cells and think about whether one needs to do a transplant early on or not – is the issue of toxicity. High-dose melphalan by itself has a small but real secondary incidence of cancer, myelodysplasia, or leukemia. If one uses lenalidomide maintenance after melphalan transplantation treatment, that risk of secondary cancer is slightly increased.

In my experience, if patients have achieved a complete response with induction therapy only, it’s not unreasonable to offer early transplant and be clear that’s the standard of care. The alternative is maintenance with lenalidomide, knowing once the stem cells have been harvested, that transplantation can be an option to treat relapsed myeloma. We have many other options available as well. Time will tell in terms of the ongoing randomized trials as to whether transplant remains central to our treatment paradigm.

DR HENRY This leads us to our second patient. Here we have an older man of 74 years. He’s a professional piano player, so we want to try to avoid peripheral neuropathy in him. He has some mild renal insufficiency and some coronary artery disease, so he’s deemed transplant-ineligible. He has IgG kappa myeloma, and he’s brand new. What would you consider to be options for him for treatment?

DR ANDERSON This brings up the issue of a transplant-ineligible patient. He has significant comorbidity that would make transplantation an increased risk. What we would recommend in such a patient is still triplet induction therapy incorporating novel agents (Figure 1). Lenalidomide, the immunomodulatory drug, can safely be given in the context of neuropathy because it does not cause significant neuropathy. It would need to be dose modified, depending on the degree of renal insufficiency. We would recommend also including proteasome inhibitors. Bortezomib, the first-generation proteasome inhibitor, would be contraindicated because it does have a small but real attendant neuropathy. If, however, it is given weekly and subcutaneously, the risk of attendant neuropathy is quite low. In this patient, therefore, one could start with lenalidomide and bortezomib weekly and subcutaneously,^1,2 with a very early and vigilant follow-up for the earliest signs of neuropathy, so as not to allow it to develop and compromise his career.

Alternatively, one could use a proteasome inhibitor that does not have attendant neuropathy. Carfilzomib, the second-generation proteasome inhibitor, does not have neuropathy.⁹ But we would need to have caution here, because this patient has a history of coronary artery disease, and carfilzomib has a very small, but real, incidence of cardiac toxicity so would need to be used judiciously in this setting. The third proteasome inhibitor, ixazomib, is the next-generation bortezomib-class proteasome inhibitor, and it’s oral.¹⁰ It has less neuropathy than does bortezomib, so in my view is a very realistic option for him together with lenalidomide. It does have a small incidence of neuropathy, so close monitoring for neuropathy would be indicated. We could use lenalidomide–dexamethasone as a doublet and avoid neuropathy,¹¹ but usually doublets are reserved only for frail patients.

My recommendation, therefore, would be RVD with the bortezomib weekly or subcutaneously, or alternatively, lenalidomide, ixazomib, dexamethasone as an all-oral regimen as induction therapy. In my view, this 74-year-old patient with comorbidity is not a transplant candidate. However, one can be very optimistic with this patient. The likelihood that he could have myeloma as a chronic illness and die from something else is quite high. Initial induction triplet therapy would achieve a very high response extent and frequency. The durability would be long, especially with lenalidomide maintenance if it’s standard-risk myeloma or lenalidomide and a proteasome inhibitor, probably ixazomib in this setting, if he were to have high-risk myeloma.

If myeloma relapses, then there are many options that could be used in this patient and achieve years of progression-free and overall survival. Indeed, he is 74 years old and will respond very well to induction triplet therapy, with many years’ duration of response due to continuous lenalidomide or lenalidomide and proteasome inhibitor maintenance. Then there are many effective options to treat relapsed therapy using triplet novel agents. Therefore, his lifespan is unlikely to be shortened by multiple myeloma.

DR HENRY It’s so incredible compared with what it was when I trained. The next patient, a 45-year-old woman with IgG lambda myeloma, has had RVD induction and responded. She had lenalidomide maintenance, but then she progressed, and she got her stem-cell transplant, and she’s progressing after that. I guess we’re looking here to fold in some of the newer agents. How you would you do that in this patient?DR ANDERSON Yes. I think one of the most remarkable and exciting developments with myeloma is the rapid approval of the novel classes of agents that I mentioned earlier – the proteasome inhibitors, the immunomodulatory drugs, the HDAC inhibitor, and the monoclonal antibodies.¹ They’re particularly relevant in a patient such as this one, whose myeloma has relapsed after what would be considered standard therapy for a young person with standard-risk myeloma. This patient had RVD and maintenance therapy, and then progressed. The transplant was given for relapsed myeloma. The opportunity to use stem-cell transplant in patients when myeloma becomes active after maintenance should not be forgotten as it can be very effective. In all the trials done to date in which early versus late transplant are compared, there have been similar outcomes. Therefore, if the transplant isn’t done early, don’t forget that it’s an option at the time the myeloma progresses. I do want to mention, that there are lots of options for relapsed myeloma (Figures 3 and 4). I mentioned RVD or CyBorD as initial triplet therapies.^2-4 In North America, those are the 2 most common regimens. If myeloma then relapses and is resistant to RVD or to CyBorD, then we need to identify alternatives.

We also need to think about the comorbidities in the patient – issues such as age, neuropathy, presence of renal dysfunction, and other clinical factors. And we need to think about what treatment they’ve had in the past. This patient has had RVD, maintenance with lenalidomide, and a stem-cell transplant. We can offer patients a variety of therapies, but in the context of resistance to the first-generation proteasome inhibitor bortezomib and the first-generation immunomodulatory drug lenalidomide, we would strongly recommend the second-generation immunomodulatory drug pomalidomide¹² together with a second-generation proteasome inhibitor, be that carfilzomib¹³ or ixazomib.¹⁴ When one uses the second-generation IMiDs and proteasome inhibitors together, there’s a very high frequency of response in the order of 70%-80%, which lasts years.

Besides carfilzomib and ixazomib proteasome inhibitors, we also have elotuzumab and daratumumab, the monoclonal antibodies.^15-17 These agents have been FDA approved to treat patients such as this one who has had 1-3 previous therapies for their myeloma. All of them have been approved in randomized phase 3 trials compared with lenalidomide-dexamethasone in the control arm.^13-15,17 They’ve all been found to be superior. Although lenalidomide-dexamethasone combined with daratumumab, ixazomib, elotuzumab, or carfilzomib is superior to lenalidomide in relapsed myeloma, the situation in North America, as in this patient, is usually that patients have had lenalidomide-dexamethasone as part of their initial treatment and their myeloma is refractory to lenalidomide.

Hence, we recommend, that we go to the second-generation pomalidomide and second-generation proteasome inhibitors, either carfilzomib or ixazomib. Having said that, the treatment paradigm is evolving. For example, the monoclonal antibody daratumumab was initially approved by the FDA in multiply relapsed disease as a single agent because it achieves a 30% response rate.¹⁶ It now has been moved earlier into the first relapse of multiple myeloma, where it achieves much higher response rates when combined with lenalidomide–dexamethasone or combined with bortezomib–dexamethasone.^17,18 Response rates of 70%-80% can be achieved, including minimal residual disease negative complete responses.

Today, in a patient who has had RVD transplant and myeloma has returned, we would recommend second-generation IMiDs, pomalidomide, and second-generation proteasome inhibitors, either carfilzomib or ixazomib. Data for daratumumab combined with lenalidomide-dexamethasone or with bortezomib-dexamethasone, look very promising. We need, however, to see more experience of daratumumab together with lenalidomide-dexamethasone or daratumumab together with bortezomib-dexamethasone in patients whose myeloma is refractory to RVD, that is, patients whose myeloma has returned after RVD induction treatment. Of note, pomalidomide, dexamethasone, and daratumumab have just been approved by the FDA and may also be active even in myeloma recurring after RVD treatment.¹⁹

Daratumumab in combination will be moving earlier and earlier and may be appropriate to treat the first relapse. I do want to stress, however, that at present I save daratumumab for the second or greater relapse. Daratumumab is active even when relapse occurs after treatment with second-generation IMiDs and proteasome inhibitors.

DR HENRY Before we close, I have a couple practical questions with these antibodies. Daratumumab has the track record of first-treatment severe reactions and long infusion times. How long are you anticipating the first daratumumab treatment takes? There has been some talk that maybe splitting it in half and going over 2 days is easier on the patient and the infusion center. Have you done that?

DR ANDERSON Yes, I think that’s a very important point. We need to be thinking – first and foremost – about efficacy of our therapy. Equally important, however, are the safety profile and the user-friendliness for the patient. Daratumumab infusions are quite long – on the order of 8 hours or longer on day 1 of infusion. And to date, all the clinical trials have used daratumumab infusions weekly for 8 treatments, followed by 8 treatments given every 2 weeks. Then monthly daratumumab is given as a maintenance therapy. Thus, there is a requirement for multiple outpatient clinic visits that can be prolonged.

One of the opportunities that’s being tested is to give daratumumab subcutaneously. While this is being evaluated in protocols now, the results that have been reported at our national meetings look to be quite promising in terms of efficacy, similar to results with the intravenous administration. Obviously, this would allow for a much more convenient clinic visit and shorter time for the patients being treated.

I should mention that the other antibody, elotuzumab, has been approved in combination with lenalidomide and dexamethasone.¹⁵ The infusions with lenalidomide, dexamethasone, and the antibody elotuzumab are much shorter, on the order of 2- or 3-hour visits. The place for elotuzumab in the management of relapsed myeloma is yet to be totally defined. We tend to use it now in the setting of more indolent relapses, where patients might have a slowly rising monoclonal protein. Elotuzumab-lenalidomide-dexamethasone has maintained an overall survival advantage at 4 years compared with lenalidomide-dexamethasone when used in relapsed myeloma.

We are quite excited about both antibodies. Daratumumab tends to get most of the activity, as it achieves responses as a single agent,¹⁶ and the depth of the responses are markedly increased when it’s combined with lenalidomide-dexamethasone or bortezomib-dexamethasone.^17,18 However, one shouldn’t forget elotuzumab¹⁵ based on its tolerability and the survival advantage I mentioned at 4 years.

The final point is that we think about myeloma genetically at the time of diagnosis and relapse in terms of standard or high-risk disease. One of the hallmarks of high-risk disease has been 17P deletion or P53 dysfunction. One of the most exciting outcomes of the development of monoclonal antibodies has been the responses observed even in the context of P53 deletion. Clearly, antibody-mediated cellular cytotoxicity, complement-mediated cytotoxicity, and other mechanisms of action of these antibodies do not require normal P53 function. The important point, therefore, is that what has previously been thought of as high-risk disease can nowadays be effectively treated with these new immune treatments, correlating with the marked improvement in survival and overall outcome.

DR HENRY We have outlined 3 kinds of myeloma patients we see, and especially interesting is the last patient, who has relapsed and then progressed, and in whom newer drugs have a role. Thank you for such a complete and thorough discussion, Dr Anderson.

In his bimonthly podcast, Dr Henry, the JCSO Editor-in-Chief, discusses a round-up by JCSO Editor Dr Howard Burris of the top takeaways from this year’s annual ASCO meeting, as well as a series of articles focusing on CAR T-cell therapies. He also looks at reports on psychosocial factors and treatment satisfaction after radical prostatectomy; the impact of inpatient rehabilitation on outcomes for patients with cancer; and the long-term effects of posttreatment exercise on pain in young women with breast cancer. Patient-specific cases of carcinoma of the colon in a child, managing severe radiation dermatitis after head and neck radiotherapy, striking rash in a patient on a checkpoint inhibitor, and a small gastric GIST with high mitotic index are also included. Dr Henry rounds off his comments with an examination of the challenges presented by tumor heterogeneity in the war on cancer.

Listen to the podcast below

In his bimonthly podcast, Dr Henry, the JCSO Editor-in-Chief, discusses a round-up by JCSO Editor Dr Howard Burris of the top takeaways from this year’s annual ASCO meeting, as well as a series of articles focusing on CAR T-cell therapies. He also looks at reports on psychosocial factors and treatment satisfaction after radical prostatectomy; the impact of inpatient rehabilitation on outcomes for patients with cancer; and the long-term effects of posttreatment exercise on pain in young women with breast cancer. Patient-specific cases of carcinoma of the colon in a child, managing severe radiation dermatitis after head and neck radiotherapy, striking rash in a patient on a checkpoint inhibitor, and a small gastric GIST with high mitotic index are also included. Dr Henry rounds off his comments with an examination of the challenges presented by tumor heterogeneity in the war on cancer.

Listen to the podcast below

In his bimonthly podcast, Dr Henry, the JCSO Editor-in-Chief, discusses a round-up by JCSO Editor Dr Howard Burris of the top takeaways from this year’s annual ASCO meeting, as well as a series of articles focusing on CAR T-cell therapies. He also looks at reports on psychosocial factors and treatment satisfaction after radical prostatectomy; the impact of inpatient rehabilitation on outcomes for patients with cancer; and the long-term effects of posttreatment exercise on pain in young women with breast cancer. Patient-specific cases of carcinoma of the colon in a child, managing severe radiation dermatitis after head and neck radiotherapy, striking rash in a patient on a checkpoint inhibitor, and a small gastric GIST with high mitotic index are also included. Dr Henry rounds off his comments with an examination of the challenges presented by tumor heterogeneity in the war on cancer.

Listen to the podcast below

In this interview, Dr David Henry, the Editor-in-Chief of JCSO, and Dr Daniel Haller, of the Abramson Cancer Center, University of Pennsylvania Perelman School of Medicine in Philadelphia, discuss the findings from recent groundbreaking studies in gastrointestinal cancers.

Listen to the podcast below.

In this interview, Dr David Henry, the Editor-in-Chief of JCSO, and Dr Daniel Haller, of the Abramson Cancer Center, University of Pennsylvania Perelman School of Medicine in Philadelphia, discuss the findings from recent groundbreaking studies in gastrointestinal cancers.

Listen to the podcast below.

In this interview, Dr David Henry, the Editor-in-Chief of JCSO, and Dr Daniel Haller, of the Abramson Cancer Center, University of Pennsylvania Perelman School of Medicine in Philadelphia, discuss the findings from recent groundbreaking studies in gastrointestinal cancers.

Listen to the podcast below.

In his bimonthly podcast, Dr David Henry, the JCSO Editor-in-Chief, discusses the approval of the biosimilars, bevacizumab-awwb and trastuzumab-dkst, and new therapies for virally associated cancers. Also in the line-up are an interview with Dr Daniel Haller on the latest advances in treating gastrointestinal cancers, and an article on hands-on advice on integrating survivorship care planning in a radiation oncology workflow. Research topics incude how to improve communication between oncology care providers and patient caregivers during hospice; the impact of patient education on enrollment in clinical trials; and organizational barriers to optimal lung cancer care in the community setting. A series of Case Reports that highlight some of the clincial challenges in treating patients with cancer round out the issue.

Listen to the podcast below

In his bimonthly podcast, Dr David Henry, the JCSO Editor-in-Chief, discusses the approval of the biosimilars, bevacizumab-awwb and trastuzumab-dkst, and new therapies for virally associated cancers. Also in the line-up are an interview with Dr Daniel Haller on the latest advances in treating gastrointestinal cancers, and an article on hands-on advice on integrating survivorship care planning in a radiation oncology workflow. Research topics incude how to improve communication between oncology care providers and patient caregivers during hospice; the impact of patient education on enrollment in clinical trials; and organizational barriers to optimal lung cancer care in the community setting. A series of Case Reports that highlight some of the clincial challenges in treating patients with cancer round out the issue.

Listen to the podcast below

In his bimonthly podcast, Dr David Henry, the JCSO Editor-in-Chief, discusses the approval of the biosimilars, bevacizumab-awwb and trastuzumab-dkst, and new therapies for virally associated cancers. Also in the line-up are an interview with Dr Daniel Haller on the latest advances in treating gastrointestinal cancers, and an article on hands-on advice on integrating survivorship care planning in a radiation oncology workflow. Research topics incude how to improve communication between oncology care providers and patient caregivers during hospice; the impact of patient education on enrollment in clinical trials; and organizational barriers to optimal lung cancer care in the community setting. A series of Case Reports that highlight some of the clincial challenges in treating patients with cancer round out the issue.

Listen to the podcast below

In this podcast, Dr Henry discusses research articles on analgesic management in radiation oncology for painful bone metastases, hospitalizations for fracture in patients with metastatic disease, measurement of physical activity and sedentary behavior in breast cancer survivors, and patient navigators’ personal experiences with cancer and their impact on treatment. He also highlights a New Therapies review article on hallmark tumor metabolism becoming a validated therapeutic target, as well as The JCSO Interview, in which Kenneth Anderson, MD, talks about new myeloma drugs and their associated improved response rates and extended survival. Comments on the approvals of abemaciclib for breast cancer and avelumab and durvalumab for metastatic bladder cancer, and Case Reports on concurrent ipilimumab and CMV colitis refractory to oral steroids, recurrent head and neck cancer presenting as a large retroperitoneal mass, massive liver metastasis from colon adenocarcinoma causing cardiac tamponade, and cardiac pleomorphic sarcoma after placement of Dacron graft round out the line-up of articles. 

Listen to the podcast below.

In this podcast, Dr Henry discusses research articles on analgesic management in radiation oncology for painful bone metastases, hospitalizations for fracture in patients with metastatic disease, measurement of physical activity and sedentary behavior in breast cancer survivors, and patient navigators’ personal experiences with cancer and their impact on treatment. He also highlights a New Therapies review article on hallmark tumor metabolism becoming a validated therapeutic target, as well as The JCSO Interview, in which Kenneth Anderson, MD, talks about new myeloma drugs and their associated improved response rates and extended survival. Comments on the approvals of abemaciclib for breast cancer and avelumab and durvalumab for metastatic bladder cancer, and Case Reports on concurrent ipilimumab and CMV colitis refractory to oral steroids, recurrent head and neck cancer presenting as a large retroperitoneal mass, massive liver metastasis from colon adenocarcinoma causing cardiac tamponade, and cardiac pleomorphic sarcoma after placement of Dacron graft round out the line-up of articles. 

Listen to the podcast below.

In this podcast, Dr Henry discusses research articles on analgesic management in radiation oncology for painful bone metastases, hospitalizations for fracture in patients with metastatic disease, measurement of physical activity and sedentary behavior in breast cancer survivors, and patient navigators’ personal experiences with cancer and their impact on treatment. He also highlights a New Therapies review article on hallmark tumor metabolism becoming a validated therapeutic target, as well as The JCSO Interview, in which Kenneth Anderson, MD, talks about new myeloma drugs and their associated improved response rates and extended survival. Comments on the approvals of abemaciclib for breast cancer and avelumab and durvalumab for metastatic bladder cancer, and Case Reports on concurrent ipilimumab and CMV colitis refractory to oral steroids, recurrent head and neck cancer presenting as a large retroperitoneal mass, massive liver metastasis from colon adenocarcinoma causing cardiac tamponade, and cardiac pleomorphic sarcoma after placement of Dacron graft round out the line-up of articles. 

Listen to the podcast below.

For the July-August issue of the Journal of Community and Supportive Oncology, the Editor-in-Chief, Dr David Henry, discusses a recap by Howard Burris, MD, of the top presentations at this year’s annual meeting of the American Society for Clinical Oncology, and a selection of articles on some of the key findings reported at the meeting. A number of articles, in keeping with the journal mission of delivering content that can inform or change daily practice in the community setting, provide ‘how-to’ clinical and supportive advice. They include an outline by Thomas J Smith of Johns Hopkins University of how to initiate goals-of-care conversations with patients and their family members; a review of managing polycythemia vera in the community oncology setting; a New Therapies feature on how immunotherapies are shaping the treatment of hematologic malignancies; and research articles on using Onodera’s Prognostic Nutritional Index to predict wound complications in patients with soft tissue sarcoma, and bone remodeling associated with CTLA-4 inhibition. A third research article assesses a multidisciplinary survivorship program in a group of predominantly Hispanic women with breast cancer. Also in the line-up for discussion are Case Reports, one on managing high-grade pleomorphic sarcoma in a patient with colon metastasis and another on intramedullary spinal cord and leptomeningeal metastases presenting as cauda equina syndrome in a patient with melanoma.

Listen to the podcast below.

For the July-August issue of the Journal of Community and Supportive Oncology, the Editor-in-Chief, Dr David Henry, discusses a recap by Howard Burris, MD, of the top presentations at this year’s annual meeting of the American Society for Clinical Oncology, and a selection of articles on some of the key findings reported at the meeting. A number of articles, in keeping with the journal mission of delivering content that can inform or change daily practice in the community setting, provide ‘how-to’ clinical and supportive advice. They include an outline by Thomas J Smith of Johns Hopkins University of how to initiate goals-of-care conversations with patients and their family members; a review of managing polycythemia vera in the community oncology setting; a New Therapies feature on how immunotherapies are shaping the treatment of hematologic malignancies; and research articles on using Onodera’s Prognostic Nutritional Index to predict wound complications in patients with soft tissue sarcoma, and bone remodeling associated with CTLA-4 inhibition. A third research article assesses a multidisciplinary survivorship program in a group of predominantly Hispanic women with breast cancer. Also in the line-up for discussion are Case Reports, one on managing high-grade pleomorphic sarcoma in a patient with colon metastasis and another on intramedullary spinal cord and leptomeningeal metastases presenting as cauda equina syndrome in a patient with melanoma.

Listen to the podcast below.

For the July-August issue of the Journal of Community and Supportive Oncology, the Editor-in-Chief, Dr David Henry, discusses a recap by Howard Burris, MD, of the top presentations at this year’s annual meeting of the American Society for Clinical Oncology, and a selection of articles on some of the key findings reported at the meeting. A number of articles, in keeping with the journal mission of delivering content that can inform or change daily practice in the community setting, provide ‘how-to’ clinical and supportive advice. They include an outline by Thomas J Smith of Johns Hopkins University of how to initiate goals-of-care conversations with patients and their family members; a review of managing polycythemia vera in the community oncology setting; a New Therapies feature on how immunotherapies are shaping the treatment of hematologic malignancies; and research articles on using Onodera’s Prognostic Nutritional Index to predict wound complications in patients with soft tissue sarcoma, and bone remodeling associated with CTLA-4 inhibition. A third research article assesses a multidisciplinary survivorship program in a group of predominantly Hispanic women with breast cancer. Also in the line-up for discussion are Case Reports, one on managing high-grade pleomorphic sarcoma in a patient with colon metastasis and another on intramedullary spinal cord and leptomeningeal metastases presenting as cauda equina syndrome in a patient with melanoma.

Listen to the podcast below.

For the May-June issue of the Journal of Community and Supportive Oncology, the Editor in Chief, Dr David Henry, discusses an editorial by Kevin Knopf, a JCSO editor, about drawing on modern portfolio theory to improve cancer care. Side effects come under scrutiny this issue, with a How We Do It article on prehabilitation for lymphedema in head and neck cancer patients, a Review article that examines pancreatitis associated with newer classes of antineoplastic therapies, and a research article that looks at prescriber adherence to antiemetic guidelines with trifluridine-tipiracil. In other research articles, investigators report on physician attitudes and prevalence of molecular testing in lung cancer; a comprehensive assessment of cancer survivors’ concerns to inform program development; and perceived financial hardship among patients with advanced cancer. Two Case Reports address the treatment of Kaposi sarcoma in patients with AIDS, and a third describes a rare case of hypoglycemia induced by a classic gastrointestinal stromal tumor. Finally, Dr Henry summarizes an in-depth interview on cardiotoxicity, which he did with his colleague, Dr Joseph Carver.

Listen to the podcast below.

For the May-June issue of the Journal of Community and Supportive Oncology, the Editor in Chief, Dr David Henry, discusses an editorial by Kevin Knopf, a JCSO editor, about drawing on modern portfolio theory to improve cancer care. Side effects come under scrutiny this issue, with a How We Do It article on prehabilitation for lymphedema in head and neck cancer patients, a Review article that examines pancreatitis associated with newer classes of antineoplastic therapies, and a research article that looks at prescriber adherence to antiemetic guidelines with trifluridine-tipiracil. In other research articles, investigators report on physician attitudes and prevalence of molecular testing in lung cancer; a comprehensive assessment of cancer survivors’ concerns to inform program development; and perceived financial hardship among patients with advanced cancer. Two Case Reports address the treatment of Kaposi sarcoma in patients with AIDS, and a third describes a rare case of hypoglycemia induced by a classic gastrointestinal stromal tumor. Finally, Dr Henry summarizes an in-depth interview on cardiotoxicity, which he did with his colleague, Dr Joseph Carver.

Listen to the podcast below.

For the May-June issue of the Journal of Community and Supportive Oncology, the Editor in Chief, Dr David Henry, discusses an editorial by Kevin Knopf, a JCSO editor, about drawing on modern portfolio theory to improve cancer care. Side effects come under scrutiny this issue, with a How We Do It article on prehabilitation for lymphedema in head and neck cancer patients, a Review article that examines pancreatitis associated with newer classes of antineoplastic therapies, and a research article that looks at prescriber adherence to antiemetic guidelines with trifluridine-tipiracil. In other research articles, investigators report on physician attitudes and prevalence of molecular testing in lung cancer; a comprehensive assessment of cancer survivors’ concerns to inform program development; and perceived financial hardship among patients with advanced cancer. Two Case Reports address the treatment of Kaposi sarcoma in patients with AIDS, and a third describes a rare case of hypoglycemia induced by a classic gastrointestinal stromal tumor. Finally, Dr Henry summarizes an in-depth interview on cardiotoxicity, which he did with his colleague, Dr Joseph Carver.

Listen to the podcast below.