77 episódios
- Episode summary
In this episode, we bring Dr. Manni Mohyuddin from Huntsman Cancer Center [Utah] to go through the biggest myeloma data from the 2026 International Myeloma Society (IMS) Annual Meeting at Glasgow.
In this episode
1. CERVINO (Phase 3): Etentamig vs. standard therapy in triple-class-exposed RRMM
Patients had at least 2 prior lines, were triple-class exposed and had no prior BCMA therapy. They were randomized to etentamig or the investigator’s choice of Kd, EPd or SVd. The co-primary endpoints were ORR and PFS.
Etentamig is dosed every 4 weeks from the start, and patients in CR could stop after 2 years.
The population was more heavily pretreated than MajesTEC-9: 51% were triple-class refractory (vs. about 30%), with a median of 3 prior lines.
Discussion: Where CERVINO fits with MajesTEC-3 and MajesTEC-9
Efficacy compared with teclistamab, elranatamab and linvoseltamab
Whether low-affinity CD3 binding really means less CRS
Infection risk
2. EXCALIBUR-RRMM (Phase 3): Iberdomide-Dara-Dex vs. DVd
The trial enrolled patients with relapsed myeloma that was not refractory to anti-CD38 therapy. About 70% had 1 prior line, about 90% had prior IMiD exposure and about 40% were IMiD-refractory. Iberdomide was given at 1 mg, the dose chosen in stage 1.
The dual primary endpoints both favored the iberdomide arm: MRD-negative CR: 41% vs. 21%
Median PFS: 42 vs. 20 months
Discussion: How this compares with MajesTEC-3 and DREAMM-7 in a similar population
Where IberDd may fit in practice: as a bridge before CAR-T, or for indolent or biochemical relapse in patients whose disease isn’t dara-refractory
Whether the more selective CELMoD design means fewer non-hematologic side effects than lenalidomide-based triplets
3. GEM-TECTAL (Spanish Myeloma Group): MRD-guided Tec-Dara and Tal-Dara in high-risk NDMM
The schema: 4 cycles of Dara-VRd
Stem cell collection and MRD assessment
6 cycles of Tec-Dara consolidation
Next step by MRD status: patients who are MRD-negative get 2 years of Tec-Dara maintenance, and patients who are MRD-positive get early rescue with 6 cycles of Tal-Dara.
63% of patients were high-risk by the IMS-IMWG definition.
MRD negativity at 10⁻⁶ by NGF was 40% after Dara-VRd and 86% after Tec-Dara consolidation. Only 1 patient was still MRD-positive.
Discussion: the safety of Tec-Dara consolidation, and whether this will be the next frontier for high-risk disease
4. TRILOGY-1: Updated Phase 1 data for ramantamig (BCMA×GPRC5D trispecific)
The patients were heavily pretreated: Median of 3 prior lines
100% triple-class exposed and 50% triple-class refractory
96% CD38-refractory
14% with prior BCMA therapy
Dosing is every 4 weeks from the start, moving to every 8 weeks after 6 months.
In BCMA/GPRC5D-naïve patients, the CR rate was about 80%, and 90% of those CRs were MRD-negative at 10⁻⁶. 2-year PFS was 81%, and about 85% in the original cohort with 26 months of follow-up.
Grade ≥3 infections occurred in 25% of patients, which is lower than in MajesTEC-9 at similar follow-up and may reflect more routine primary IVIG prophylaxis.
Skin, nail and oral side effects were milder than with talquetamab, and mean weight loss was under 5%. - Topics Covered
1. KOMET-007 and SNDX-5613-0708: Menin Inhibitors with Intensive Chemotherapy
KOMET-007: Phase 1a/b study adding ziftomenib 600 mg once daily, starting on day 8, to 7+3 induction and continuing it through consolidation, in 99 patients with newly diagnosed NPM1-mutated (n=49; median age 60) or KMT2A-rearranged (n=50; median age 43) AML. Presented by Amer Zeidan at EHA 2026 (Abstract S130; NCT05735184).
SNDX-5613-0708: Phase 1 dose-escalation study adding revumenib to cytarabine plus daunorubicin or idarubicin for up to two induction cycles in induction-eligible adults aged 18–75 (ECOG 0–2) with newly diagnosed KMT2A-rearranged, NPM1-mutated, or NUP98-rearranged AML. Two dose levels were tested: DL1 (110/220 mg) and DL2 (160/270 mg, the approved monotherapy dose). 31 patients were treated (13 at DL1, 18 at DL2) as of October 2025. Presented by Ibrahim Aldoss at EHA 2026 (Abstract PF489; NCT06226571).
Key results (KOMET-007 median follow-up 17.6 months NPM1-m, 11.0 months KMT2A-r):
• KOMET-007 CRc 96% (47/49) in NPM1-m and 90% (45/50) in KMT2A-r, 93% (92/99) overall; MRD negativity among CRs ~85%
• KOMET-007 12-month OS 94% (NPM1-m) vs. 71% (KMT2A-r); median OS not reached in either cohort; 60-day mortality 2% and 4%
• KOMET-007 safety: grade 3 differentiation syndrome 4%, no grade 4; no ziftomenib-related QTc prolongation
• Revumenib + intensive chemotherapy, response-evaluable patients: DL1 (n=12) ORR/CRc 100%, CR 92%; DL2 (n=14) ORR 93%, CRc 86%, CR 79%; MRD-negative CR 100% (DL1) and 70% (DL2); responses similar across dose levels
• Revumenib safety: no differentiation syndrome; one grade 3 QTcF prolongation DLT; any-grade QTcF prolongation ~15% at DL1
Discussion points: Both studies start the menin inhibitor after the cytotoxic days of induction, when there is less leukemia left to differentiate. Dr. Zeidner credits that timing and the chemotherapy itself for differentiation syndrome rates of 3–4%, compared with roughly 15–30% for single-agent menin inhibitors in relapsed/refractory disease. He saw no new QTc signal and no clear delay in count recovery. He cautioned that single-arm data can only be judged against historical expectations, and that the low early mortality reflects selected patients at academic centers. Ashwin questioned how much a high CR rate adds in NPM1-mutated disease, where 7+3 already works well. Dr. Zeidner agreed the two genotypes need separate readouts. In NPM1-mutated, FLT3 wild-type disease the goal is cure with chemotherapy, so relapse and survival are the open questions, and the randomized phase 3 KOMET-017 (7+3 plus ziftomenib or placebo) will answer them. In KMT2A-rearranged disease remission is a bridge to transplant, so he asks whether azacitidine-venetoclax plus a menin inhibitor could replace intensive induction. He is leading a single-arm study of that approach (RAVEN) in younger fit KMT2A-rearranged patients. Choosing between the two drugs, he finds differentiation syndrome rates comparable in NPM1-mutated disease (about 20–25%) and more severe in KMT2A-rearranged disease. Both drugs prolong the QTc. Revumenib carries the boxed warning and somewhat more grade 3 events, and he checks ECGs weekly when starting either one.
2. HOVON156/AMLSG28-18/PASHA
Phase 3, open-label trial randomizing 768 adults with newly diagnosed FLT3-mutated AML fit for intensive chemotherapy 1:1 to gilteritinib 120 mg daily or midostaurin 50 mg twice daily, each with 7+3 induction and consolidation and followed by FLT3 inhibitor maintenance. Median age 59; FLT3-ITD allelic ratio ≥0.5 in 48%, FLT3-TKD in 21%, NPM1 co-mutation in 58%. The primary endpoint was OS. Presented by Marc Raaijmakers at EHA 2026 (Abstract LB5005; NCT04027309).
Key results (43.2-month median follow-up):
• OS (primary endpoint): median not reached in either arm; HR 1.02 (95% CI 0.81–1.28; P=0.86)
• Median EFS 51.1 vs. 19.9 months (HR 0.83; P=0.052)
• Post-CR morphologic relapse 21% (gilteritinib) vs. 36% (midostaurin) (HR 0.68; P=0.003)
• Among relapsing patients, median OS 7.2 months with gilteritinib vs. 10.2 months with midostaurin; 50% of midostaurin-arm relapses received salvage gilteritinib vs. 17% in the gilteritinib arm
• CR rates did not differ between arms; early mortality, infection rates, and myelosuppression were numerically higher with gilteritinib
Discussion points: Dr. Zeidner called it a negative trial with OS curves that overlap completely. Gilteritinib lowered relapse in patients who reached CR. Midostaurin-arm patients who relapsed could still be salvaged with gilteritinib and transplant, while gilteritinib-arm patients had no equally effective option left. He did not use gilteritinib off-label before this trial and will not now. He offered a thought experiment: if EFS had been the powered primary endpoint and crossed significance, the same data would have been called positive and a new standard, so endpoint choice drives the interpretation as much as the data do. The hosts compared this with PARADIGM, where an EFS benefit without an OS difference has already shifted practice, and with the earlier randomized phase 2 PrECOG 0905 comparison of the same two drugs. Raj noted that in myeloma an EFS gain usually carries into OS because several effective lines follow, while in FLT3-mutated AML little works after upfront gilteritinib. Dr. Zeidner added that midostaurin may now be an outdated control for FLT3-ITD disease, since many centers have moved to quizartinib.
3. Quizartinib vs. Midostaurin with Intensive Chemotherapy (Multicenter Cohort)
Retrospective cohort study across 12 US centers (2017–2025) of patients with newly diagnosed FLT3-ITD AML treated with intensive chemotherapy plus midostaurin (n=127) or quizartinib (n=88); median age 56; 89% ELN intermediate risk. Primary endpoint 1-year OS. Median follow-up was 667 days with midostaurin vs. 324 days with quizartinib. Presented by Michelle Lee at EHA 2026 (Abstract S133); Dr. Zeidner is a co-author.
Key results:
• 1-year OS 93% (quizartinib) vs. 78% (midostaurin) (HR 0.19; 95% CI 0.07–0.52)
• 1-year EFS 77% vs. 56% (HR 0.44)
• CRc 85% vs. 73%
• FLT3 clearance similar in both groups (~39–40%)
• The quizartinib group had roughly half the follow-up and fewer triple-mutated (NPM1/DNMT3A/FLT3-ITD) patients
Discussion points: Dr. Zeidner stressed the retrospective design. Most midostaurin patients were treated earlier, the quizartinib group has shorter follow-up, and the investigators chose 1-year OS to fit that follow-up. He reads the cohort as support for current practice rather than a reason to change it. For fit patients he gives 7+3 plus quizartinib for FLT3-ITD and 7+3 plus midostaurin for FLT3-TKD. He avoids quizartinib in patients with significant QTc prolongation or cardiac comorbidity and is more cautious above age 60, given higher early mortality in that subgroup on QuANTUM-First. He still uses quizartinib in older patients with the NPM1/DNMT3A/FLT3-ITD genotype, which depends heavily on FLT3 signaling and did well with quizartinib on ... - Blood Cancer Talks — Show Notes
Episode: Best of ASCO/EHA 2026 — Multiple Myeloma & AL Amyloidosis
Guest: Dr. Prashant Kapoor, MD Professor of Medicine, Mayo Clinic, Rochester, MN Chair, Myeloma, Amyloidosis and Dysproteinemia Group, Mayo Clinic
Episode Overview
In this episode, the hosts sit down with Dr. Prashant Kapoor to review the highest-impact multiple myeloma and AL amyloidosis data from the 2026 ASCO and EHA annual meetings. The discussion centers on the rapidly shifting relapsed/refractory myeloma landscape, where a wave of phase 3 trials of T-cell engaging immunotherapies (bispecific antibodies and CAR T) have now each demonstrated superiority over traditional triplet regimens.
Topics Covered
1. MajesTEC-3
Phase 3, open-label trial of teclistamab + daratumumab SC (n=291) vs. investigator's choice of DPd or DVd (n=296) in 587 patients with relapsed/refractory myeloma and 1–3 prior lines; prior BCMA-directed therapy and anti-CD38-refractory disease were exclusions (only 5% CD38-exposed, none were refractory). Initially presented at ASH 2025, with cytogenetic subgroup data updated at EHA 2026.
Key results (34.5-month median follow-up):
Median PFS not reached with Tec-Dara vs. 18.1 months with DPd/DVd; 36-month PFS 83.4% vs. 29.7% (HR 0.17)
36-month OS 83.3% vs. 65.0% (HR 0.46)
Severe infection rate front-loaded: ~35% → ~17% between the first and second 6-month windows, plateauing at ~10–11%/window beyond 12 months; overall grade 3–4 infection 54%, 4.6% fatal infections (mostly without IVIG prophylaxis)
EHA 2026 cytogenetic subgroup: 2-year PFS 90% (0 HRCA), 82% (1 HRCA), 76% (≥2 HRCA) — vs. only 14% with DPd/DVd in patients with ≥2 HRCA
Discussion points: Applicability to patients at 1st/2nd relapse seen in clinic today; whether infection risk limits use of Tec-Dara at first relapse; implications of the high-risk cytogenetic subgroup data.
2. MajesTEC-9
Phase 3 trial of teclistamab monotherapy vs. investigator's choice of PVd or Kd in relapsed/refractory myeloma enrolling a heavily anti-CD38-refractory population (100% CD38-exposed, 85% refractory) — the population MajesTEC-3 excluded. Natural comparator: CARTITUDE-4 (phase 3, cilta-cel vs. DPd/PVd in Len-refractory myeloma, 1–3 prior lines, ~25% CD38-refractory/exposed).
Key results (~18-month median follow-up):
18-month PFS 70% vs. 27% (HR 0.29); 18-month OS 79% vs. 69% (HR 0.6), despite ~2/3 of control-arm patients receiving BsAb/CAR T as subsequent therapy
Discussion points: Cross-trial comparison with CARTITUDE-4 — comparable 18-month PFS on cross-trial comparison, but differing populations (CARTITUDE-4 required Len-refractory disease; MajesTEC-9 enrolled a more CD38-refractory population) and differing maturity (~3-year vs. ~1.5-year follow-up); how Dr. Kapoor chooses between teclistamab and cilta-cel at earlier-line relapse in Len- and CD38-refractory patients, given the divergent toxicity profiles — ongoing infection risk with continuous BsAb dosing vs. the one-time cilta-cel infusion with its rare but potentially irreversible delayed neurotoxicity, IEC-enterocolitis, and CTTLN risk.
3. MonumenTAL-3
Phase 3 trial — the first phase 3 study of a GPRC5D-targeted bispecific — randomizing 864 patients with relapsed/refractory myeloma (mostly Len-refractory, ~10% CD38-exposed but none refractory) 1:1:1 to Tal-Dara-Pom (n=287), Tal-Dara (n=287), or DPd (n=290), each Talq arm compared against the common DPd control. Presented by Peter Voorhees at EHA 2026 and simultaneously published in NEJM.
Key results (24.6-month median follow-up):
Both Talq arms significantly improved PFS over DPd: Tal-DP HR 0.28, Tal-D HR 0.33 (both P<0.0001); 24-month PFS 81.3% (Tal-DP) and 77.6% (Tal-D) vs. ~51% (DPd)
OS also favored both Talq arms, up to 89.2% vs. 79.1% (DPd) at 24 months
Safety reflected regimen composition: more neutropenia/grade 3–4 infection with the Pom-containing arm; Talq arms showed frequent but mostly low-grade CRS, rare ICANS, and expected dysgeusia/skin-nail toxicity with weight loss (up to ~46% in Tal-DP)
Discussion points: Not powered for a Tal-Dara vs. Tal-Dara-Pom comparison — did adding pomalidomide meaningfully change efficacy or safety; how to choose between a BCMA-directed and a GPRC5D-directed bispecific at first relapse given overlapping eligible populations with MajesTEC-3.
4. LINKER-AL2 — AL Amyloidosis
Phase 1/2, open-label study of single-agent, fixed-duration linvoseltamab in patients with relapsed, refractory, or suboptimally responding systemic AL amyloidosis after ≥1 prior therapy (~60% prior daratumumab-containing regimen). Data presented in 20 patients at 80 mg (n=7) or 240 mg (n=13).
Key results:
No grade ≥3 CRS at either dose; any-grade CRS in 50% (35% grade 1, 15% grade 2); infusion-related reactions in 45% (mostly during step-up dosing); no DLTs, no notable ICANS
Hematologic ORR 100% (80 mg) and ~92% (240 mg); hematologic CR reached 100% at the 240 mg dose in the most recent update
Rapid responses — involved FLC often normalized within ~15 days; median time to hematologic CR ~47 days
Discussion points: Frames LINKER-AL2 alongside other BCMA-targeting BsAbs in AL amyloidosis (etentamig, elranatamab) as promising options for patients with suboptimal hematologic response to frontline Dara-CyBorD, particularly transplant-ineligible patients; how Dr. Kapoor would choose among BCMA-targeting BsAbs as 2nd-line therapy (trial or off-label) for a transplant-eligible patient with a suboptimal response to Dara-CyBorD - BloodCancerTalks: ASCO/EHA 2026 Lymphoma Round-Up with Dr. Thomas Lew
Guest: Dr. Thomas Lew, Peter MacCallum Cancer Centre (Melbourne, Australia) — hematologist specializing in lymphoid malignancies.
In this episode, we break down the biggest lymphoma and CLL data from ASCO and EHA 2026 (Chicago and Stockholm), covering mantle cell lymphoma genomics, bispecific antibodies in DLBCL and follicular lymphoma, a practice-changing (or not) CNS prophylaxis study, transplant-eligible relapsed DLBCL, fixed-duration BTK/BCL2 combinations in CLL, and the first in vivo CAR T data in lymphoma.
1. TRIANGLE: TP53-Mutated MCL Molecular Subgroup Analysis
Molecular subgroup data from the practice-shaping TRIANGLE trial presented by Dr. Marta Grau.
Discussion: Where TP53-mutated MCL stands today, and whether ibrutinib-containing regimens are changing the natural history of this historically dismal subgroup.
2. EPCORE DLBCL-1: Epcoritamab vs. Chemotherapy in R/R DLBCL
Randomized phase 3 trial (n=483) of bispecific antibody epcoritamab vs. investigator's choice chemotherapy (72% R-GemOx, 28% BR) in second-line-or-later, transplant-ineligible R/R DLBCL, presented by Prof. Chris Fox.
Discussion: A PFS benefit without an OS signal, set against a meaningfully higher infection-related mortality — what this means for patient selection and infection mitigation strategies.
3. CNS Prophylaxis in Ultra-High-Risk DLBCL: Does HD-MTX Help?
Pooled analysis of two large multicenter retrospective cohorts (n=1,923 ultra-high-risk patients — CNS-IPI 5–6, testicular/renal/adrenal/breast involvement, or ≥3 extranodal sites), presented by Dr. Matt Wilson (Glasgow) and simultaneously published in JCO.
Discussion: Whether these data close the door on routine HD-MTX in ultra-high-risk DLBCL, and if any subgroup still warrants prophylaxis.
4. Pola-R-ICE: A Negative Trial in Transplant-Eligible R/R DLBCL
Randomized phase 3 study (4 European cooperative groups; n=294) of polatuzumab vedotin added to R-ICE in transplant-eligible R/R DLBCL, with ASCT/alloSCT/CAR-T permitted as consolidation.
Discussion: Why this trial missed, and what it tells us about the ceiling of intensive salvage chemo-immunotherapy platforms in the CAR-T era.
5. BRUIN-CLL-322: Fixed-Duration Pirtobrutinib + Venetoclax-Rituximab in R/R CLL
Randomized phase 3 trial (n=639) of fixed-duration pirtobrutinib (non-covalent BTKi) plus venetoclax-rituximab (PVR) vs. venetoclax-rituximab (VR, the MURANO-based control) in second-line-or-later R/R CLL.
6. SOUNDTRACK-F1: Surovatamig (CD19 Bispecific) Safety Run-In in Untreated Follicular Lymphoma
Safety run-in from a randomized trial (surovatamig vs. chemoimmunotherapy) in untreated FL meeting GELF criteria, presented by Prof. Chan Cheah — building on EPCORE-FL-1 data presented at ASH.
Discussion: How this CD19-directed bispecific compares to CD20-targeting agents in frontline FL.
7. LB2501: First In Vivo CAR T Data in B-Cell Lymphoma
Late-breaking data from Dr. Lei Fan and Legend Biotech on LB2501, an in vivo CD19/CD20 dual-targeted CAR T therapy — a third-generation, self-inactivating, replication-incompetent lentiviral vector that generates CAR T cells directly in vivo, without lymphodepletion. Builds on the in vivo CAR T myeloma data first presented at ASH and updated at EHA.
Discussion: What these very early but striking data suggest about the feasibility of in vivo CAR T generation in lymphoma, and how it might reshape access to cellular therapy.
BloodCancerTalks is co-hosted by Rajshekhar Chakraborty, Ashwin Kishtagari and Eddie Cliff. Subscribe wherever you get your podcasts. - Episode Overview
For the second time in two decades, a phase 3 trial has shown a statistically significant improvement over R-CHOP in newly diagnosed diffuse large B-cell lymphoma (DLBCL). In this episode, Eddie, Raj, and Ashwin sit down with Professor Charles Herbaux to unpack the data, debate the clinical implications, and ask the question that's on every hematologist's mind: is this enough to change practice?
Background: Setting the Stage for Tafasitamab
Before diving into frontMIND, the episode provides context on tafasitamab, a CD19-targeting monoclonal antibody
L-MIND (Phase 2 — relapsed/refractory DLBCL):
81 patients with R/R DLBCL
ORR 58%, complete response rate 41%
Established activity of tafasitamab + lenalidomide in the relapsed setting
https://pubmed.ncbi.nlm.nih.gov/32511983/
First-MIND (Phase 1b — frontline DLBCL, IPI 2–5):
66 patients randomized: tafa-R-CHOP (n=33) vs. tafa-len-R-CHOP (n=33)
ORR: 75.8% vs. 81.8%, respectively
Serious treatment-emergent adverse events: 42.4% vs. 51.5%
Provided the signal (and the safety caution) to move to phase 3
https://pubmed.ncbi.nlm.nih.gov/37369099/
The frontMIND Trial
Design: Phase 3, double-blind, placebo-controlled randomized trial
Intervention: R-CHOP + tafasitamab (12 mg/kg IV days 1, 8, 15 per cycle) + lenalidomide (25 mg/day, days 1–10 per cycle)
Control: R-CHOP + placebos
GCSF mandatory (given double-blind design); VTE prophylaxis (heparin or aspirin) mandatory given lenalidomide
Enrollment: May 2021 – March 2023; 899 patients randomized
Primary endpoint: Investigator-assessed progression-free survival (PFS)
Patient Population:
Age 18–80; DLBCL or high-grade B-cell lymphoma, IPI 3–5
Median age: 65 years
96% advanced stage; 54% bulky disease; 31% ECOG PS 2; 82% elevated LDH
55% IPI 3 / aaIPI 2; 43% IPI 4–5 / aaIPI 3
8% double/triple hit — a high-risk subgroup included despite R-CHOP being the control
Broad histologic inclusion: transformed lymphoma, grade 3B FL, T-cell/histiocyte-rich LBCL, EBV+ DLBCL, ALK+ LBCL, HHV8+ DLBCL Note: On retrospective central review, ~7% of patients had a different histology (roughly half had FL grade 1–3A), underscoring the diagnostic challenges in DLBCL
~40% received pre-phase steroids; 8% rituximab; 4% vincristine prior to cycle 1
Key Efficacy Results
(Primary analysis at median follow-up 35.2 months)
| Endpoint | Tafa-Len-R-CHOP | R-CHOP | HR / p-value | 2-year PFS | 71.1% | 62.9% | HR 0.75, p=0.0194
| 3-year PFS | 67.3% | 60.7% | ~6.6% absolute difference
| Overall Survival | — | — | HR 0.85, p=0.27 (immature)
Points of Discussion:
Absolute PFS benefit at 2 years: ~8.2%; at 3 years: ~6.6% — a modest but statistically significant improvement
OS curves cross early, then separate slightly from ~18 months; data remain immature
Early censoring observed: ~17% (intervention) and ~14% (control) censored by 9 months — raises questions about off-protocol therapy
Subgroup consistency: PFS benefit appeared consistent across prespecified subgroups; specific subgroups discussed in the episode
Safety
Adverse Event | Tafa-Len-R-CHOP | R-CHOP
| Fatal treatment-emergent AEs | 6% (26 pts) | 4% (17 pts)
| Diarrhea (any grade) | 25% | 17%
| Febrile neutropenia | 17% (incl. 1 death) | 13%
| Grade ≥3 anemia | 24% | 17%
| Grade ≥3 thrombocytopenia | 27% | 14%
The addition of tafasitamab and lenalidomide to R-CHOP adds meaningful hematologic toxicity, particularly thrombocytopenia and anemia, as well as diarrhea and febrile neutropenia.
Key Discussion Points from the Episode
Did the early-phase L-MIND and First-MIND data justify bringing tafasitamab into the front-line setting, and was tafa-len-R-CHOP the right intervention arm to take forward?
Is R-CHOP the appropriate control for a patient population that includes 8% double/triple hit lymphoma?
What are the implications of using investigator-assessed PFS as the primary endpoint — and how critical is effective blinding to the integrity of that endpoint?
How do we interpret the early OS curve crossing and currently non-significant OS benefit?
Is the ~8% absolute PFS improvement at 2 years clinically meaningful enough to change practice — particularly given the added toxicity?
How should we think about patient selection: who would you prioritize for tafa-len-R-CHOP over standard R-CHOP in clinical practice?
What does frontMIND mean for the DLBCL treatment landscape alongside polatuzumab-R-CHP (POLARIX)?
Resources & Further Reading
frontMIND trial: Lenz et al. Lancet. https://pubmed.ncbi.nlm.nih.gov/42217458/
POLARIX: Tilly H, et al. NEJM 2022
About BloodCancerTalks
BloodCancerTalks is a medical education podcast hosted by Raj, Ashwin, and Eddie, dedicated to the latest advances in hematologic malignancies. New episodes available wherever you listen to podcasts.
Follow us on X/Twitter for episode updates and hematology/oncology content.
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Sobre Blood Cancer Talks
This is a podcast on latest advances in the understanding and management of blood cancers. Here, we will bring a wide range of experts within hematologic malignancies to discuss various topics in depth.
Host: Raj Chakraborty, MD from Columbia University, New York, Ashwin Kishtagari, MD, from Vanderbilt University, Nashville, and Edward Cliff, MD, from Harvard University, Boston
Tweet your suggestions and feedback to @rajshekharucms @AshKishtagari @Eddie_Cliff @BloodCancerTalk
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