Welcome to Dana-Farber's Research News
November 15, 2025
This twice-monthly newsletter highlights recently published research where Dana-Farber faculty are listed as first or senior authors. The information is pulled from PubMed and this issue notes papers published from October 16 - October 31.
If you are a Dana-Farber faculty member and you think your paper is missing from Research News, please let us know by emailing dfciresearchnews@dfci.harvard.edu.
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Blood Davids MS The treatment landscape for chronic lymphocytic leukemia (CLL) has been transformed by the advent of covalent Bruton tyrosine kinase (BTK) inhibitors (cBTKis) and B-cell lymphoma 2 (BCL-2) inhibitors, leading to markedly improved outcomes and, for many, near-normal life expectancy. However, patients progressing after both classes of therapy (double-refractory) have limited options and poor prognoses. This review outlines a practical approach to managing double-exposed or double-refractory CLL, incorporating clinical cases, trial data, and expert perspectives. For cBTKi intolerance, second-generation agents may remain effective. Venetoclax retreatment is reasonable after prior fixed-duration use. In true double-refractory disease, noncovalent BTK inhibitors (eg, pirtobrutinib) and CD19-directed chimeric antigen receptor T-cell (CAR-T) therapy (lisocabtagene maraleucel) are standard-of-care options. Pirtobrutinib induces rapid responses, though often of limited duration, underscoring the need for early consolidation planning with CAR-T or allogeneic stem cell transplant. Persistent disease after CAR-T therapy warrants close monitoring and timely transplant referral in eligible patients. Phosphoinositide 3-kinase inhibitors remain available but are limited by toxicity and modest benefit. Emerging agents, including BTK degraders, bispecific antibodies, and novel cellular therapies, offer promising future directions. Optimizing outcomes in double-refractory CLL requires an individualized, nuanced strategy integrating available treatments with innovative approaches under investigation. |
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Blood Hantel A, Wang Y, Cronin A, Walsh TP, Gallagher E, Luskin MR, Lathan CS, Uno H, DeAngelo DJ, Abel GA Clinical trial eligibility criteria select a target population and reduce anticipated risks for participants but may unnecessarily limit participation both overall and differently across demographic groups. We previously abstracted eligibility criteria for 190 phase II/III acute myeloid leukemia (AML) trials and used Food and Drug Administration and professional society guidance on modernizing criteria to develop alternative, safety-based eligibility criteria for each trial. In this analysis, these trial- and safety-based eligibility criteria sets were applied to a retrospective cohort of 2226 newly-diagnosed patients across 8 hospitals to assess impacts on eligibility. Eligibility proportions increased from a median of 47.9% with trial-based criteria to 84.2% with safety-based criteria (median difference 30.0%; p<0.001); excluding age criteria, the increase was 11.5% (p<0.001). Non-Hispanic (NH)-Asian, NH-Black, NH-White, and Hispanic patients were eligible for median proportions of 41.1%, 44.0%, 47.9%, and 50.0% with trial-based criteria, increasing by 27.9-31.6% when using safety-based criteria (within group changes all p<0.001; between-group changes all p>0.05). Excluding age criteria, increases were between 10.0-11.9%. Moving from trial- to safety-based criteria decreased the proportion of trials with significant eligibility differences between NH-White and NH-Asian (-11.1%), NH-Black (-4.2%), and Hispanic (-12.1%) patients. Criteria significantly associated with increased eligibility and decreased between-group differences in eligibility were coronary artery disease, congestive heart failure, aspartate transaminase level, upper age limits, and prior malignancy. These data suggest that modernization of eligibility for AML trials to focus on safety-based criteria can improve both overall enrollment and population representation. |
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Blood NK Cell Exhaustion in VEXAS: Another Piece in the Puzzle Belizaire R In this issue of Blood, Breillat et al describe a profound impairment in natural killer (NK) cell function in VEXAS (vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic) syndrome, shedding light on how innate immune exhaustion contributes to its complex inflammatory phenotype. Since its initial description, VEXAS syndrome has stood out as a prototypical hematoinflammatory disorder linking acquired somatic mutations in UBA1 to systemic inflammation and hematological abnormalities. Although the role of myeloid cells in driving inflammation has been well described, the contribution of cytotoxic lymphocytes has remained relatively understudied. |
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Blood Vianna P, Hossain S, Miller S, Rossi A, Cuddy SAM, Falk RH, Laubach JP, Bianchi G Immunoglobulin light-chain (AL) amyloidosis is a plasma cell disorder characterized by progressive organ dysfunction secondary to deposition of organized immunoglobulin light-chain aggregates. Achievement of rapid and deep normalization of involved immunoglobulin free light chains is necessary to maximize chances of reversibility of organ dysfunction, which, in turn, results in improved quality and length of life. There are no US Food and Drug Administration (FDA)-approved therapies for patients with relapsed AL amyloidosis. B-cell maturation antigen-targeting (BCMA)-bispecific T-cell engagers teclistamab and elranatamab have shown high activity and acceptable safety profile in patients with relapsed and/or refractory multiple myeloma, leading to their FDA approval. Herein, we report on safety and efficacy of elranatamab for patients with relapsed and/or refractory AL amyloidosis. We treated 9 consecutive patients with advanced-stage AL amyloidosis with single-agent elranatamab, observing a 100% overall response and 67% complete response rate, including minimal residual disease negativity, with expected toxicities. Median time to hematological response was 9 days (range, 6-24), with deep suppression in involved free light chains observed within 1 cycle of therapy, translating in cardiac and renal responses at 3 to 6 months. These data support prospective studies exploring elranatamab for patients with relapsed AL amyloidosis. |
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JAMA Early-Onset Gastrointestinal Cancers: A Review Jayakrishnan T, Ng K IMPORTANCE: Early-onset gastrointestinal (GI) cancer is typically defined as GI cancer diagnosed in individuals younger than 50 years. The incidence of early-onset GI cancer is rising globally, and early-onset GI cancers represent the most rapidly increasing early-onset cancer in the US. OBSERVATIONS: Worldwide, among early-onset GI cancers reported in 2022, colorectal cancer (CRC) was the most common (54.3%; 184?709 cases), followed by gastric cancer (23.8%; 80?885 cases), esophageal cancer (13.2%; 45?056 cases), and pancreatic cancer (8.6%; 29?402 cases). In the US, among early-onset GI cancers reported in 2022, 20?805 individuals were diagnosed with early-onset CRC, 2689 with early-onset gastric, 2657 with early-onset pancreatic, and 875 with early-onset esophageal cancer. Most early-onset GI cancers are associated with modifiable risk factors including obesity, poor-quality diet (eg, sugar-sweetened beverages, ultraprocessed foods), sedentary lifestyle, cigarette smoking, and alcohol consumption. Nonmodifiable risk factors include family history, hereditary syndromes (eg, Lynch syndrome), and inflammatory bowel disease for patients with early-onset CRC. Approximately 15% to 30% of early-onset GI cancers have pathogenic germline variants in genes such as DNA mismatch repair genes and BRCA1/2. All patients with early-onset GI cancers should undergo germline and somatic genetic testing to guide treatment, screen for other cancers (eg, endometrial cancer in Lynch syndrome), and assess familial risk. Treatment for early-onset GI cancers is similar to later-onset GI cancers and may include chemotherapy, surgery, radiation, and therapies such as poly-adenosine diphosphate ribose polymerase inhibitors for BRCA-associated pancreatic cancer. Compared with GI cancers diagnosed after age 50 years, patients with early-onset GI cancers typically receive more treatments but often have similar or shorter survival. Specialized centers and multidisciplinary teams can support patients with challenges around fertility preservation, parenting with cancer, financial difficulty, and psychosocial distress. Currently, screening is not recommended for most early-onset GI cancers, although in the US, screening for CRC is recommended for average-risk individuals starting at age 45 years. High-risk individuals (eg, those with Lynch syndrome, a first-degree relative with CRC, or advanced colorectal adenoma) should begin CRC screening earlier, at an age determined by the specific risk factor. CONCLUSIONS AND RELEVANCE: Early-onset GI cancers, typically defined as cancer diagnosed in individuals younger than 50 years, are among the largest subset of early-onset cancers globally. Treatment is similar to later-onset GI cancers and typically involves a combination of chemotherapy, surgery, and radiation, depending on the cancer type and stage. The prognosis for patients with early-onset GI cancers is similar to or worse than that for patients with later-onset GI cancers, highlighting the need for improved methods of prevention and early detection. |
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JAMA Wong JMW, Kao PC, Kim London WB, Grace RF IMPORTANCE: Eltrombopag, a thrombopoietin receptor agonist, is approved by the US Food and Drug Administration for children with chronic immune thrombocytopenia. Efficacy of eltrombopag during the newly diagnosed phase of pediatric immune thrombocytopenia is unknown. OBJECTIVE: To determine if the proportion of patients with a platelet response is significantly greater in patients with newly diagnosed immune thrombocytopenia treated with eltrombopag than in those treated with standard therapy (first-line treatments). DESIGN, SETTING, AND PARTICIPANTS: This phase 3, randomized clinical trial enrolled patients (aged 1-<18 years) with newly diagnosed primary immune thrombocytopenia (platelet count <30?×?109/L who required pharmacological treatment but did not have severe bleeding or need a rapid increase in platelet count) from May 7, 2019, to January 25, 2024, at 23 centers participating in the Pediatric ITP Consortium of North America. Final follow-up occurred on February 26, 2025. INTERVENTIONS: Eltrombopag was administered orally based on a standard dosing schedule (n?=?78) vs standard therapy (investigator choice of glucocorticoids, intravenous immunoglobulin, or anti-D immunoglobulin) (n?=?40). MAIN OUTCOMES AND MEASURES: The primary outcome was a sustained platelet response defined as 3 or more of 4 platelet counts greater than 50?×?109/L during weeks 6 to 12 without rescue treatment. The secondary outcomes included bleeding scores, change in health-related quality of life, and serious adverse events. RESULTS: Of 118 pediatric patients (median age, 8 years [IQR, 4-12 years]; 49% were male), 63% experienced an initial treatment failure after observation or medical therapy. Enrollment ended after a planned interim analysis met a prespecified threshold for efficacy. Of 71 patients in the eltrombopag group, 46 (65% [95% CI, 54%-76%]) had a sustained platelet response compared with 13 of 37 patients (35% [95% CI, 20%-51%]) in the standard therapy group (between-group difference, 30% [95% CI, 11%-49%]; P?=?.002), which crossed the monitoring boundary for efficacy. Overall, there was no between-group difference in the number and type of adverse events. CONCLUSIONS AND RELEVANCE: In pediatric patients with newly diagnosed immune thrombocytopenia requiring pharmacological treatment, eltrombopag resulted in a higher rate of sustained platelet response compared with standard therapy. Eltrombopag may be an effective option for pediatric patients with newly diagnosed immune thrombocytopenia with nonsevere bleeding who warrant medical intervention. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT03939637. |
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Journal of Clinical Oncology Jacobson CA Axicabtagene ciloleucel (axi-cel) is an autologous anti-CD19 chimeric antigen receptor (CAR) T-cell therapy approved for relapsed/refractory (R/R) follicular lymphoma (FL). Here, we report updated clinical outcomes from ZUMA-5 in 159 enrolled patients with R/R indolent non-Hodgkin lymphoma (iNHL; 127 with FL and 31 with marginal zone lymphoma) after a median follow-up of 64.6 months. Patients underwent leukapheresis and received lymphodepleting chemotherapy and axi-cel (2 × 106 CAR T cells/kg). The overall response rate was 90% (75% complete response rate). The median duration of response was 60.4 months, and the median progression-free survival (PFS) was 62.2 months; median time to next treatment and overall survival were not reached (NR). At data cutoff, 55% of patients were alive without requiring subsequent anticancer therapy. Median lymphoma-specific PFS in patients with FL was NR; 34% had progression or death due to lymphoma or study treatment. Notably, after 30 months postinfusion, progression or lymphoma-related deaths were rare. Late-onset toxicities were infrequent and largely unrelated to axi-cel. Durable response and prolonged survival in FL were associated with robust early CAR T-cell expansion and naïve product phenotype. These findings confirm sustained responses and manageable safety with axi-cel in the long term among patients with R/R iNHL and its potential as a curative therapy in FL. |
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Nature Genetics St Laurent JD, Xu GD, Ying AW, Patil A, Paulo JA, Cervantes KS, Feng WW, Sankar A, Samé Guerra DD, Qi J, Neel DS, Hornick JL, Kolin DL, Gygi SP, Kadoch C The mammalian (m)SWI/SNF family of chromatin remodelers govern cell type-specific chromatin accessibility and gene expression and assemble as three distinct complexes: canonical BRG1-associated or BRM-associated factor (cBAF), poly(bromo)-associated BAF (PBAF) and noncanonical BAF (ncBAF). ARID1A and ARID1B are paralog subunits that specifically nucleate the assembly of cBAF complexes and are frequently co-mutated in highly aggressive dedifferentiated or undifferentiated endometrial carcinomas (DDEC/UECs). Here in cellular models and primary human tumors, we find that ARID1A and/or ARID1B (ARID1A/B) deficiency-mediated cBAF loss results in increased ncBAF and PBAF biochemical abundance and chromatin-level functions to maintain the DDEC oncogenic state. Furthermore, treatment with clinical-grade SMARCA4 and/or SMARCA2 ATPase inhibitors markedly attenuates DDEC cell proliferation and tumor growth in vivo and synergizes with carboplatin-based chemotherapy to extend survival. These findings reveal the oncogenic contributions of shifted mSWI/SNF family complex stoichiometry and resulting gene-regulatory dysregulation and suggest therapeutic utility of mSWI/SNF small molecule inhibitors in DDEC/UECs and other cBAF-disrupted cancer types. |
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New England Journal of Medicine Sacituzumab Govitecan in Untreated, Advanced Triple-Negative Breast Cancer Tolaney SM BACKGROUND: Patients with previously untreated, locally advanced, unresectable or metastatic triple-negative breast cancer who are not candidates for inhibitors of programmed cell death protein 1 (PD-1) or programmed death ligand 1 (PD-L1) have limited treatment options. METHODS: In this international, phase 3, open-label, randomized trial, we enrolled patients with previously untreated, advanced triple-negative breast cancer who were not candidates for PD-1 or PD-L1 inhibitors owing to previous use or coexisting conditions. Patients had either PD-L1-negative tumors with a combined positive score (CPS; the number of PD-L1-staining tumor cells, lymphocytes, and macrophages divided by the total number of viable tumor cells, multiplied by 100) of less than 10 or PD-L1-positive tumors with a CPS of 10 or higher and were assigned in a 1:1 ratio to receive sacituzumab govitecan or chemotherapy (paclitaxel, nanoparticle albumin-bound paclitaxel, or gemcitabine plus carboplatin). The primary end point was progression-free survival, assessed by blinded independent central review. Secondary end points included overall survival, objective response, the duration of response, and safety. RESULTS: Among 558 patients, median progression-free survival was 9.7 months (95% confidence interval [CI], 8.1 to 11.1) with sacituzumab govitecan and 6.9 months (95% CI, 5.6 to 8.2) with chemotherapy (stratified hazard ratio for disease progression or death, 0.62; 95% CI, 0.50 to 0.77; P<0.001). An objective response was confirmed in 48% of patients (95% CI, 42 to 54) who received sacituzumab govitecan and 46% (95% CI, 40 to 52) who received chemotherapy; the median response duration was 12.2 months (95% CI, 9.7 to 13.8) and 7.2 months (95% CI, 5.7 to 8.4), respectively. Adverse events of grade 3 or higher occurred in 66% of patients who received sacituzumab govitecan (most frequently neutropenia [in 43%], diarrhea [in 9%], and leukopenia [in 7%]) and in 62% of patients who received chemotherapy (most frequently neutropenia [in 41%], anemia [in 16%], and leukopenia [in 13%]). The incidence of adverse events that led to discontinuation of sacituzumab govitecan or at least one chemotherapy drug was 4% and 12%, respectively. CONCLUSIONS: Sacituzumab govitecan led to significantly longer progression-free survival than chemotherapy among patients with advanced triple-negative breast cancer who were not candidates for treatment with PD-1 or PD-L1 inhibitors. The incidence of adverse events of grade 3 or higher with sacituzumab govitecan was similar to that with chemotherapy, but adverse events were common. (Funded by Gilead Sciences; ASCENT-03 ClinicalTrials.gov number, NCT05382299.). |
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New England Journal of Medicine Survival with Osimertinib plus Chemotherapy in EGFR-Mutated Advanced NSCLC Jänne PA BACKGROUND: The primary analysis of this trial showed that first-line treatment with osimertinib plus chemotherapy with a platinum-based agent and pemetrexed led to significantly longer progression-free survival than osimertinib monotherapy among patients with epidermal growth factor receptor (EGFR)-mutated advanced non-small-cell lung cancer (NSCLC). Results from the planned final analysis of overall survival are needed. METHODS: In this phase 3, international, open-label trial, we randomly assigned in a 1:1 ratio patients with EGFR-mutated (exon 19 deletion or L858R mutation) advanced NSCLC who had not previously received treatment for advanced disease to receive either osimertinib (80 mg once daily) plus chemotherapy with pemetrexed (500 mg per square meter of body-surface area) and a platinum-based agent (cisplatin [75 mg per square meter] or carboplatin [pharmacologically guided dose]) or osimertinib monotherapy (80 mg once daily). The key secondary end point was overall survival. RESULTS: A total of 557 patients were randomly assigned to the osimertinib plus platinum-pemetrexed group (279 patients) or the osimertinib monotherapy group (278 patients). The median overall survival was 47.5 months in the osimertinib plus platinum-pemetrexed group and 37.6 months in the osimertinib monotherapy group (hazard ratio for death, 0.77; 95% confidence interval, 0.61 to 0.96; P?=?0.02). Grade 3 or higher adverse events of any cause were reported in 70% of the patients in the osimertinib plus platinum-pemetrexed group and in 34% of the patients in the osimertinib monotherapy group; adverse events leading to the discontinuation of osimertinib were reported in 12% and 7%, respectively. CONCLUSIONS: Among patients with EGFR-mutated advanced NSCLC, first-line treatment with osimertinib plus platinum-pemetrexed led to significantly longer overall survival than osimertinib monotherapy and was associated with an increased risk of reversible adverse events of grade 3 or higher. (Funded by AstraZeneca; FLAURA2 ClinicalTrials.gov number, NCT04035486.). |
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New England Journal of Medicine Trastuzumab Deruxtecan plus Pertuzumab for HER2-Positive Metastatic Breast Cancer Tolaney SM BACKGROUND: Trastuzumab deruxtecan has shown efficacy in patients with previously treated human epidermal growth factor receptor 2 (HER2)-positive advanced or metastatic breast cancer. The efficacy and safety of trastuzumab deruxtecan in patients with no previous therapy for HER2-positive advanced or metastatic breast cancer are unclear. METHODS: We conducted a phase 3 trial involving patients with HER2-positive advanced or metastatic breast cancer and no previous chemotherapy or HER2-directed therapy for metastatic disease. Patients were randomly assigned in a 1:1:1 ratio to receive trastuzumab deruxtecan plus pertuzumab; trastuzumab deruxtecan plus placebo; or a taxane, trastuzumab, and pertuzumab (THP). The primary end point was progression-free survival as assessed by blinded independent central review. Secondary end points included objective response, duration of response, and safety. RESULTS: For this prespecified interim analysis, data for trastuzumab deruxtecan plus pertuzumab and for THP are reported; data for trastuzumab deruxtecan plus placebo remain blinded until the final analysis of progression-free survival. At the data-cutoff date (February 26, 2025), the median progression-free survival was 40.7 months with trastuzumab deruxtecan plus pertuzumab (383 patients) and 26.9 months with THP (387 patients) (hazard ratio for progression or death, 0.56; 95% confidence interval [CI], 0.44 to 0.71; P<0.00001 [P-value boundary for superiority, 0.00043]). The incidence of a confirmed response was 85.1% with trastuzumab deruxtecan plus pertuzumab and 78.6% with THP (complete responses in 15.1% and 8.5%, respectively), with a median duration of response of 39.2 months and 26.4 months. Safety was consistent with the known profiles of the individual treatments. The incidence of grade 3 or higher adverse events was 63.5% with trastuzumab deruxtecan plus pertuzumab and 62.3% with THP; the most common were neutropenia, hypokalemia, and anemia with trastuzumab deruxtecan plus pertuzumab and neutropenia, leukopenia, and diarrhea with THP. Adjudicated drug-related interstitial lung disease or pneumonitis occurred in 12.1% of patients receiving trastuzumab deruxtecan plus pertuzumab (grade 1 or 2 in 44 patients and grade 5 [death] in 2 patients) and in 1.0% of those receiving THP (all grade 1 or 2). CONCLUSIONS: Trastuzumab deruxtecan plus pertuzumab led to a significantly lower risk of progression or death than THP when used as first-line treatment for HER2-positive advanced or metastatic breast cancer, with no new safety signals. (Funded by AstraZeneca and Daiichi Sankyo; DESTINY-Breast09 ClinicalTrials.gov number, NCT04784715.). |
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Proceedings of the National Academy of Sciences of the U.S.A. Small-Molecule Allosteric Activator of Ubiquitin-Specific Protease 7 (USP7) Jaen Maisonet I, Sharafi M, Salazar-Chaparro A, Bratt AS, Varca AC, Shah B, Darnowski M, Chung M, Teh WP, Che J, Buhrlage SJ Ubiquitin-specific protease 7 (USP7) is a deubiquitylase essential for cell homeostasis, DNA repair, and regulation of both tumor suppressors and oncogenes. Recently, haploinsufficiency of USP7 has been associated with Hao-Fountain syndrome (HAFOUS), a rare neurodevelopmental disorder. Although a range of USP7 inhibitors have been developed over the last decade, in the context of HAFOUS, USP7 activators may represent a more relevant approach. To address this challenge, we report the identification and characterization of a small-molecule activator of USP7 called MS-8. Structural and functional studies show that MS-8 allosterically activates USP7, mimicking the endogenous autoactivation mechanism of the enzyme. We observed that MS-8 engages and activates mutant USP7 in a cellular context, impacting downstream proteins. Taken together, our study provides validation of the USP7 activator that paves the way toward activation-driven USP7 pharmacology. |
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Blood Advances Ethical Considerations for Hematologic Precursor Conditions Blackstone EC, Weeks LD, Abel GA |
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Blood Advances Tsakmaklis N, Hunter ZR, Guerrera ML, Guijosa A, Sarosiek S, Treon SP, Castillo JJ |
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Blood Advances Murdock HM, Kim HT, Maurer K, Kelkar AH, Shapiro RM, Gooptu M, Romee R, Nageshwar PK, Garrity HM, Shimony S, Luskin MR, Winer ES, Vedula RS, Chen EC, Volpe VO, Garcia JS, Wadleigh M, DeAngelo DJ, Stone RM, Wu CJ, Cutler CS, Koreth J, Ritz J, Antin JH, Ho VT, Nikiforow S, Soiffer RJ |
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Blood Advances Wong WJ, Zon RL, Gibson CJ, Pozdnyakova O, Neuberg D, Battinelli EM, Luskin MR, Tothova Z, Morgan EA, Ebert BL |
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Blood Cancer Discovery Fulciniti M, Fong Ng J, Encinas Mayoral J, Epstein CB, White CM, Ott CJ, Sperling AS, Samur MK, Anderson KC, Munshi NC |
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BMJ Supportive and Palliative Care How to Build a Thriving Integrative Oncology Programme Martyniuk I, Kennedy V, Berman T, Bao T |
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Breast Sammons S, Lamba N, Lin NU |
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British Journal of Haematology BCL-2 Inhibition in Waldenström Macroglobulinaemia and Marginal Zone Lymphoma Sarosiek S, Fernandez-Turizo M, Sarosiek KA, Castillo JJ |
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British Journal of Haematology Itzhaki Ben Zadok O, Simitsis P, Jacobson C, Nadeem O, Frigault MJ, Raje N, Duffy C, Costello P, Cruz JD, Looka A, Nohria A |
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Cancer Epidemiology, Biomarkers, and Prevention Pradhan P, Ghobrial IM, Marinac CR, O'Donnell EK, Syngal S, Weeks LD, Rebbeck TR |
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Cell Cycle Kolodziejczyk A, Liu S, Strobel F, Martinez Alonso D, Butter D, ?nioch K, Chu C, Long H, Li Q, Dougan SK, Sicinski P |
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Clinical Cancer Research Janeway KA, Dubois SG |
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Clinical Cancer Research Tesch ME, Zheng Y, Guzman-Arocho YD, Collins LC, Heng YJJ, Tayob N, Peppercorn J, Come SE, Snow C, Winer E, Mittendorf EA, Partridge AH |
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European Journal of Epidemiology Ogino S, Ugai S, Ugai T |
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European Journal of Medicinal Chemistry Allosteric Inhibition of JAK2 with Lysine-Reactive Compounds that Bind the Pseudokinase Domain Primi MC, Tavares MT, Hatcher JM, Kang H, Kresina TAC, Chakraborty S, Leroy E, Schmoker AM, Jeon H, Weisberg EL, Akatsu T, Griffin JD, Scott DA, Eck MJ |
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Expert Opinion on Emerging Drugs Mezigdomide for Multiple Myeloma: A Focus on Phase 2 Trial Data Mo CC, Liu Y, Nadeem O, Midha S, Laubach JP, Salman TJ, Nicholson T, Donnelly K, Bianchi G, Sperling AS, Hartley-Brown MA, Richardson PG |
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Haematologica Falade AS, Merryman R, LaCasce A |
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Human Genetics and Genomics Advances Carver S, Taraszka K, Groha S, Gusev A |
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Immunity Myeloid Cells Mediate Interferon-Driven Resistance to Immunotherapy in Advanced Renal Cell Carcinoma Bi K, Camp SY, Meli K, Saad E, Titchen BM, Labaki C, Pimenta EM, Park J, Shannon E, Fu J, Xirenayi S, Horst J, Choueiri TK, Van Allen EM |
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Journal of General Internal Medicine Erfani P, Zhang T, Orav EJ, Lathan CS, Lam MB |
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Journal of Nuclear Medicine Radiopharmaceutical Therapy: Rapid Growth, Rising Challenges, and the Critical Need for Expertise Jacene HA |
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Journal of Pediatric Psychology Chevalier L, Paul MA, Lokko L, Bona K, Zhou ES |
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Journal of the American Chemical Society Structure-Guided Design of a Bioactive Covalent Small Molecule Targeting a Riboswitch Li C, Munshi NC |
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mBio Zhang Z, Anang S, Wang Q, Nguyen HT, Sodroski JG |
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Medicine Dosimetry Han Z, Lee HY, Yu S, Hsu SH, Fitzgerald KJ, Kann BH, Kozono D, Leeman JE, van Dams R, Mak RH |
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Nature Reviews Urology Optimizing Local Control in the Surgical Management of Bladder Cancer Egger M, D'Andrea VD, Steiner C, Onochie NO, Clinton TN, Pan CX, Kibel AS, Mouw KW, Mossanen M |
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Neurology Goulart TO, Wang C, Fuse K, Zambrano D, Bukhari Y, Rhee JY |
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NPJ Digital Medicine Chen S, Fan L, Aerts H, Gallifant J, Bitterman DS |
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Pediatric Blood and Cancer Vital Voices: Patient/Family Perspectives to Improve Treatment for Pediatric B-ALL Greenzang KA |
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Pediatric Critical Care Medicine Gouda SR, Snaman JM, D'Anna R, Upham EJ, Dahlberg SE, Rosenberg AR, DeCourcey DD |
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Prostate Cancer and Prostatic Diseases Gagnon A, Zhong C, Xie W, Morlock L, Freeman D, Trowbridge R, Kilbridge KL, McGregor BA, Taplin ME, Choudhury AD |
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Radiotherapy and Oncology Zhu LL, Bredfeldt JS, Hu YH, Hancox C, Guthier CV, Quirk S, Pursley J, Kamran SC, McClatchy D, Nguyen PL, D'Amico AV, Sayan M, Kim E, Mouw KW, King MT, Martin NE, Leeman JE |