Welcome to Dana-Farber's Research News
October 1, 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 September 1 through September 15.
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 Loke J, Kim PG, Nguyen TTP, Boileau M, McConkey M, Miller A, Shin W, Hergott CB, Ericsson M, Nordstrom A, Llopis PM, Armstrong SA, Mancias JD, Ebert BL TET2 is among the most commonly mutated genes in both clonal hematopoiesis and myeloid malignancies; thus, the ability to identify selective dependencies in TET2-deficient cells has broad translational significance. Here, we identify regulators of Tet2 knockout (KO) hematopoietic stem and progenitor cell (HSPC) expansion using an in vivo CRISPR-Cas9 KO screen, in which nucleotide barcoding enabled large-scale clonal tracing of Tet2-deficient HSPCs in a physiologic setting. Our screen identified candidate genes, including Ncoa4, that are selectively required for Tet2 KO clonal outgrowth compared with wild type. Ncoa4 targets ferritin for lysosomal degradation (ferritinophagy), maintaining intracellular iron homeostasis by releasing labile iron in response to cellular demands. In Tet2-deficient HSPCs, increased mitochondrial adenosine triphosphate production correlates with increased cellular iron requirements and, in turn, promotes Ncoa4-dependent ferritinophagy. Restricting iron availability reduces Tet2 KO stem cell numbers, revealing a dependency in TET2-mutated myeloid neoplasms. |
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Blood Distinct Molecular Subtypes in Waldenström Macroglobulinemia Hunter ZR, Treon SP In this issue of Blood, Gagler et al report a single-cell multi-omic study of MYD88-mutated (MYD88Mut) Waldenström macroglobulinemia (WM), identifying 2 distinct subtypes of disease: memory B-cell–like (MBC-like) and plasma cell–like (PC-like). The MBC-like subtype showed a blockade in differentiation at the memory B-cell stage, whereas the PC-like subtype showed partial differentiation toward a plasma cell. Among their key findings are that CXCR4 mutations (CXCR4Mut), along with MAP3K14 and ARID1A mutations, were prevalent in the MBC-like subtype, whereas chromosome 6q deletions (del6q) occurred in the PC-like subtype. Distinct mutations and transcriptional and epigenomic features were also observed in both MYD88Mut WM subsets. |
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Cancer Cell Engineering Myeloid Cells for Cancer Immunotherapy Liu F, Romee R Macrophages naturally infiltrate tumors, modulate tumor microenvironment, phagocytose tumor cells, and present antigens to induce T cell responses. These properties have been leveraged to develop chimeric antigen receptor-macrophages (CAR-Ms) for cancer immunotherapy. We discuss key findings from CAR-M studies to assess their potential to overcome major limitations of current CAR-T cell therapies and outline research directions to optimize CAR-Ms as a safe, efficacious, and cost-effective cancer immunotherapy. |
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JAMA Reducing Drug Prices – The Most Favored Nation Policy vs. Price Negotiation Kelkar AH On May 12, 2025, an executive order was issued seeking to establish a most favored nation (MFN) pricing policy for prescription drugs, an attempt to curb soaring US drug prices, which remain 2 to 3 times higher than in other high-income countries and are a key driver of health spending. An MFN policy would cap Medicare payments at the lowest price paid by a group of comparable countries; for example, a $17?000 Medicare payment for a 1-month supply of lenalidomide would be reduced to match Australia’s $900 price for the same cancer drug. Although the MFN policy correctly captures the urgency of addressing unaffordable US drug prices, it is unlikely to meaningfully reduce prices due to legal, operational, and market barriers; a more effective and sustainable solution would be to expand and accelerate drug price negotiation within (and ideally beyond) Medicare. |
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Journal of Clinical Oncology Liu JF PURPOSE: This phase IIb, single-arm, multicenter, global study (ADAGIO; ClinicalTrials.gov identifier: NCT04590248) assessed the efficacy and safety of adavosertib in patients with recurrent/persistent uterine serous carcinoma (USC) who had previously received platinum-based chemotherapy. METHODS: Eligible patients were age 18 years and older and had histologically confirmed recurrent/persistent USC, previously treated with at least one platinum-based chemotherapy regimen, and with evidence of measurable disease. Adavosertib was administered orally at 300 mg once daily on days 1-5 and 8-12 of a 21-day cycle until discontinuation criteria were met. The primary end point was objective response rate (ORR) by blinded independent central review (BICR). Secondary end points included duration of response (DoR), progression-free survival (PFS), safety, and tolerability. Biomarkers previously associated with adavosertib response in other settings were assessed in archival tissue samples. RESULTS: In 104 evaluable patients, one complete response and 26 partial responses were observed, for an ORR by BICR of 26.0% (95% CI, 17.9 to 35.5). Median DoR was 4.7 months (95% CI, 3.8 to 8.3); median PFS was 2.8 months (95% CI, 2.6 to 3.9). Biomarker analysis identified no single predictive alteration for adavosertib response, although a trend was observed for CCNE1 amplification or high cyclin E1 protein expression. Most patients (97.2%) experienced treatment-related adverse events (TRAEs), most frequently diarrhea (59.6%), nausea (59.6%), and anemia (58.7%). Grade ?3 TRAEs occurred in 60.6% of patients, with neutropenia (21.1%) and fatigue (13.8%) most common. 17.4% of patients discontinued adavosertib due to AEs (treatment-related in 14.7%). CONCLUSION: Adavosertib showed some antitumor activity in patients with recurrent/persistent USC. However, at 300 mg once daily dosing, it was not well tolerated in this population. Exploratory biomarker studies suggest CCNE1/cyclin E1 expression may enrich for response to Wee1 inhibition in USC. |
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Journal of Clinical Oncology Jänne PA PURPOSE: Patritumab deruxtecan (HER3-DXd; MK-1022) is an investigational HER3-directed antibody-drug conjugate composed of a human immunoglobulin G1 monoclonal antibody to HER3 (patritumab) covalently linked via a stable tetrapeptide-based cleavable linker to a topoisomerase I inhibitor payload that has shown durable antitumor activity in previously treated patients with EGFR-mutated advanced non-small cell lung cancer (NSCLC). We extend these observations to patients with advanced NSCLC with other/no identified driver genomic alterations. METHODS: Patients with advanced squamous or nonsquamous NSCLC without a common EGFR-activating mutation whose disease had progressed on previous therapies including platinum-based chemotherapy, immune checkpoint inhibitors, and targeted therapy (for patients with known actionable genomic alterations) received HER3-DXd 5.6 mg/kg intravenously once every 3 weeks. The primary end point was confirmed objective response rate (cORR). RESULTS: Forty-seven patients were treated with HER3-DXd (median treatment duration, 4.2 [range, 0.7-19.8] months). The cORR was 27.7% (95% CI, 15.6% to 42.6%), and the median duration of response was 8.1 (95% CI, 4.2 to not evaluable) months. The median progression-free survival was 5.5 (95% CI, 4.0 to 11.2) months, and the median overall survival was 15.2 (95% CI, 10.8 to 17.7) months. Similar efficacy was observed in patients with NSCLC harboring identified driver genomic alterations and in those without such genomic features. The rate of study drug discontinuation associated with treatment-emergent adverse events (TEAEs) was 12.8%. Study drug-related grade ?3 TEAEs occurred in 51.1% of patients and were serious in 12.8% (none were associated with death). Adjudicated treatment-related interstitial lung disease occurred in five patients (10.6%; all grade 1 or 2). CONCLUSION: The previously reported efficacy and safety of HER3-DXd in heavily pretreated patients with EGFR-mutated NSCLC are also observed in those with other NSCLC subtypes and warrant further clinical evaluation. |
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Journal of Clinical Oncology Jänne PA PURPOSE: WU-KONG1B (ClinicalTrials.gov identifier: NCT03974022) is a multinational phase II, dose-randomized study to assess the antitumor efficacy of sunvozertinib in pretreated patients with advanced non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) exon 20 insertion mutations (exon20ins). METHODS: Eligible patients with advanced-stage EGFR exon20ins NSCLC were randomly assigned by 1:1 ratio to receive sunvozertinib 200 mg or 300 mg once daily (200 and 300 mg-rand cohorts). After predefined interim analysis, additional patients were enrolled and treated with the 300 mg dose once daily. The primary end point was blinded independent review committee (IRC)-assessed confirmed objective response rate (cORR), and the key secondary end point was duration of response (DoR). RESULTS: Among 85, 89, and 107 efficacy-evaluable patients in 200 mg-rand, 300 mg-rand, and 300 mg-all (including randomly assigned and nonrandomized patients) cohorts, the cORRs were 45.9% (97.5% CI, 33.6% to 58.5%), 47.2% (97.5% CI, 35.1% to 59.5%), and 45.8% (97.5% CI, 34.8% to 57.0%), respectively, per IRC assessment. The predefined null hypothesis was rejected with statistical significance (P < .0001). Comparing 300 and 200 mg-rand cohorts, higher cORRs were observed in patients with baseline brain metastasis (52.4% v 28.6%) and previous amivantamab treatment (41.7% v 25%), as well as longer DoR (13.8 v 11.1 months). At 200 and 300 mg once daily, the most common treatment-related adverse events with grade ?3 included diarrhea (2.2% v 18%), blood creatine phosphokinase increased (6.6% v 12.6%), and anemia (4.4% v 6.3%). CONCLUSION: Sunvozertinib is efficacious at both 200 and 300 mg once daily in treating platinum-pretreated patients with advanced EGFR exon20ins NSCLC. The treatment-related adverse events of sunvozertinib were consistent with an EGFR tyrosine kinase inhibitor, with a more favorable safety profile at 200 mg than 300 mg once daily. |
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Journal of Clinical Oncology Konstantinopoulos PA, Matulonis UA PURPOSE: Patients with platinum-resistant/platinum-refractory high-grade serous ovarian cancer (HGSOC) without a BRCA mutation have poor prognosis and limited treatment options. We report efficacy and biomarker data from EPIK-O, which investigated alpelisib + olaparib versus single-agent chemotherapy in these patients. PATIENTS AND METHODS: EPIK-O was an open-label, phase III trial that randomly assigned patients with platinum-resistant/platinum-refractory HGSOC with no germline or known somatic BRCA mutation 1:1 to alpelisib 200 mg once daily + olaparib 200 mg twice daily or treatment of physician's choice (TPC; paclitaxel 80 mg/m2 once weekly or pegylated liposomal doxorubicin 40-50 mg/m2 once every 28 days). Patients had 1-3 previous systemic therapies. Previous bevacizumab was required (unless contraindicated); previous poly(adenosine diphosphate-ribose) polymerase inhibitors were allowed. Primary end point was progression-free survival (PFS) per RECIST 1.1 (blinded independent review committee [BIRC]). Secondary efficacy end points included overall response rate (ORR; per BIRC), duration of response (per BIRC), and overall survival (OS; key secondary end point). RESULTS: A total of 358 patients (alpelisib + olaparib [n = 180], TPC [n = 178]) were included. The median follow-up time was 9.3 months. At data cutoff (April 21, 2023), 33 (18.3%) and 30 (16.9%) patients remained on treatment with alpelisib + olaparib and TPC, respectively. The median PFS (BIRC) was 3.6 versus 3.9 months (hazard ratio [HR], 1.14 [95% CI, 0.88 to 1.48]; one-sided P = .84) for alpelisib + olaparib versus TPC. The ORR was 15.6% (95% CI, 10.6% to 21.7%) versus 13.5% (95% CI, 8.8% to 19.4%). The median OS was 10.0 versus 10.6 months (HR, 1.22; 95% CI, 0.87 to 1.71). The safety profile of alpelisib + olaparib was consistent with that observed for the individual agents. CONCLUSION: The primary objective, PFS improvement, was not met in EPIK-O. No new or unexpected adverse events were observed. Biomarker analyses provided new insights for responders to alpelisib + olaparib. |
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Journal of Clinical Oncology Meyerhardt JA PURPOSE: Patients with advanced, well-differentiated extrapancreatic neuroendocrine tumors (epNETs) have limited systemic treatment options. Pazopanib, an oral multikinase inhibitor with activity against vascular endothelial growth factor receptor (VEGFR)-2 and -3, PDGFR-alpha and-beta, and c-Kit, was tested for efficacy in epNET. PATIENTS AND METHODS: We conducted a multicenter, randomized, double-blind, phase II study of pazopanib (800 mg once daily) versus placebo in low- to intermediate-grade epNET with radiologic progressive disease (PD) within 12 months of study entry. Previous somatostatin analog (SSA) was required for midgut tumors, and concurrent SSA was allowed. The primary end point was progression-free survival (PFS) by blinded independent central review. Unblinding and crossover were allowed if PD was confirmed by central review. RESULTS: One hundred seventy-one patients (97 pazopanib and 74 placebo) were randomly assigned between September 2013 and October 2015. The majority had a midgut primary site (75%) and previous SSA treatment (93%). About half (49%) of the patients had functional tumors. The median follow-up was 61 months (95% CI, 60 to 63). Median PFS was 11.8 versus 7.6 months in pazopanib versus placebo, respectively (hazard ratio, 0.54 [95% CI, 0.37 to 0.79]; P < .001); 49 placebo patients crossed over to pazopanib. There was no significant difference in overall survival between the treatment arms. Rates of grade 3 or greater adverse events (regardless of attribution) were higher in pazopanib versus placebo (84% v 47%; P < .001), as were grade 5 death events (8% v 0%, P = .017). CONCLUSION: Pazopanib compared with placebo significantly improves PFS in patients with progressive epNET, confirming that the VEGF signaling pathway is a valid target for therapy in epNET. However, after integrating the associated risks relative to the benefits, further development of pazopanib in this clinical context is not planned. |
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Journal of Clinical Oncology Dougan M, Dougan SK Resistance to apoptosis is a hallmark of cancer. Multiple nodes in the apoptosis pathway have been targeted for cancer therapy, including the inhibitor of apoptosis proteins (IAPs). In the Original Report that accompanies this article,1 a phase III trial of the IAP inhibitor xevinapant combined with chemoradiation for locally advanced squamous cell carcinoma of the head and neck (SCCHN) showed poorer outcomes in the experimental arm, necessitating a reassessment of the role of IAPs in human cancer. |
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Journal of Clinical Oncology Haddad R, Schoenfeld JD PURPOSE: TrilynX was a randomized, double-blind, phase III study evaluating the addition of xevinapant (an inhibitor of apoptosis proteins inhibitor) or placebo to chemoradiotherapy (CRT) in patients with unresected locally advanced squamous cell carcinoma of the head and neck (LA SCCHN). METHODS: Patients with unresected LA SCCHN (oropharynx [p16-negative only], hypopharynx, or larynx) were randomly assigned 1:1 to six cycles of oral xevinapant 200 mg/day or matched placebo (once daily on Days 1-14 of a 21-day cycle) plus CRT for the first three cycles (cisplatin [100 mg/m2 once on Day 2 of every cycle] plus intensity-modulated radiotherapy [70 Gy; 35 fractions of 2 Gy/day, 5 days/week]). The primary end point was event-free survival (EFS) assessed by the blinded independent review committee. Progression-free survival, overall survival (OS), and safety were secondary end points. RESULTS: Between September 20, 2020, and February 27, 2023, 730 patients were randomly assigned to xevinapant plus CRT (n = 364) or placebo plus CRT (n = 366). The median (95% CI) EFS was 19.4 months (14.5 to not estimable) with xevinapant and 33.1 months (21.0 to not estimable) with placebo (hazard ratio [HR], 1.33 [95% CI, 1.05 to 1.67]; P = .9919). OS was worse in the xevinapant arm (HR, 1.39 [95% CI, 1.04 to 1.86]). Grade ?3 treatment-emergent adverse events (TEAEs) occurred in 320 (87.9%; xevinapant) and 286 (80.3%; placebo) patients; anemia (78 [21.4%] v 51 [14.3%]) and neutropenia (71 [19.5%] v 69 [19.4%]) were the most common. Serious TEAEs occurred in 194 (53.3%; xevinapant) and 129 (36.2%; placebo) patients. TEAEs leading to death occurred in 22 (6.0%; xevinapant) and 13 (3.7%; placebo) patients. CONCLUSION: Xevinapant plus CRT did not improve EFS (EFS was shorter with xevinapant v placebo) and demonstrated an unfavorable safety profile versus placebo plus CRT in patients with unresected LA SCCHN. |
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Journal of the National Cancer Institute Greenzang KA, Janeway K Understanding the patient experience of treatment toxicities and their impact on health-related quality of life from cancer treatments requires asking patients using patient-reported outcomes. Over the past 20 years, the National Institutes of Health has sponsored several tools-namely, Patient-Reported Outcomes Measurement Information System measures and the Patient-Reported Outcomes version of the Common Terminology Criteria for Adverse Events-for precisely this purpose: to ensure valid, reliable tools to collect and detect patient-reported toxicities or adverse events and their impact on health-related quality of life. These patient-reported outcomes measures have been widely incorporated in clinical trials for adults with cancer. Yet, despite considerable work developing and validating developmentally appropriate versions of these measures for pediatric and adolescent self-report, patient-reported outcomes inclusion in pediatric and adolescent and young adult clinical trials has lagged. Here, we discuss optimal strategies to integrate validated patient-reported outcomes tools and sound analytic methodologies in clinical trials for children and adolescent and young adults with cancer, highlighting lessons learned from recent successes and ongoing experiences developing and opening cross-network trials for children and adolescent and young adults through the Children's Oncology Group for patients with classic Hodgkin lymphoma, osteosarcoma, and acute lymphoblastic leukemia. |
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Nature Communications Jang DM, Boxer K, Ha BH, Tkacik E, Levitz T, Rawson S, Metivier RJ, Schmoker A, Jeon H, Eck MJ CRAF (RAF1) is one of three RAF-family kinases that initiate MAP kinase signaling in response to activated RAS and is essential for oncogenic signaling from mutant KRAS. Like BRAF, CRAF is regulated by 14-3-3 engagement and by intramolecular autoinhibitory interactions of its N-terminal regulatory region. Unlike BRAF, it is thought to require tyrosine phosphorylation in its N-terminal acidic (NtA) motif for full catalytic activation. Here we describe cryo-EM reconstructions of full-length CRAF in complex with MEK1 and a 14-3-3 dimer. These structures reveal a fully autoinhibited conformation analogous to that observed for BRAF and two "open monomer" states in which the inhibitory interactions of the CRD and 14-3-3 dimer are released or rearranged, but the kinase domain remains inactive. Structure-function studies of the NtA motif indicate that phosphorylation or acidic mutations in this segment increase catalytic activity by destabilizing the inactive conformation of the kinase domain. Collectively, these studies provide a structural foundation for understanding the shared and unique regulatory features of CRAF and will inform efforts to selectively block CRAF signaling in cancer. |
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Nature Genetics Tamoxifen Induces PI3K Activation in Uterine Cancer Kübler K, Nardone A, Anand S, Hermida-Prado F, Akhshi T, Feiglin A, Feit AS, Cohen Feit G, Pun M, Kuang Y, Cha J, Miller M, Gibson WJ, Paweletz CP, Van Allen EM, Nguyen QD, Leshchiner I, Stewart C, Matulonis UA, Getz G, Jeselsohn R Mutagenic processes and clonal selection contribute to the development of therapy-associated secondary neoplasms, a known complication of cancer treatment. The association between tamoxifen therapy and secondary uterine cancers is uncommon but well established; however, the genetic mechanisms underlying tamoxifen-driven tumorigenesis remain unclear. We find that oncogenic PIK3CA mutations, common in spontaneously arising estrogen-associated de novo uterine cancer, are significantly less frequent in tamoxifen-associated tumors. In vivo, tamoxifen-induced estrogen receptor stimulation activates phosphoinositide 3-kinase (PI3K) signaling in normal mouse uterine tissue, potentially eliminating the selective benefit of PI3K-activating mutations in tamoxifen-associated uterine cancer. Together, we present a unique pathway of therapy-associated carcinogenesis in which tamoxifen-induced activation of the PI3K pathway acts as a non-genetic driver event, contributing to the multistep model of uterine carcinogenesis. While this PI3K mechanism is specific to tamoxifen-associated uterine cancer, the concept of treatment-induced signaling events may have broader applicability to other routes of tumorigenesis. |
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Proceedings of the National Academy of Sciences of the U.S.A. Making Sense of Low-Complexity Domains: The 2025 Lasker Basic Science Award Kaelin WG Jr Up to 10 to 20% of the proteome contains regions with much lower amino acid diversity than would be expected by chance. This year's Lasker Basic Science Award is given to Steven McKnight and Dirk Görlich for their pioneering work on such low-complexity domains (LCDs). They showed, using a variety of elegant approaches, that such LCDs can form homotypic and heterotypic interactions that lead to reversible phase separations in cells. These phase separations, which in the laboratory manifest as hydrogels and in cells as membrane free structures (liquid condensates) such as P bodies and stress granules, form hubs for molecular processes such as transcription and messenger RNA (mRNA) splicing and also underlie the selectivity of nuclear pore complexes (NPCs), which act a barriers to large molecules unless they are escorted by specific LCD containing nuclear transporters that interact with LCD containing nucleoporins within NPC channels. Naturally occurring LCD mutations linked to neurodegeneration and other diseases cause the formation of irreversible (rather than reversible) LCD polymers, resulting in insoluble, amyloid-like, fibrils, underscoring the critical importance of these domains. |
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Advances in Radiation Oncology Doyle P, Sayan M, Lam M, Moningi S |
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American Journal of Critical Care Arciprete EGB, Eche-Ugwu IJ, DeCourcey DD, Rosenberg AR, Snaman JM |
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American Journal of Hematology Kim HT, Liney DJ, Rizza K, Cutler CS, Koreth J, Nikiforow S, Shapiro RM, Kelkar AH, Gooptu M, Romee R, Wu CJ, Antin JH, Ritz J, Soiffer RJ, Ho VT |
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American Journal of Hematology Regression of Monosomy 7 Clone in Patient with RECQL4-Associated Syndrome Nunes SC, Reed HD, Pellin D, Harris C, Andresen F, Abu-El-Haija A, Barbera C, Schienda J, Madden JA, Bledsoe JR, Brundige K, Day-Lewis M, Nguyen AA, Shimamura A, Williams DA |
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Annual Review of Pathology Role of Chromatin Looping Factors in Leukemia Glushakow-Smith SG, Tothova Z |
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Best Practice and Research Clinical Haematology Ghobrial IM, Nadeem O |
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Blood Advances Kelkar AH, Achebe MO, Hantel A |
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British Journal of Haematology ZIP10 as a Potential Therapeutic Target in Acute Myeloid Leukaemia Rolles B, Hillerbrand AC, Romine KA, Stahl M |
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British Journal of Haematology Hantel A, Merz LE |
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Cancer Florez N, Rotow J, Sands J |
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Cancer Immunology Research Brea EJ, Baldacci S, Savage N, Facchinetti F, Hinchey C, Chakravarti S, Mottram A, Ngo K, Vo H, Leeper BA, Tuladhar B, Ganapathy S, Ivanova EV, Saldanha A, Locquet MA, Salamah A, Holterhus M, Mesler EB, De Vizio M, Stornante C, Campisi M, Thai TC, Haggerty TJ, Li Z, Barbie TU, Gokhale PC, Paweletz CP, Ramasubramanian A, Janne PA, Barbie DA, Smith EL |
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Cell Chemical Biology Pharmacologic Interrogation of USP28 Cellular Function in p53 Signaling Bratt AS, Kilgas S, Tarazona Guzman MI, Magin RS, Jaen Maisonet I, Starnbach CA, Teh WP, Varca AC, Hu B, Tarazona Guzman E, Seo HS, Dhe-Paganon S, Girardi NM, Adelmant G, Marto JA, Chowdhury D, Buhrlage SJ |
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Cell Genomics Detection of Heterogeneous Resistance Mechanisms to Tyrosine Kinase Inhibitors from Cell-Free DNA Parsons HA, Messer C, Santos K, Weiss J, Merrell D, Danysh BP, Hughes ME, Kirkner GJ, Patel A, Hess J, Sendrick K, Stewart C, Grant E, Schlueter-Kuck K, Grinshpun A, Wagle N, Leone JP, Freedman RA, Metzger O, Schiff R, Tolaney SM, Getz G, Lin NU |
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Clinical Cancer Research Molecular Characterization of NUT Carcinoma: A Report from the NUT Carcinoma Registry Kim JJ, Walton SA, Mahadevan NR, Haradon J, Paoloni F, Jänne PA, Barbie DA, Sholl LM, DuBois SG, Hanna GJ, Shapiro GI, French CA, Luo J |
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Contemporary Clinical Trials Cao C, Tanasijevic AM, Diguglielmo KA, Nguyen TL, Kemp W, Oppenheim JB, Ligibel JA |
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EMBO Reports p300/CBP is an Essential Driver of Pathogenic Enhancer Activity and Gene Expression in Ewing Sarcoma Godfrey LC, Regalado B, Schweber SR, Hatton C, Wenge DV, Wen Y, Boileau M, Wessels M, Qi J, Ott CJ, Stegmaier K, Rivera MN, Armstrong SA |
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European Journal of Nuclear Medicine and Molecular Imaging Ng TSC, Liu M, Robertson M, Könik A, Cheng SC, Bakht MK, Harrington K, Wolanski A, Gilbert L, Preston M, Mossanen M, Beltran H, Hirsch MS, Sonpavde G, Jacene HA |
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European Journal of Nuclear Medicine and Molecular Imaging Borges N, Liu M, Cheng SC, Könik A, Ritzer J, Wolanski A, Ng TSC, Choudhury AD, Taplin ME, Ravi P, Jacene H |
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European Urology Refining the Role of Androgen Deprivation Therapy after Radical Prostatectomy Sayan M, Nguyen PL |
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Genes and Development Lineage Rewiring in Lung Adenocarcinoma via HNF4? and NKX2-1 Dynamics Feng A, Yermalovich A, Meyerson M |
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Gynecologic Oncology The RAS-MEK-ERK Pathway in Low-Grade Serous Ovarian Cancer Stover EH, Lee EK, Shapiro GI, Brugge JS, Matulonis UA, Liu JF |
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Haematologica Kim HT, Soiffer RJ, Cutler C, Koreth J, Nikiforow S, Shapiro RM, Kelkar A, Gooptu M, Romee R, Wu CJ, Antin JH, Ritz J, Ho VT |
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Hospital Pediatrics Rising Incidence of Pediatric Catatonia and Medical Etiology: Multiyear Trends Lichtor SA, Dunn E, Ray A, Wulff C, Anglero-Diaz Y, O'Connor R, Schneider M, Warwick AB, Samsel CB |
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JACC: Advances Yi-Frazier JP, Rosenberg AR |
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JACC: CardioOncology Raman HS, Nohria A, Upshaw JN, LaCasce AS |
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JAMA Network Open Frailty and Postoperative Complications in Older Adults with Nonmetastatic Breast Cancer Lorentzen EH, Chen YJ, Morton C, King TA, Mittendorf EA, Minami CA |
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JAMA Network Open Patient-Centered Measures of Goal Concordance in Geriatrics and Palliative Care: A Scoping Review Chua IS, Bain PA, Fromme EK, Edelen M, Pusic AL, Ritchie CS, Bates DW |
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JAMA Network Open Smartphone-Based Measures as Indicators of Functional Status in Patients with Advanced Cancer Straczkiewicz M, Keating NL, Schonholz SM, Matulonis UA, Horowitz N, Campos S, Onnela JP, Wright AA |
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JCO Oncology Practice Raman HS, Abel GA, Lindvall C, Odejide OO |
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JCO Precision Oncology Alessi JV, Lindsay JR, Giobbie-Hurder A, Sharma B, Felt K, Kumari P, Mazor T, Cerami E, Lotter W, Altreuter J, Weirather J, Dryg I, Hoebel K, Manos M, Adib E, Curtis JD, Ricciuti B, Di Federico A, Ghandour F, Saad E, Wang XA, Pecci F, Holovatska M, Gandhi MM, Hughes ME, O'Meara TA, Chan SJ, Pfaff K, Konstantinopoulos PA, Hodi FS, Shipp MA, Signoretti S, Choueiri T, Wei XX, Santagata S, Hanna GJ, Lin NU, Tolaney SM, Liu J, Sorger PK, Lindeman N, Sholl LM, Nowak JA, Barbie D, Awad MM, Johnson BE, Rodig SJ |
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JCO Precision Oncology Surana R, Morgado M, Bockorny B, Weekes CD, Coleman EC, Bird A, Wang J, Williams HL, Zheng H, Brais LK, Saxena N, Graham C, Ritterband L, Sawin M, Peters ML, Whooley P, Bullock A, Zerillo J, Clark JW, Parikh AR, Yurgelun MB, Patel AK, Mayer RJ, Cleary JM, Enzinger P, Rubinson DA, McCleary NJ, Enzinger A, Slater S, Ng K, Biller LH, Abrams TA, Huffman BM, Singh H, Raghavan S, Mancias JD, Nowak JO, Aguirre AJ, Wolpin BM, Perez K |
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JCO Oncology Practice Paudel R, Uno H, Cronin C, Dizon Hassett MJ |
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Journal of the American College of Radiology Peers C, Lacson R, Ledbetter MS, Wagner AJ, Giess CS, Khorasani R, DiPiro PJ |
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Journal of Clinical Investigation Abeykoon JP, Asada S, Zhu G, Hirohashi Y, Moreau L, Iyer D, Mukkavalli S, Parmar K, Zambrano G, Shapiro GI, D'Andrea A |
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Journal of Geriatric Oncology Thompson LL, Lipson SM, Yoon J, Florissi C, Gregg AT, Amin PM, Shah S, Anabaraonye N, Jiang S, Baxter E, Saraf A, Fitzgerald K, Kann B, Kozono D, Mak RH |
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Journal for ImmunoTherapy of Cancer Regan MM, McDermott DF, Stephen Hodi F |
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Journal of the National Cancer Institute - Monograms The Multidisciplinary Community of Exercise Oncology Practice: Current Status and Future Directions Cao C, Campbell N, Cleary C, Ligibel JA |
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Journal of Pain and Symptom Management Nurses' Experiences of Serious Illness Conversations with Marginalized Patients in COVID-19 Tabata-Kelly M, Bulger AL, Reich AJ, Gray TF, Wichmann L, Rinaldi S, Bernacki RE |
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Leukemia Research
Brunner AM, Stone RM |
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