Latest Conference Articles

Experts unpack key melanoma data shared during the 2026 ASCO Annual Meeting.

Tacabrutideg's safety profile was tolerable, and the drug had antitumor activity in BTK inhibitor–naive patients with CLL/SLL and other B-cell malignancies.

LB2501, an off-the-shelf in vivo dual-target CAR T-cell therapy, produced a 100% ORR at dose level 2 across DLBCL, MCL, and follicular lymphoma.

Zanubrutinib yielded sustained progression-free survival and a tolerable safety profile in older patients with CLL/SLL treated in the SEQUOIA trial.

Treatment with subcutaneous blinatumomab generated high CR rates across 2 dosing regimens in pretreated, relapsed/refractory, Ph-positive B-ALL.

ASCO 2026 highlights show dostarlimab may deliver curative potential in dMMR endometrial cancer, while novel ADCs and fasting reshape ovarian care.

Tuspetinib/venetoclax/azacitidine produced high CR and MRD-negativity rates across molecular subgroups of older or unfit patients newly diagnosed AML.

The first-in-class BTK degrader tacabrutideg produced an ORR of 94.1% at the recommended phase 2 dose in relapsed/refractory CLL/SLL.

Gilteritinib generated comparable OS outcomes vs midostaurin in newly diagnosed FLT3-mutated AML, failing to meet the phase 3 trial primary end point.

Peter Voorhees, MD, discusses efficacy data for talquetamab plus daratumumab with or without pomalidomide from MonumenTAL-3.

Stephan Stilgenbauer, MD, discusses safety considerations for BGB-16673 and where its development is headed in chronic lymphocytic leukemia.

Ziftomenib plus 7+3 yielded high CR and MRD-negativity rates with manageable safety in newly diagnosed NPM1/KMT2A-mutated AML.

Fixed-duration pirtobrutinib plus venetoclax and rituximab reduced the risk of progression or death by 45% in previously treated CLL.

Obe-cel delivered durable remissions in relapsed/refractory B-ALL, with the best efficacy and safety seen in patients with low disease burden.

Phase 1 data showed that INCA033989 produced rapid and durable responses as monotherapy and in a combination regimen in CALR-mutated myelofibrosis.

The type II JAK2 inhibitor AJ1-11095 produced SVRs, deep symptom responses, and mutation VAF reductions in type I JAK inhibitor–exposed myelofibrosis.

Epcoritamab improved PFS and produced durable complete responses vs chemoimmunotherapy in relapsed/refractory large B-cell lymphoma.

RevCAR T did not cause GVHD or ICANS and achieved complete remission in patients with CD123-positive relapsed/refractory AML.

Talquetamab plus daratumumab, with or without pomalidomide, significantly improved PFS and deepened responses in relapsed/refractory myeloma.

Luspatercept produced clinically meaningful improvements in RBC transfusion independence in myelofibrosis-associated anemia.

A phase 2 study of dose-adjusted EPOCH plus tafasitamab with or without rituximab met its primary end point of MRD negativity after the first cycle.

Fixed-duration venetoclax/obinutuzumab more than doubled median PFS vs chlorambucil/obinutuzumab in previously untreated CLL.

Branko Cuglievan, MD, discusses data for revumenib in the pediatric R/R KMT2AR-acute leukemias subgroup from AUGMENT-101.

Jennifer Marvin-Peek, MD, discusses data for azacitidine, venetoclax, and ivosidenib, in IDH1-mutated acute myeloid leukemia and their significance.

In the MAXILUS primary analysis, luspatercept initiated at 1.75 mg/kg yielded high RBC transfusion independence rates in lower-risk MDS.

Revumenib yielded responses across subgroups with relapsed/refractory, NPM1-mutated AML and co-mutations, as well as in KMT2A-rearranged acute leukemia.

Partial response to bridging therapy before cilta-cel was associated with improved PFS and OS outcomes in relapsed/refractory multiple myeloma.

Experts recap of the most pivotal lung cancer data to surface at the 2026 ASCO Annual Meeting.

EPCORE FL-1 showed that epcoritamab/lenalidomide/rituximab yielded superior efficacy vs lenalidomide/rituximab across follicular lymphoma populations.

Azacitidine plus venetoclax and ivosidenib produced robust responses and induced high rates of MRD negativity in IDH1-mutated newly diagnosed AML.