NCCN Hematologic Malignancies 2017

SAN FRANCISCO – Pursue a deep remission that allows a patient to stay treatment free for some period of time, or go for long-term disease control that might not allow for a drug holiday?

It’s a key decision facing physicians in the frontline setting of chronic lymphocytic leukemia, William Wierda, MD, PhD, said at the annual congress on Hematologic Malignancies held by the National Comprehensive Cancer Network.

SAN FRANCISCO – Pursue a deep remission that allows a patient to stay treatment free for some period of time, or go for long-term disease control that might not allow for a drug holiday?

It’s a key decision facing physicians in the frontline setting of chronic lymphocytic leukemia, William Wierda, MD, PhD, said at the annual congress on Hematologic Malignancies held by the National Comprehensive Cancer Network.

SAN FRANCISCO – Pursue a deep remission that allows a patient to stay treatment free for some period of time, or go for long-term disease control that might not allow for a drug holiday?

It’s a key decision facing physicians in the frontline setting of chronic lymphocytic leukemia, William Wierda, MD, PhD, said at the annual congress on Hematologic Malignancies held by the National Comprehensive Cancer Network.

SAN FRANCISCO – After years of stagnation in the field of acute myeloid leukemia – with most standard therapies developed in the 1970s – times are changing, Bruno Medeiros, MD, said at the annual congress on hematologic malignancies held by the National Comprehensive Cancer Network.

“2017 is the year of AML,” he said. Four new therapies have been approved by the FDA since April. They include midostaurin for newly diagnosed, FLT-3–mutated patients; enasidenib, for relapsed/refractory IDH2-mutated patients; CPX-351, for high-risk AML patients; and gemtuzumab ozogamicin for newly diagnosed, CD-33–positive patients.

SAN FRANCISCO – After years of stagnation in the field of acute myeloid leukemia – with most standard therapies developed in the 1970s – times are changing, Bruno Medeiros, MD, said at the annual congress on hematologic malignancies held by the National Comprehensive Cancer Network.

“2017 is the year of AML,” he said. Four new therapies have been approved by the FDA since April. They include midostaurin for newly diagnosed, FLT-3–mutated patients; enasidenib, for relapsed/refractory IDH2-mutated patients; CPX-351, for high-risk AML patients; and gemtuzumab ozogamicin for newly diagnosed, CD-33–positive patients.

SAN FRANCISCO – After years of stagnation in the field of acute myeloid leukemia – with most standard therapies developed in the 1970s – times are changing, Bruno Medeiros, MD, said at the annual congress on hematologic malignancies held by the National Comprehensive Cancer Network.

“2017 is the year of AML,” he said. Four new therapies have been approved by the FDA since April. They include midostaurin for newly diagnosed, FLT-3–mutated patients; enasidenib, for relapsed/refractory IDH2-mutated patients; CPX-351, for high-risk AML patients; and gemtuzumab ozogamicin for newly diagnosed, CD-33–positive patients.

SAN FRANCISCO – The approach to relapsed/refractory multiple myeloma (MM) has to be tailored patient by patient based on the biology of the disease, frailty measures, comorbidities, and prior treatment regimens, Natalie Callander, MD, director of the myeloma clinical program at the University of Wisconsin Carbone Cancer Center, Madison, said at the annual congress on Hematologic Malignancies held by the National Comprehensive Cancer Network.

Despite major treatment breakthroughs in recent years and a wide swath of therapeutic options, multiple myeloma is still an incurable disease that eventually relapses in most patients, Dr. Callander, vice chair of the NCCN Multiple Myeloma Panel, said. “If you are having trouble with your relapsed or refractory patients, you’re not alone.”

As a guide to individualize the treatment approach, the NCCN has put together recommendations for patients with relapsed/recalcitrant MM. “Preferred regimens” include bortezomib-lenalidomide-dexamethasone and other well-established combinations supported by evidence from Phase 1 trials. When relapse occurs more than 6 months after primary induction, one option is simply to repeat the induction therapy.

A long list of “other recommended regimens” includes 21 combination options supported by “very strong Phase 2 data,” she said. The NCCN also has a third list of regimens for the most aggressive disease and certain special circumstances. Two powerful combinations that are used to get the disease under control quickly include high-dose cyclophosphamide or dexamethasone/thalidomide/cisplatin/doxorubicin/cyclophosphamide/etoposide, (DT-PACE) with or without bortezomib.

Dr. Callander underscored the importance of differentiating biochemical relapse, such as increases in serum M protein or other indicators, from clinical relapse, such as new soft tissue plasmacytomas or hypercalcemia.

Patients with clinical relapse typically need a quicker and more vigorous therapeutic response, she said. Studies have found that those in biochemical relapse tend to do better than those in symptomatic relapse.

“This whole concept of biochemical versus symptomatic is really important,” Dr. Callander said.

Among the tips she offered for managing patients with relapse, were to perform a repeat bone marrow biopsy with cytogenetics to gauge the presence of high-risk biology, since this category of patients tends to do far worse and to need a more aggressive treatment approach.

“Getting that kind of information with that follow-up bone marrow biopsy might be very important,” she said.

It’s important to be aware of the phenomenon of “light chain escape,” in which patients with relapsed/refractory disease can stop making intact immunoglobulin G. It’s thought to be due to clonal evolution, in which the clone that was making intact immunoglobulin becomes less dominant. These patients tend to do worse than similar patients who don’t exhibit this phenomenon, Dr. Callander said.

Dr. Callander reported no relevant financial disclosures.

SAN FRANCISCO – The approach to relapsed/refractory multiple myeloma (MM) has to be tailored patient by patient based on the biology of the disease, frailty measures, comorbidities, and prior treatment regimens, Natalie Callander, MD, director of the myeloma clinical program at the University of Wisconsin Carbone Cancer Center, Madison, said at the annual congress on Hematologic Malignancies held by the National Comprehensive Cancer Network.

Despite major treatment breakthroughs in recent years and a wide swath of therapeutic options, multiple myeloma is still an incurable disease that eventually relapses in most patients, Dr. Callander, vice chair of the NCCN Multiple Myeloma Panel, said. “If you are having trouble with your relapsed or refractory patients, you’re not alone.”

As a guide to individualize the treatment approach, the NCCN has put together recommendations for patients with relapsed/recalcitrant MM. “Preferred regimens” include bortezomib-lenalidomide-dexamethasone and other well-established combinations supported by evidence from Phase 1 trials. When relapse occurs more than 6 months after primary induction, one option is simply to repeat the induction therapy.

A long list of “other recommended regimens” includes 21 combination options supported by “very strong Phase 2 data,” she said. The NCCN also has a third list of regimens for the most aggressive disease and certain special circumstances. Two powerful combinations that are used to get the disease under control quickly include high-dose cyclophosphamide or dexamethasone/thalidomide/cisplatin/doxorubicin/cyclophosphamide/etoposide, (DT-PACE) with or without bortezomib.

Dr. Callander underscored the importance of differentiating biochemical relapse, such as increases in serum M protein or other indicators, from clinical relapse, such as new soft tissue plasmacytomas or hypercalcemia.

Patients with clinical relapse typically need a quicker and more vigorous therapeutic response, she said. Studies have found that those in biochemical relapse tend to do better than those in symptomatic relapse.

“This whole concept of biochemical versus symptomatic is really important,” Dr. Callander said.

Among the tips she offered for managing patients with relapse, were to perform a repeat bone marrow biopsy with cytogenetics to gauge the presence of high-risk biology, since this category of patients tends to do far worse and to need a more aggressive treatment approach.

“Getting that kind of information with that follow-up bone marrow biopsy might be very important,” she said.

It’s important to be aware of the phenomenon of “light chain escape,” in which patients with relapsed/refractory disease can stop making intact immunoglobulin G. It’s thought to be due to clonal evolution, in which the clone that was making intact immunoglobulin becomes less dominant. These patients tend to do worse than similar patients who don’t exhibit this phenomenon, Dr. Callander said.

Dr. Callander reported no relevant financial disclosures.

SAN FRANCISCO – The approach to relapsed/refractory multiple myeloma (MM) has to be tailored patient by patient based on the biology of the disease, frailty measures, comorbidities, and prior treatment regimens, Natalie Callander, MD, director of the myeloma clinical program at the University of Wisconsin Carbone Cancer Center, Madison, said at the annual congress on Hematologic Malignancies held by the National Comprehensive Cancer Network.

Despite major treatment breakthroughs in recent years and a wide swath of therapeutic options, multiple myeloma is still an incurable disease that eventually relapses in most patients, Dr. Callander, vice chair of the NCCN Multiple Myeloma Panel, said. “If you are having trouble with your relapsed or refractory patients, you’re not alone.”

As a guide to individualize the treatment approach, the NCCN has put together recommendations for patients with relapsed/recalcitrant MM. “Preferred regimens” include bortezomib-lenalidomide-dexamethasone and other well-established combinations supported by evidence from Phase 1 trials. When relapse occurs more than 6 months after primary induction, one option is simply to repeat the induction therapy.

A long list of “other recommended regimens” includes 21 combination options supported by “very strong Phase 2 data,” she said. The NCCN also has a third list of regimens for the most aggressive disease and certain special circumstances. Two powerful combinations that are used to get the disease under control quickly include high-dose cyclophosphamide or dexamethasone/thalidomide/cisplatin/doxorubicin/cyclophosphamide/etoposide, (DT-PACE) with or without bortezomib.

Dr. Callander underscored the importance of differentiating biochemical relapse, such as increases in serum M protein or other indicators, from clinical relapse, such as new soft tissue plasmacytomas or hypercalcemia.

Patients with clinical relapse typically need a quicker and more vigorous therapeutic response, she said. Studies have found that those in biochemical relapse tend to do better than those in symptomatic relapse.

“This whole concept of biochemical versus symptomatic is really important,” Dr. Callander said.

Among the tips she offered for managing patients with relapse, were to perform a repeat bone marrow biopsy with cytogenetics to gauge the presence of high-risk biology, since this category of patients tends to do far worse and to need a more aggressive treatment approach.

“Getting that kind of information with that follow-up bone marrow biopsy might be very important,” she said.

It’s important to be aware of the phenomenon of “light chain escape,” in which patients with relapsed/refractory disease can stop making intact immunoglobulin G. It’s thought to be due to clonal evolution, in which the clone that was making intact immunoglobulin becomes less dominant. These patients tend to do worse than similar patients who don’t exhibit this phenomenon, Dr. Callander said.

Dr. Callander reported no relevant financial disclosures.

SAN FRANCISCO – Routine testing for minimal residual disease is probably not of value in acute myeloid leukemia, as there is no evidence that changing treatment based on MRD status currently makes a difference in patient outcomes, experts said at the annual congress on Hematologic Malignancies held by the National Comprehensive Cancer Network.

“If we find minimal residual disease, we don’t always have a better therapy to offer our patients,” Jessica Altman, MD, associate professor of hematology and oncology at the Northwestern University Feinberg School of Medicine, said.

Beyond that therapeutic reality, there are no clear guidelines and standards for MRD testing. The optimal timing for MRD testing and a standard threshold for an MRD classification are not yet established, she said.

“Having MRD is bad, not having it is better,” Richard Stone, MD, PhD, clinical director of the adult leukemia program at the Dana-Farber Cancer Institute, said. The problem in AML, he said, is, “So?” There is no reliable “MRD eraser” in AML, he said. Until then, there is not much point in knowing whether a patient is MRD positive or not.

A recent survey conducted by researchers at Moffitt Cancer Center, Tampa, addressed MRD testing at 13 major cancer centers. While most centers reported that they test for MRD, many physicians said that they are unsure about what to do with the results.

A 2013 study by the HOVON group found that patients who were in complete remission but MRD positive after their first course of therapy, subsequently became MRD negative after their second course of therapy. But the second regimen would not have been different based on knowledge of MRD status, according to the HOVON/SAKK AML 42A study (J Clin Oncol. 2013; 31:3889-97).

The AML community is awaiting guidelines on MRD use from the NCCN and other groups, Dr. Altman said. An option for using NPM1 mutations to assess MRD should be available soon, and could be an improvement on existing options (N Engl J Med 2016; 374:422-33).

Given the treatment limitations, knowing about MRD status can have a negative mental toll on patients, Dr. Stone said. “I would not underplay the psychological burden.” Nevertheless, MRD should be measured in clinical trials, and it could be a valuable surrogate marker by which to compare drug efficacy.

One of the biggest hopes is that MRD status could eventually be useful in determining the need for allogeneic stem cell transplant in patients deemed intermediate risk, Dr. Altman said. “I think we are finally on the brink of this being actionable.”

Dr. Altman reports financial relationships with Astellas, Bristol-Myers Squibb, Celgene, Janssen, Novartis, and Syros. Dr. Stone reports financial relationships with AbbVie, Actinium, Agios, Amgen and many other companies.

SAN FRANCISCO – Routine testing for minimal residual disease is probably not of value in acute myeloid leukemia, as there is no evidence that changing treatment based on MRD status currently makes a difference in patient outcomes, experts said at the annual congress on Hematologic Malignancies held by the National Comprehensive Cancer Network.

“If we find minimal residual disease, we don’t always have a better therapy to offer our patients,” Jessica Altman, MD, associate professor of hematology and oncology at the Northwestern University Feinberg School of Medicine, said.

Beyond that therapeutic reality, there are no clear guidelines and standards for MRD testing. The optimal timing for MRD testing and a standard threshold for an MRD classification are not yet established, she said.

“Having MRD is bad, not having it is better,” Richard Stone, MD, PhD, clinical director of the adult leukemia program at the Dana-Farber Cancer Institute, said. The problem in AML, he said, is, “So?” There is no reliable “MRD eraser” in AML, he said. Until then, there is not much point in knowing whether a patient is MRD positive or not.

A recent survey conducted by researchers at Moffitt Cancer Center, Tampa, addressed MRD testing at 13 major cancer centers. While most centers reported that they test for MRD, many physicians said that they are unsure about what to do with the results.

A 2013 study by the HOVON group found that patients who were in complete remission but MRD positive after their first course of therapy, subsequently became MRD negative after their second course of therapy. But the second regimen would not have been different based on knowledge of MRD status, according to the HOVON/SAKK AML 42A study (J Clin Oncol. 2013; 31:3889-97).

The AML community is awaiting guidelines on MRD use from the NCCN and other groups, Dr. Altman said. An option for using NPM1 mutations to assess MRD should be available soon, and could be an improvement on existing options (N Engl J Med 2016; 374:422-33).

Given the treatment limitations, knowing about MRD status can have a negative mental toll on patients, Dr. Stone said. “I would not underplay the psychological burden.” Nevertheless, MRD should be measured in clinical trials, and it could be a valuable surrogate marker by which to compare drug efficacy.

One of the biggest hopes is that MRD status could eventually be useful in determining the need for allogeneic stem cell transplant in patients deemed intermediate risk, Dr. Altman said. “I think we are finally on the brink of this being actionable.”

Dr. Altman reports financial relationships with Astellas, Bristol-Myers Squibb, Celgene, Janssen, Novartis, and Syros. Dr. Stone reports financial relationships with AbbVie, Actinium, Agios, Amgen and many other companies.

SAN FRANCISCO – Routine testing for minimal residual disease is probably not of value in acute myeloid leukemia, as there is no evidence that changing treatment based on MRD status currently makes a difference in patient outcomes, experts said at the annual congress on Hematologic Malignancies held by the National Comprehensive Cancer Network.

“If we find minimal residual disease, we don’t always have a better therapy to offer our patients,” Jessica Altman, MD, associate professor of hematology and oncology at the Northwestern University Feinberg School of Medicine, said.

Beyond that therapeutic reality, there are no clear guidelines and standards for MRD testing. The optimal timing for MRD testing and a standard threshold for an MRD classification are not yet established, she said.

“Having MRD is bad, not having it is better,” Richard Stone, MD, PhD, clinical director of the adult leukemia program at the Dana-Farber Cancer Institute, said. The problem in AML, he said, is, “So?” There is no reliable “MRD eraser” in AML, he said. Until then, there is not much point in knowing whether a patient is MRD positive or not.

A recent survey conducted by researchers at Moffitt Cancer Center, Tampa, addressed MRD testing at 13 major cancer centers. While most centers reported that they test for MRD, many physicians said that they are unsure about what to do with the results.

A 2013 study by the HOVON group found that patients who were in complete remission but MRD positive after their first course of therapy, subsequently became MRD negative after their second course of therapy. But the second regimen would not have been different based on knowledge of MRD status, according to the HOVON/SAKK AML 42A study (J Clin Oncol. 2013; 31:3889-97).

The AML community is awaiting guidelines on MRD use from the NCCN and other groups, Dr. Altman said. An option for using NPM1 mutations to assess MRD should be available soon, and could be an improvement on existing options (N Engl J Med 2016; 374:422-33).

Given the treatment limitations, knowing about MRD status can have a negative mental toll on patients, Dr. Stone said. “I would not underplay the psychological burden.” Nevertheless, MRD should be measured in clinical trials, and it could be a valuable surrogate marker by which to compare drug efficacy.

One of the biggest hopes is that MRD status could eventually be useful in determining the need for allogeneic stem cell transplant in patients deemed intermediate risk, Dr. Altman said. “I think we are finally on the brink of this being actionable.”

Dr. Altman reports financial relationships with Astellas, Bristol-Myers Squibb, Celgene, Janssen, Novartis, and Syros. Dr. Stone reports financial relationships with AbbVie, Actinium, Agios, Amgen and many other companies.

SAN FRANCISCO – A growing number of immunotherapy options for adults with acute lymphocytic leukemia (ALL) – rituximab, inotuzumab ozogamicin, blinatumomab and chimeric antigen receptor (CAR) T-cell therapy – have improved remission rates, but their collective effects on patient outcomes remain to be seen, David Maloney, MD, PhD, said at the National Comprehensive Cancer Network Annual Congress: Hematologic Malignancies.

The main challenge for the field is deciding when and how to use a variety of therapies, he said. “How are we going to put these together? What’s the order?” he asked. “Are we going to be able to decrease the need for allogeneic stem cell transplant? And, obviously, that’s the goal.”

About 30%-50% of adults with ALL exhibit CD20-positive cells, making them potentially treatable with rituximab. Data show a better event-free survival rate and a reduced relapse rate when rituximab is added to standard chemotherapy as compared with standard chemotherapy alone, Dr. Maloney of the clinical research division at the Fred Hutchinson Cancer Research Center, Seattle, noted (N Engl J Med. 2016 Sep 15;375[11]:1044-53). But the improvement was only “modest,” he said.

The anti-CD22 antibody inotuzumab ozogamicin has produced complete remission in 81% of relapsed or refractory ALL patients, compared with those getting standard therapy (N Engl J Med. 2016 Aug 25;375:740-53). Dr. Maloney said it seems well tolerated, but there is concern about an increase in veno-occlusive disease in patients who have undergone or will undergo an allogeneic stem cell transplant.

Blinatumomab produces moderate response rates and minimal residual disease–negative remissions, but delivery of the drug is “cumbersome,” requiring a 4-week continuous infusion, he said. The drug seems to be more effective in those with a lower burden of disease, he noted.

CAR T-cell therapy has produced MRD-negative complete responses in 94% of patients, based on results from a clinical trial at Fred Hutchinson. And using the chemotherapy drug fludarabine in combination with this therapy “dramatically” boosts the peak number of the CAR T cells and how long they persist, Dr. Maloney said. Still, CAR T-cell therapy is a work-intensive treatment requiring cells harvested from the patient, and the procedure often brings on cytokine-release syndrome and neurotoxicity, though both adverse events are typically reversible, he said.

It may be that using fewer CAR T cells can reduce toxicity without compromising treatment response, he said.

Questions remain over whether to transplant patients who are in remission after CAR T-cell therapy. “This is a hot debate,” he said. The decision will likely depend on their prior therapy, whether they’ve had a prior transplant, and the how robust the CAR T-cell expansion has been, he said.

Dr. Maloney reports financial relationships with Celgene, Gilead Sciences, Kite Pharma, and Roche.

SAN FRANCISCO – A growing number of immunotherapy options for adults with acute lymphocytic leukemia (ALL) – rituximab, inotuzumab ozogamicin, blinatumomab and chimeric antigen receptor (CAR) T-cell therapy – have improved remission rates, but their collective effects on patient outcomes remain to be seen, David Maloney, MD, PhD, said at the National Comprehensive Cancer Network Annual Congress: Hematologic Malignancies.

The main challenge for the field is deciding when and how to use a variety of therapies, he said. “How are we going to put these together? What’s the order?” he asked. “Are we going to be able to decrease the need for allogeneic stem cell transplant? And, obviously, that’s the goal.”

About 30%-50% of adults with ALL exhibit CD20-positive cells, making them potentially treatable with rituximab. Data show a better event-free survival rate and a reduced relapse rate when rituximab is added to standard chemotherapy as compared with standard chemotherapy alone, Dr. Maloney of the clinical research division at the Fred Hutchinson Cancer Research Center, Seattle, noted (N Engl J Med. 2016 Sep 15;375[11]:1044-53). But the improvement was only “modest,” he said.

The anti-CD22 antibody inotuzumab ozogamicin has produced complete remission in 81% of relapsed or refractory ALL patients, compared with those getting standard therapy (N Engl J Med. 2016 Aug 25;375:740-53). Dr. Maloney said it seems well tolerated, but there is concern about an increase in veno-occlusive disease in patients who have undergone or will undergo an allogeneic stem cell transplant.

Blinatumomab produces moderate response rates and minimal residual disease–negative remissions, but delivery of the drug is “cumbersome,” requiring a 4-week continuous infusion, he said. The drug seems to be more effective in those with a lower burden of disease, he noted.

CAR T-cell therapy has produced MRD-negative complete responses in 94% of patients, based on results from a clinical trial at Fred Hutchinson. And using the chemotherapy drug fludarabine in combination with this therapy “dramatically” boosts the peak number of the CAR T cells and how long they persist, Dr. Maloney said. Still, CAR T-cell therapy is a work-intensive treatment requiring cells harvested from the patient, and the procedure often brings on cytokine-release syndrome and neurotoxicity, though both adverse events are typically reversible, he said.

It may be that using fewer CAR T cells can reduce toxicity without compromising treatment response, he said.

Questions remain over whether to transplant patients who are in remission after CAR T-cell therapy. “This is a hot debate,” he said. The decision will likely depend on their prior therapy, whether they’ve had a prior transplant, and the how robust the CAR T-cell expansion has been, he said.

Dr. Maloney reports financial relationships with Celgene, Gilead Sciences, Kite Pharma, and Roche.

SAN FRANCISCO – A growing number of immunotherapy options for adults with acute lymphocytic leukemia (ALL) – rituximab, inotuzumab ozogamicin, blinatumomab and chimeric antigen receptor (CAR) T-cell therapy – have improved remission rates, but their collective effects on patient outcomes remain to be seen, David Maloney, MD, PhD, said at the National Comprehensive Cancer Network Annual Congress: Hematologic Malignancies.

The main challenge for the field is deciding when and how to use a variety of therapies, he said. “How are we going to put these together? What’s the order?” he asked. “Are we going to be able to decrease the need for allogeneic stem cell transplant? And, obviously, that’s the goal.”

About 30%-50% of adults with ALL exhibit CD20-positive cells, making them potentially treatable with rituximab. Data show a better event-free survival rate and a reduced relapse rate when rituximab is added to standard chemotherapy as compared with standard chemotherapy alone, Dr. Maloney of the clinical research division at the Fred Hutchinson Cancer Research Center, Seattle, noted (N Engl J Med. 2016 Sep 15;375[11]:1044-53). But the improvement was only “modest,” he said.

The anti-CD22 antibody inotuzumab ozogamicin has produced complete remission in 81% of relapsed or refractory ALL patients, compared with those getting standard therapy (N Engl J Med. 2016 Aug 25;375:740-53). Dr. Maloney said it seems well tolerated, but there is concern about an increase in veno-occlusive disease in patients who have undergone or will undergo an allogeneic stem cell transplant.

Blinatumomab produces moderate response rates and minimal residual disease–negative remissions, but delivery of the drug is “cumbersome,” requiring a 4-week continuous infusion, he said. The drug seems to be more effective in those with a lower burden of disease, he noted.

CAR T-cell therapy has produced MRD-negative complete responses in 94% of patients, based on results from a clinical trial at Fred Hutchinson. And using the chemotherapy drug fludarabine in combination with this therapy “dramatically” boosts the peak number of the CAR T cells and how long they persist, Dr. Maloney said. Still, CAR T-cell therapy is a work-intensive treatment requiring cells harvested from the patient, and the procedure often brings on cytokine-release syndrome and neurotoxicity, though both adverse events are typically reversible, he said.

It may be that using fewer CAR T cells can reduce toxicity without compromising treatment response, he said.

Questions remain over whether to transplant patients who are in remission after CAR T-cell therapy. “This is a hot debate,” he said. The decision will likely depend on their prior therapy, whether they’ve had a prior transplant, and the how robust the CAR T-cell expansion has been, he said.

Dr. Maloney reports financial relationships with Celgene, Gilead Sciences, Kite Pharma, and Roche.