Welcome to Dana-Farber's Research News
August 1, 2024
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 July 1 through July 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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Annals of Oncology
Freedman RA, Heiling HM, Li T, Tayob N, Davis R, Pereslete AM, DeMeo MK, Cotter C, Chen WY, Parsons HA, Moy B, Savoie J, Lin NU
PURPOSE: Treatment options for HER2-positive breast cancer brain metastases (BCBM) remain limited. We previously reported central nervous system (CNS) activity for neratinib and neratinib-capecitabine. Preclinical data suggest that neratinib may overcome resistance to ado-trastuzumab-emtansine (T-DM1) when given in combination. In TBCRC 022's cohort 4, we examined the efficacy of neratinib plus T-DM1 in patients with HER2-positive BCBM.
PATIENTS AND METHODS: In this multicenter, phase II study, patients with measurable HER2-positive BCBM received neratinib 160 mg daily plus T-DM1 3.6 mg/kg intravenously every 21 days in three parallel-enrolling cohorts (cohort 4A-previously untreated BCBM, cohorts 4B and 4C- BCBM progressing after local CNS-directed therapy without [4B] and with [4C] prior exposure to T-DM1). Cycle 1 diarrheal prophylaxis was required. The primary endpoint was the Response Assessment in Neuro-Oncology-Brain Metastases (RANO-BM) by cohort. Overall survival (OS) and toxicity were also assessed.
RESULTS: Between 2018-2021, 6, 17, and 21 patients enrolled to cohorts 4A, 4B, and 4C. Enrollment was stopped prematurely for slow accrual. The CNS objective response rate in cohorts 4A, 4B, and 4C was 33.3% (95% confidence interval [CI]: 4.3-77.7%), 35.3% (95% CI: 14.2-61.7%), and 28.6% (95% CI: 11.3-52.2%), respectively; 38.1-50% experienced stable disease for ?6 months or response. Diarrhea was the most common grade 3 toxicity (22.7%). Median OS was 30.2 months (cohort 4A; 95% CI: 21.9, not reached [NR]), 23.3 months (cohort 4B; 95% CI: 17.6, NR), and 20.9 months (cohort 4C; 95% CI: 14.9, NR).
CONCLUSION: We observed Intracranial activity for neratinib plus T-DM1, including those with prior T-DM1 exposure, suggesting synergistic effects with neratinib. Our data provide additional evidence for neratinib-based combinations in patients with HER2-positive BCBM, even those who are heavily pre-treated.
Blood
Kaminski J, Fleming RA, Alvarez-Calderon F, Winschel MB, McGuckin C, Rui X, Keskula P, Cagnin L, Charles J, Zavistaski J, Margossian SP, Kapadia MA, Lane J, Baumeister SHC, Tkachev V, Shalek AK, Kean LS, Gerdemann U
Chimeric antigen receptor (CAR) T cells hold promise as a therapy for B-cell-derived malignancies, and despite their impressive initial response rates, a significant proportion of patients ultimately experience relapse. Although recent studies have explored the mechanisms of in vivo CAR T-cell function, little is understood about the activation of surrounding CARneg bystander T cells and their potential to enhance tumor responses. We performed single-cell RNA sequencing on nonhuman primate (NHP) and patient-derived T cells to identify the phenotypic and transcriptomic hallmarks of bystander activation of CARneg T cells following B-cell-targeted CAR T-cell therapy. Using a highly translatable CD20 CAR NHP model, we observed a distinct population of activated CD8+ CARneg T cells emerging during CAR T-cell expansion. These bystander CD8+ CARneg T cells exhibited a unique transcriptional signature with upregulation of natural killer-cell markers (KIR3DL2, CD160, and KLRD1), chemokines, and chemokine receptors (CCL5, XCL1, and CCR9), and downregulation of naïve T-cell-associated genes (SELL and CD28). A transcriptionally similar population was identified in patients after a tisagenlecleucel infusion. Mechanistic studies revealed that interleukin-2 (IL-2) and IL-15 exposure induced bystander-like CD8+ T cells in a dose-dependent manner. In vitro activated and patient-derived T cells with a bystander phenotype efficiently killed leukemic cells through a T-cell receptor-independent mechanism. Collectively, to our knowledge, these data provide the first comprehensive identification and profiling of CARneg bystander CD8+ T cells following B-cell-targeting CAR T-cell therapy and suggest a novel mechanism through which CAR T-cell infusion might trigger enhanced antileukemic responses. Patient samples were obtained from the trial #NCT03369353, registered at www.ClinicalTrials.gov.
Blood
CRISPR-Based Rapid Molecular Diagnostic Tests for Fusion-Driven Leukemias
Vedula RS, Karp HQ, Koob J, Lim F, Garcia JS, Winer ES, Luskin MR, Kim AS, Abudayyeh O, Zhang F, Lindsley RC
Fusion oncogenes can be cancer-defining molecular alterations that are essential for diagnosis and therapy selection.1,2 Rapid and accessible molecular diagnostics for fusion-driven leukemias such as acute promyelocytic leukemia (APL), Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL), and chronic myeloid leukemia (CML) are unavailable, creating a barrier to timely diagnosis and effective targeted therapy in many healthcare settings, including community hospitals and low-resource environments. We developed CRISPR-based RNA-fusion transcript detection assays using SHERLOCK (Specific High-sensitivity Enzymatic Reporter unLOCKing) for the diagnosis of fusion-driven leukemias. We validated these assays using diagnostic APL and CML patient samples from academic centers and dried blood spots from low-resource environments, demonstrating 100% sensitivity and specificity. We identified assay optimizations to enable the use of these tests outside of tertiary cancer centers and clinical laboratories, enhancing the potential impact of this technology. Rapid point-of-care diagnostics can improve outcomes in cancer patients by expanding access to therapies for highly treatable diseases that would otherwise lead to serious adverse outcomes due to delayed or missed diagnoses.
Cancer Discovery
Mechanisms of Resistance to Oncogenic KRAS Inhibition in Pancreatic Cancer
Dilly J, Hoffman MT, Abbassi L, Li Z, Parent BD, Hennessey CJ, Jordan AC, Morgado M, Dasgupta S, Uribe GA, Yang A, Kapner KS, Hambitzer FP, Qiang L, Feng H, Geisberg J, Wang J, Evans KE, Roth JA, Cristea S, Van Allen EM, Mancias JD, Chugh S, Wolpin BM, Raghavan S, Nowak JA, Dougan SK, Aguirre AJ
KRAS inhibitors demonstrate clinical efficacy in pancreatic ductal adenocarcinoma (PDAC); however, resistance is common. Among patients with KRASG12C-mutant PDAC treated with adagrasib or sotorasib, mutations in PIK3CA and KRAS, and amplifications of KRASG12C, MYC, MET, EGFR, and CDK6 emerged at acquired resistance. In PDAC cell lines and organoid models treated with the KRASG12D inhibitor MRTX1133, epithelial-to-mesenchymal transition and PI3K-AKT-mTOR signaling associate with resistance to therapy. MRTX1133 treatment of the KrasLSL-G12D/+;Trp53LSL-R172H/+;p48-Cre (KPC) mouse model yielded deep tumor regressions, but drug resistance ultimately emerged, accompanied by amplifications of Kras, Yap1, Myc, and Cdk6/Abcb1a/b, and co-evolution of drug-resistant transcriptional programs. Moreover, in KPC and PDX models, mesenchymal and basal-like cell states displayed increased response to KRAS inhibition compared to the classical state. Combination treatment with KRASG12D inhibition and chemotherapy significantly improved tumor control in PDAC mouse models. Collectively, these data elucidate co-evolving resistance mechanisms to KRAS inhibition and support multiple combination therapy strategies.
Cell Stem Cell
Singh PNP, Madha S, Lynch AW, Cejas P, He R, Bhattacharya S, Muñoz Gomez M, Oser MG, Brown M, Long HW, Meyer CA, Shivdasani RA
Enteroendocrine cells (EECs) secrete serotonin (enterochromaffin [EC] cells) or specific peptide hormones (non-EC cells) that serve vital metabolic functions. The basis for terminal EEC diversity remains obscure. By forcing activity of the transcription factor (TF) NEUROG3 in 2D cultures of human intestinal stem cells, we replicated physiologic EEC differentiation and examined transcriptional and cis-regulatory dynamics that culminate in discrete cell types. Abundant EEC precursors expressed stage-specific genes and TFs. Before expressing pre-terminal NEUROD1, post-mitotic precursors oscillated between transcriptionally distinct ASCL1+ and HES6hi cell states. Loss of either factor accelerated EEC differentiation substantially and disrupted EEC individuality; ASCL1 or NEUROD1 deficiency had opposing consequences on EC and non-EC cell features. These TFs mainly bind cis-elements that are accessible in undifferentiated stem cells, and they tailor subsequent expression of TF combinations that underlie discrete EEC identities. Thus, early TF oscillations retard EEC maturation to enable accurate diversity within a medically important cell lineage.
JAMA Oncology
Postoperative Management of Prostate Cancer-Optimizing Prostate Cancer Care
Sayan M, D'Amico AV
The current standard-of-care follow-up protocol for patients who have undergone a radical prostatectomy—irrespective of prostatectomy (p) stage, margin status, or Gleason score—is monitoring with an ultrasensitive prostate-specific antigen (PSA) test and the initiation of salvage radiation therapy (RT) if the PSA level reaches or exceeds 0.1 ng/mL (to convert PSA to µg/L, multiply by 1). This practice is supported by a meta-analysis of 3 prospective randomized clinical trials (RCTs), which derived its conclusion from examination of the end point of progression-free survival (PFS), primarily influenced by PSA failure. However, it is important to note that the primary end point of the RADICALS-RT trial,2 the largest of the 3 RCTs included in this meta-analysis, was freedom from distant metastases (FFDM). However, as the other 2 RCTs approached the reporting of their primary end point, being PFS, a decision was made to consolidate the data and evaluate PFS, even though it was a secondary end point in the RADICALS-RT study.
Journal of Clinical Oncology
Individualized Local Recurrence Estimates for Ductal Carcinoma In Situ
Warren LEG, Bellon JR
In 2020, there were 2.26 million new cases of breast cancer worldwide, making it the most common cancer in the world excluding nonmelanoma skin cancers. In countries with robust screening programs, ductal carcinoma in situ (DCIS) accounts for 15%-25% of these cases. The American Cancer Society estimates that there are over 51,000 new cases of DCIS in the United States annually. Although DCIS is considered to be a precursor to invasive breast cancer, there is a variable likelihood of progression, with studies suggesting that up to 50% of DCIS may not progress to invasive cancer. Given the variability in disease course, there has been increasing interest in individualizing treatment strategies to minimize overtreatment. Proposed de-escalation strategies have included omission of surgery, for example, in the COMET (Comparison of Operative versus Monitoring and Endocrine Therapy) trial (ClinicalTrials.gov identifier NCT02926911). Despite shorter treatment courses and reduced toxicities with modern radiation planning, omission of adjuvant radiation therapy (RT) to avoid acute and long-term side effects remains of interest.
Journal of Clinical Oncology
Cao C, Ligibel JA
PURPOSE: To examine the prevalence and cancer-specific patterns of functional disabilities among US cancer survivors.
METHODS: Data from 47,768 cancer survivors and 2,432,754 noncancer adults age 18 years and older from the 2017 to 2022 Behavioral Risk Factor Surveillance System were analyzed. Functional disabilities assessed included mobility disability (ie, serious difficulty walking or climbing stairs) and self-care disability (ie, self-reported difficulty dressing or bathing). Multivariable logistic regression models were used to assess the associations between functional disabilities and sociodemographic, lifestyle, and health-related factors.
RESULTS: Cancer survivors tended to be older and non-Hispanic White than noncancer adults. The prevalence of mobility disability (27.9% v 13.4%) and self-care disability (7.4% v 3.8%) were higher among cancer survivors compared with noncancer adults. After multivariable adjustments, cancer survivors were more likely to report mobility (odds ratio [OR], 1.21 [95% CI, 1.16 to 1.26]) and self-care (OR, 1.19 [95% CI, 1.10 to 1.29]) disability than noncancer adults. The prevalence of mobility (34.9% v 26.3%) and self-care disability (9.8% v 6.7%) was higher in cancer survivors who were receiving active cancer treatment than in those who had completed cancer treatment. Higher prevalence of mobility and self-care disabilities was observed in cancer survivors who were racial/ethnic minorities and with higher BMI, low physical activity, lower levels of education and/or income, comorbidities, and those experiencing cancer/treatment-related pain. Patterns of mobility and self-care disabilities varied across cancer types.
CONCLUSION: Over a quarter of US cancer survivors reported mobility disability, and nearly 10% reported self-care disability, with patterns varying across cancer types and treatment status. Racial/ethnic minorities, along with underserved groups and individuals with unhealthy lifestyles or comorbidities, were notably more affected by functional disabilities, underscoring the need for targeted disability prevention efforts.
Journal of the National Cancer Institute
Paudel R, Enzinger AC, Uno H, Cronin C, Hassett MJ
BACKGROUND: Optimal methods for deploying electronic patient-reported outcomes to manage symptoms in routine oncologic practice remain uncertain. The electronic symptom management (eSyM) program asks chemotherapy and surgery patients to self-report 12 common symptoms regularly. Feedback from nurses and patients led to changing the recall period from the past 7?days to the past 24?hours.
METHODS: Using questionnaires submitted during the 16 weeks surrounding the recall period change, we assessed the likelihood of reporting severe or moderate and severe symptoms across 12 common symptoms and separately for the 5 most prevalent symptoms. Interrupted time-series analyses modeled the effects of the change using generalized linear mixed-effects models. Surgery and chemotherapy cohorts were analyzed separately. Study-wide effects were estimated using a meta-analysis method.
RESULTS: In total, 1692 patients from 6 institutions submitted 7823 eSyM assessments during the 16 weeks surrounding the recall period change. Shortening the recall period was associated with lower odds of severe symptom reporting in the surgery cohort (odds ratio?=?0.65, 95% confidence interval?=?0.46 to 0.93; P?=?.02) and lower odds of moderate and severe symptom reporting in the chemotherapy cohort (odds ratio?=?0.83, 95% confidence interval?=?0.71 to 0.97; P?=?.02). Among the most prevalent symptoms, 24-hour recall was associated with a lower rate of reporting postoperative constipation but no differences in reporting rates for other symptoms.
CONCLUSION: A shorter recall period was associated with a reduction in the proportion of patients reporting moderate-severe symptoms. The optimal recall period may vary depending on whether electronic patient-reported outcomes are collected for active symptom management, as a clinical trial endpoint, or another purpose. ClinicalTrials.gov ID NCT03850912.
Journal of the National Cancer Institute
Gonzalo-Encabo P, Dieli-Conwright CM
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BACKGROUND: Postmenopausal women with cancer experience an accelerated physical dysfunction beyond what is expected through aging alone due to cancer and its treatments. The aim of this study was to determine whether declines in physical function after cancer diagnosis are associated with all-cause mortality and cancer-specific mortality. METHODS: This prospective cohort study included 8068 postmenopausal women enrolled in the Women's Health Initiative with a cancer diagnosis and who had physical function assessed within 1 year of that diagnosis. Self-reported physical function was measured using the 10-item physical function subscale of the 36-Item Short Form Health Survey. Cause of death was determined by medical record review, with central adjudication and linkage to the National Death Index. Death was adjudicated through February 2022. RESULTS: Over a median follow-up of 7.7?years from cancer diagnosis, 3316 (41.1%) women died. Our results showed that for every 10% difference in the physical function score after cancer diagnosis versus pre-diagnosis, all-cause mortality and cancer-specific mortality were reduced by 12% (hazard ratio?[HR] =?0.88, 95% confidence interval? [95% CI] =?0.87 to 0.89 and HR?=?0.88, 95% CI?=?0.86 to 0.91, respectively). Further categorical analyses showed a significant dose-response relationship between postdiagnosis physical function categories and mortality outcomes (P?
Journal of the National Cancer Institute Use of Cancer-Directed Therapy at the End of Life Among Adolescents and Young Adults Mack JW, Cernik C, Fisher L, Lakin JR, Uno H
BACKGROUND: Adolescents and young adults frequently receive chemotherapy near death. We know less about the use of targeted agents and immunotherapy or trends over time. METHODS: We conducted a retrospective cohort study of 1836 adolescents and young adults with cancer who died between 2009 and 2019 after receiving care at 1 of 3 sites (Dana-Farber Cancer Institute, Kaiser Permanente Northern California, and Kaiser Permanente Southern California). We reviewed electronic health data and medical records to examine use of cancer-directed therapy in the last 90?days of life, including chemotherapy, targeted therapy, immunotherapy, and investigational drugs. RESULTS: Over the study period, 35% of adolescents and young adults received chemotherapy in the last 90?days of life; 24% received targeted therapy, 7% immunotherapy, and 5% investigational drugs. Additionally, 56% received at least 1 form of systemic cancer-directed therapy in the last 90?days of life. After adjustment for patient sex, race, ethnicity, age, site of care, diagnosis, and years from diagnosis to death, the proportion of adolescents and young adults receiving targeted therapy (odds ratio [OR] = 1.05 per year of death, 95% confidence interval [CI] = 1.02 to 1.10; P?=?.006), immunotherapy (OR = 1.27, 95% CI = 1.18 to 1.38; P?
Molecular Cell Polymerization of ZBTB Transcription Factors Regulates Chromatin Occupancy Park PMC, Park J, Brown J, Hunkeler M, Roy Burman SS, Donovan KA, Yoon H, Nowak RP, S?abicki M, Ebert BL, Fischer ES BCL6, an oncogenic transcription factor (TF), forms polymers in the presence of a small-molecule molecular glue that stabilizes a complementary interface between homodimers of BCL6's broad-complex, tramtrack, and bric-à-brac (BTB) domain. The BTB domains of other proteins, including a large class of TFs, have similar architectures and symmetries, raising the possibility that additional BTB proteins self-assemble into higher-order structures. Here, we surveyed 189 human BTB proteins with a cellular fluorescent reporter assay and identified 18 ZBTB TFs that show evidence of polymerization. Through biochemical and cryoelectron microscopy (cryo-EM) studies, we demonstrate that these ZBTB TFs polymerize into filaments. We found that BTB-domain-mediated polymerization of ZBTB TFs enhances chromatin occupancy within regions containing homotypic clusters of TF binding sites, leading to repression of target genes. Our results reveal a role of higher-order structures in regulating ZBTB TFs and suggest an underappreciated role for TF polymerization in modulating gene expression.
Nature Communications Forrest SJ, Gupta H, Ward A, Li YY, Doan D, Al-Ibraheemi A, Alexandrescu S, Bandopadhayay P, Shusterman S, Mullen EA, Collins NB, Chi SN, Wright KD, Kumari P, Mazor T, Ligon KL, Shivdasani P, Manam M, MacConaill LE, Ceca E, Benich SN, London WB, Cerami E, Rollins BJ, Meyerson ML, Johnson BE, Cherniak AD, Church AJ, Janeway KA To inform clinical trial design and real-world precision pediatric oncology practice, we classified diagnoses, assessed the landscape of mutations, and identified genomic variants matching trials in a large unselected institutional cohort of solid tumors patients sequenced at Dana-Farber / Boston Children's Cancer and Blood Disorders Center. Tumors were sequenced with OncoPanel, a targeted next-generation DNA sequencing panel. Diagnoses were classified according to the International Classification of Diseases for Oncology (ICD-O-3.2). Over 6.5 years, 888 pediatric cancer patients with 95 distinct diagnoses had successful tumor sequencing. Overall, 33% (n?=?289/888) of patients had at least 1 variant matching a precision oncology trial protocol, and 14% (41/289) were treated with molecularly targeted therapy. This study highlights opportunities to use genomic data from hospital-based sequencing performed either for research or clinical care to inform ongoing and future precision oncology clinical trials. Furthermore, the study results emphasize the importance of data sharing to define the genomic landscape and targeted treatment opportunities for the large group of rare pediatric cancers we encounter in clinical practice.
Nature Medicine A Comprehensive Cancer Center in the Cloud Powered by AI Can Reduce Health Disparities Ngwa W, Quintana Y, Chipidza F Recent reports by the American Association for Cancer Research have highlighted cancer-associated health inequalities for those who are Black, Indigenous, or people of color. Black Americans have the highest overall death rates from cancer of any racial or ethnic group in the USA: for example, death rates from prostate cancer for Black men are more than double those for every other racial or ethnic group, and Black women over the age of 50 are twice as likely to die of breast cancer as white women. Geography, race, earnings, attitude and technology (sometimes abbreviated ‘GREAT’) are structural barriers to health equity. Integrated, multilevel and customized interventions are urgently needed to address these health barriers.
Nature Medicine A Systematic Review and Meta-Analysis of Nonrelapse Mortality After CAR T Cell Therapy Cordas Dos Santos DM, Alberge JB, Cliff ERS, Ghobrial IM Although chimeric antigen receptor (CAR) T cell therapy represents a transformative immunotherapy, it is also associated with distinct toxicities that contribute to morbidity and mortality. In this systematic review and meta-analysis, we searched MEDLINE, Embase and CINAHL (Cochrane) for reports of nonrelapse mortality (NRM) after CAR T cell therapy in lymphoma and multiple myeloma up to March 2024. After extraction of causes and numbers of death, we analyzed NRM point estimates using random-effect models. We identified 7,604 patients across 18 clinical trials and 28 real-world studies. NRM point estimates varied across disease entities and were highest in patients with mantle-cell lymphoma (10.6%), followed by multiple myeloma (8.0%), large B cell lymphoma (6.1%) and indolent lymphoma (5.7%). Entity-specific meta-regression models for large B cell lymphoma and multiple myeloma revealed that axicabtagene ciloleucel and ciltacabtagene autoleucel were independently associated with increased NRM point estimates, respectively. Of 574 reported nonrelapse deaths, over half were attributed to infections (50.9%), followed by other malignancies (7.8%) and cardiovascular/respiratory events (7.3%). Conversely, the CAR T cell-specific side effects, immune effector cell-associated neurotoxicity syndrome/neurotoxicity, cytokine release syndrome and hemophagocytic lymphohistiocytosis, represented only a minority of nonrelapse deaths (cumulatively 11.5%). Our findings underline the critical importance of infectious complications after CAR T cell therapy and support the comprehensive reporting of NRM, including specific causes and long-term outcomes.
Advanced Science Transmural Flow Upregulates PD-L1 Expression in Microvascular Networks Wan Z, Shelton SE, Barbie DA, Hodi FS
American Journal of Hematology Castillo JJ
American Journal of Hematology Laubach J, Richardson PG
American Journal of Transplantation Bhatia U, Tadman S, Rocha A, Rudraboina R, Contreras-Ruiz L, Guinan EC
Annals of Internal Medicine Best Practices in Caring for Seriously Ill Patients Bernacki R
Annals of Surgical Oncology Breast Articles From 2023: Informing Practice Across the Continuum of Care King TA, Mittendorf EA
Arthritis Care and Research Goldschen L, Peng CS, Mufson MJ, Feldman CH, Case SM, Costenbader KH, Amonoo HL
Biostatistics Uncertainty Directed Factorial Clinical Trials Kotecha G, Trippa L
Blood Advances Davids MS
Blood Advances Evans B, Chen T, Moscvin M, Boullt S, Bianchi G
Blood Cancer Journal Laubach J, Richardson PG
Blood Reviews Mo CC, Calabretta E, Corrado F, Baron RM, Connors JM, Wei LJ, Richardson PG
BMJ Open Rosenberg SM, Zheng Y, Poorvu PD, Snow C, Kirkner GJ, Meyer ME, Peppercorn J, Come S, Gelber S, Collins L, Winer EP, Partridge AH
Brain, Behavior, and Immunity - Health Sannes TS, Yusufov M, Sutherland J, Stefanik J, Andrade N, Gray TF, Braun IM, Pirl WF
Breast Cancer Research Treatment Leonard S, Jones AN, Freedman RA, Mayer EL, Mittendorf EA, King TA, Kantor O
Cancer Walburn T, Loffredo M, McMahon E, Orio PF, Nguyen PL, D'Amico AV, Sayan M
CA Cancer Journal for Clinicians Pohl SA, Nelson BA, Patwary TR, Benz EJ Jr, Lathan CS
Cancer Immunology Research Dias Costa A, Cardot-Ruffino V, Rahma OE, Singh H, Abrams TA, Biller LH, Cleary J, Enzinger P, Huffman BM, McCleary NJ, Perez KJ, Rubinson DA, Schlechter BL, Surana R, Yurgelun MB, Wang SJ, Remland J, Brais LK, Bollenrucher N, Chang E, Ali LR, Lenehan PJ, Lima C, Keheler CE, Sullivan KM, Dougan M, Wolpin BM, Nowak JA, Dougan SK
Cancer Research ASPSCR1::TFE3 Drives Alveolar Soft Part Sarcoma by Inducing Targetable Transcriptional Programs Sicinska E, Kerfoot JA, Taddei ML, Al-Ibraheemi A, Church AJ
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