Welcome to Dana-Farber's Research News
May 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 April 1 through April 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 ericd_schuller@dfci.harvard.edu.
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Blood
Bourgeois W, Cutler JA, Aubrey BJ, Wenge DV, Perner F, Martucci C, Henrich JA, Klega K, Nowak RP, Donovan KA, Boileau M, Wen Y, Hatton C, Apazidis AA, Olsen SN, Kirmani N, Pikman Y, Pollard JA, Perry JA, Sperling AS, Ebert BL, Crompton BD, Fischer ES, Armstrong SA
Small molecules that target the menin-KMT2A protein-protein interaction (menin inhibitors) have recently entered clinical trials in lysine methyltransferase 2A (KMT2A or MLL1)-rearranged (KMT2A-r) and nucleophosmin-mutant (NPM1c) acute myeloid leukemia (AML) and are demonstrating encouraging results. However, rationally chosen combination therapy is needed to improve responses and prevent resistance. We have previously identified IKZF1/IKAROS as a target in KMT2A-r AML and shown in preclinical models that IKAROS protein degradation with lenalidomide or iberdomide has modest single-agent activity yet can synergize with menin inhibitors. Recently, the novel IKAROS degrader mezigdomide was developed with greatly enhanced IKAROS protein degradation. In this study, we show that mezigdomide has increased preclinical activity in vitro as a single-agent in KMT2A-r and NPM1c AML cell lines, including sensitivity in cell lines resistant to lenalidomide and iberdomide. Further, we demonstrate that mezigdomide has the greatest capacity to synergize with and induce apoptosis in combination with menin inhibitors, including in MEN1 mutant models. We show that the superior activity of mezigdomide compared with lenalidomide or iberdomide is due to its increased depth, rate, and duration of IKAROS protein degradation. Single-agent mezigdomide was efficacious in 5 patient-derived xenograft models of KMT2A-r and 1 NPM1c AML. The combination of mezigdomide with the menin inhibitor VTP-50469 increased survival and prevented and overcame MEN1 mutations that mediate resistance in patients receiving menin inhibitor monotherapy. These results support prioritization of mezigdomide for early phase clinical trials in KMT2A-r and NPM1c AML, either as a single agent or in combination with menin inhibitors.
Cancer Discovery
Pecci F, Nakazawa S, Ricciuti B, Alessi JV, Barrichello A, Vaz VR, Lamberti G, Gandhi MM, Gazgalis D, Feng WW, Jiang J, Baldacci S, Locquet MA, Gottlieb FH, Lee E, Haradon D, Smokovich A, Voligny E, Nguyen T, Wang X, Bahcall M, Heist RS, Iqbal S, Che J, Janne PA, Awad MM
Activating point mutations in the MET tyrosine kinase domain (TKD) are oncogenic in a subset of papillary renal cell carcinomas (PRCC). Here, using comprehensive genomic profiling among >600,000 patients, we identify activating MET TKD point mutations as putative oncogenic driver across diverse cancers, with a frequency of ~0.5%. The most common mutations in the MET TKD defined as oncogenic or likely oncogenic according to OncoKB resulted in amino acid substitutions at positions H1094, L1195, F1200, D1228, Y1230, M1250, and others. Preclinical modeling of these alterations confirmed their oncogenic potential, and also demonstrated differential patterns of sensitivity to type I and type II MET inhibitors. Two patients with metastatic lung adenocarcinoma harboring MET TKD mutations (H1094Y, F1200I) and no other known oncogenic drivers achieved confirmed partial responses to a type I MET inhibitor. Activating MET TKD mutations occur in multiple malignancies and may confer clinical sensitivity to currently available MET inhibitors.
Cancer Discovery
Stopsack KH, Peng C, Wang M, Ogino S, Sasamoto N, Ugai T
Biological characteristics of tumors are heterogeneous, forming spectra in terms of several factors such as age at onset, anatomic spatial localization, tumor subtyping, and the degree of tumor aggressiveness (encompassing a neoplastic property spectrum). Instead of blindly using dichotomized approaches, the application of the multicategorical and continuous analysis approaches to detailed cancer spectrum data can contribute to a better understanding of the etiology of cancer, ultimately leading to effective prevention and precision oncology. We provide examples of cancer spectra and emphasize the importance of integrating the cancer spectrum theory into large-scale population cancer research.
Journal of Clinical Oncology
Ricciuti B, Lamberti G, Puchala SR, Mahadevan NR, Lin JR, Alessi JV, Chowdhury A, Li YY, Wang X, Spurr L, Pecci F, Di Federico A, Venkatraman D, Barrichello AP, Gandhi M, Vaz VR, Pangilinan AJ, Haradon D, Lee E, Gupta H, Pfaff KL, Welsh EL, Nishino M, Cherniack AD, Johnson BE, Weirather JL, Dryg ID, Rodig SJ, Sholl LM, Sorger P, Santagata S, Umeton R, Awad MM
PURPOSE: Although immune checkpoint inhibitors (ICI) have extended survival in patients with non-small-cell lung cancer (NSCLC), acquired resistance (AR) to ICI frequently develops after an initial benefit. However, the mechanisms of AR to ICI in NSCLC are largely unknown.
METHODS: Comprehensive tumor genomic profiling, machine learning-based assessment of tumor-infiltrating lymphocytes, multiplexed immunofluorescence, and/or HLA-I immunohistochemistry (IHC) were performed on matched pre- and post-ICI tumor biopsies from patients with NSCLC treated with ICI at the Dana-Farber Cancer Institute who developed AR to ICI. Two additional cohorts of patients with intervening chemotherapy or targeted therapies between biopsies were included as controls.
RESULTS: We performed comprehensive genomic profiling and immunophenotypic characterization on samples from 82 patients with NSCLC and matched pre- and post-ICI biopsies and compared findings with a control cohort of patients with non-ICI intervening therapies between biopsies (chemotherapy, N = 32; targeted therapies, N = 89; both, N = 17). Putative resistance mutations were identified in 27.8% of immunotherapy-treated cases and included acquired loss-of-function mutations in STK11, B2M, APC, MTOR, KEAP1, and JAK1/2; these acquired alterations were not observed in the control groups. Immunophenotyping of matched pre- and post-ICI samples demonstrated significant decreases in intratumoral lymphocytes, CD3e+ and CD8a+ T cells, and PD-L1-PD1 engagement, as well as increased distance between tumor cells and CD8+PD-1+ T cells. There was a significant decrease in HLA class I expression in the immunotherapy cohort at the time of AR compared with the chemotherapy (P = .005) and the targeted therapy (P = .01) cohorts.
CONCLUSION: These findings highlight the genomic and immunophenotypic heterogeneity of ICI resistance in NSCLC, which will need to be considered when developing novel therapeutic strategies aimed at overcoming resistance.
Journal of Clinical Oncology
Choueiri TK
Clinical trials frequently include multiple end points that mature at different times. The initial report, typically based on the primary end point, may be published when key planned co-primary or secondary analyses are not yet available. Clinical trial updates provide an opportunity to disseminate additional results from studies, published in JCO or elsewhere, for which the primary end point has already been reported. We present the final prespecified overall survival (OS) analysis of the open-label, phase III CLEAR study in treatment-naïve patients with advanced renal cell carcinoma (aRCC). With an additional follow-up of 23 months from the primary analysis, we report results from the lenvatinib plus pembrolizumab versus sunitinib comparison of CLEAR. Treatment-naïve patients with aRCC were randomly assigned to receive lenvatinib (20 mg orally once daily in 21-day cycles) plus pembrolizumab (200 mg intravenously once every 3 weeks) or sunitinib (50 mg orally once daily [4 weeks on/2 weeks off]). At this data cutoff date (July 31, 2022), the OS hazard ratio (HR) was 0.79 (95% CI, 0.63 to 0.99). The median OS (95% CI) was 53.7 months (95% CI, 48.7 to not estimable [NE]) with lenvatinib plus pembrolizumab versus 54.3 months (95% CI, 40.9 to NE) with sunitinib; 36-month OS rates (95% CI) were 66.4% (95% CI, 61.1 to 71.2) and 60.2% (95% CI, 54.6 to 65.2), respectively. The median progression-free survival (95% CI) was 23.9 months (95% CI, 20.8 to 27.7) with lenvatinib plus pembrolizumab and 9.2 months (95% CI, 6.0 to 11.0) with sunitinib (HR, 0.47 [95% CI, 0.38 to 0.57]). Objective response rate also favored the combination over sunitinib (71.3% v 36.7%; relative risk 1.94 [95% CI, 1.67 to 2.26]). Treatment-emergent adverse events occurred in >90% of patients who received either treatment. In conclusion, lenvatinib plus pembrolizumab achieved consistent, durable benefit with a manageable safety profile in treatment-naïve patients with aRCC.
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
TP53-Associated Early Breast Cancer: New Observations from a Large Cohort
Sandoval RL, Tianyu L, Bychkovsky BL, Cahill S, Tayob N, Garber JE
BACKGROUND: A large well-annotated recent international cohort of Li-Fraumeni (LFS) patients with early-stage breast cancer (BC) was examined for shared features.
METHODS: This multicentre cohort study included females with a germline TP53 pathogenic or likely pathogenic variant and nonmetastatic BC diagnosed between 2002-2022. Clinical and genetic data were obtained from institutional registries and clinical charts. Descriptive statistics were utilized to summarize proportions and differences were assessed by Chi square or Wilcoxon rank sum tests. Metachronous contralateral breast cancer (CBC) risk, radiation-induced sarcoma risk, and recurrence-free survival (RFS) were analyzed by Kaplan-Meier methodology.
RESULTS: Among 227 females who met study criteria, the median age of first BC diagnosis was 37?years (range 21-71), 11.9% presented with bilateral synchronous BC and 18.1% had ductal carcinoma in situ (DCIS) only. In total, 166 (73.1%) underwent mastectomies including 67 bilateral mastectomies as first BC surgery. Among those with retained breast tissue, CBC rate was 25.3% at 5-years. Among 186 invasive tumors, 72.1% were stages I-II, 48.9% node-negative, and the most common subtypes were HR+/HER2- (40.9%) and HR+/HER2?+?(34.4%). At a median follow-up of 69.9?months (IQR 32.6-125.9), invasive HR+/HER2- disease had the highest recurrence risk among the subtypes (5-year RFS 61.1%, p?=?.0012). Among those who received radiation therapy (n?=?79), the 5-year radiation-induced sarcoma rate was 4.8%.
CONCLUSION: We observed high rates of DCIS, HR+ and HER2+ breast cancers, with a worse outcome in the HR+/HER2- luminal tumors despite appropriate treatment. Confirmation of these findings in further studies could have implications for BC care in LFS.
JAMA Oncology
Second Primary Breast Cancer in Young Breast Cancer Survivors
Brantley KD, Collins LC, Come SE, Zheng Y, Kirkner GJ, Snow C, Partridge AH
IMPORTANCE: Among women diagnosed with primary breast cancer (BC) at or younger than age 40 years, prior data suggest that their risk of a second primary BC (SPBC) is higher than that of women who are older when they develop a first primary BC.
OBJECTIVE: To estimate cumulative incidence and characterize risk factors of SPBC among young patients with BC.
DESIGN, SETTING, AND PARTICIPANTS: Participants were enrolled in the Young Women's Breast Cancer Study, a prospective study of 1297 women aged 40 years or younger who were diagnosed with stage 0 to III BC from August 2006 to June 2015. Demographic, genetic testing, treatment, and outcome data were collected by patient surveys and medical record review. A time-to-event analysis was used to account for competing risks when determining cumulative incidence of SPBC, and Fine-Gray subdistribution hazard models were used to evaluate associations between clinical factors and SPBC risk. Data were analyzed from January to May 2023.
MAIN OUTCOMES AND MEASURES: The 5- and 10- year cumulative incidence of SPBC.
RESULTS: In all, 685 women with stage 0 to III BC (mean [SD] age at primary BC diagnosis, 36 [4] years) who underwent unilateral mastectomy or lumpectomy as the primary surgery for BC were included in the analysis. Over a median (IQR) follow-up of 10.0 (7.4-12.1) years, 17 patients (2.5%) developed an SPBC; 2 of these patients had cancer in the ipsilateral breast after lumpectomy. The median (IQR) time from primary BC diagnosis to SPBC was 4.2 (3.3-5.6) years. Among 577 women who underwent genetic testing, the 10-year risk of SPBC was 2.2% for women who did not carry a pathogenic variant (12 of 544) and 8.9% for carriers of a pathogenic variant (3 of 33). In multivariate analyses, the risk of SPBC was higher among PV carriers vs noncarriers (subdistribution hazard ratio [sHR], 5.27; 95% CI, 1.43-19.43) and women with primary in situ BC vs invasive BC (sHR, 5.61; 95% CI, 1.52-20.70).
CONCLUSIONS: Findings of this cohort study suggest that young BC survivors without a germline pathogenic variant have a low risk of developing a SPBC in the first 10 years after diagnosis. Findings from germline genetic testing may inform treatment decision-making and follow-up care considerations in this population.
Lancet Oncology
Jänne PA
BACKGROUND: DESTINY-Lung01 is a multicentre, open-label, phase 2 study evaluating the antitumour activity and safety of trastuzumab deruxtecan, a HER2-directed antibody-drug conjugate, in patients with HER2-overexpressing or HER2 (ERBB2)-mutant unresectable or metastatic non-small-cell lung cancer (NSCLC). The results of the HER2-mutant cohort (cohort 2) have been reported elsewhere. Herein, we report the primary analysis of cohorts 1 and 1A, which aimed to evaluate the activity and safety of trastuzumab deruxtecan 5·4 mg/kg and 6·4 mg/kg in patients with HER2-overexpressing NSCLC.
METHODS: Patients aged 18 years or older with unresectable or metastatic (or both unresectable and metastatic) non-squamous NSCLC who had relapsed following or were refractory to standard treatment or for whom no standard treatment was available, with an HER2 immunohistochemistry score of 3+ or 2+ (without known HER2 mutations) and an Eastern Cooperative Oncology Group performance status score of 0 or 1, were enrolled at 20 specialist hospitals in France, Japan, the Netherlands, Spain, and the USA. Patients were assigned to cohorts sequentially, first to cohort 1, to receive trastuzumab deruxtecan 6·4 mg/kg (cohort 1), then to cohort 1A, to receive trastuzumab deruxtecan 5·4 mg/kg, both administered intravenously once every 3 weeks. The primary endpoint was confirmed objective response rate by independent central review and was assessed in the full analysis set, which included all patients who signed an informed consent form and were enrolled in the study. Safety was assessed in all enrolled patients who received at least one dose of trastuzumab deruxtecan. This trial is registered with ClinicalTrials.gov, NCT03505710, and is ongoing (closed to recruitment).
FINDINGS: Between Aug 27, 2018, and Jan 28, 2020, 49 patients were enrolled in cohort 1 (median age 63·0 years [IQR 58·0-68·0], 30 [61%] male, 19 [39%] female, and 31 [63%] White), and from June 16 to Dec 9, 2020, 41 patients were enrolled in cohort 1A (median age 62·0 years [IQR 56·0-66·0], 22 [54%] male, 19 [46%] female, and 31 [76%] White). As of data cutoff (Dec 3, 2021), the median treatment duration was 4·1 months (IQR 1·4-7·1) in cohort 1 and 5·5 months (1·4-8·7) in cohort 1A, and median follow-up was 12·0 months (5·4-22·4) in cohort 1 and 10·6 months (4·5-13·5) in cohort 1A. Confirmed objective response rate by independent central review was 26·5% (95% CI 15·0-41·1; 13 of 49, all partial responses) in cohort 1 and 34·1% (20·1-50·6; 14 of 41; two complete responses and 12 partial responses) in cohort 1A. The most common treatment-emergent adverse events of grade 3 or worse were neutropenia (12 [24%] of 49 in cohort 1, none in cohort 1A), pneumonia (six [12%] and two [5%], respectively), fatigue (six [12%] and three [7%], respectively), and disease progression (six [12%] and four [10%], respectively). Drug-related treatment-emergent adverse events of grade 3 or worse occurred in 26 (53%) of 41 patients in cohort 1 and nine (22%) of 49 patients in cohort 1A. Drug-related serious adverse events were reported in ten (20%) patients and three (7%) patients, respectively. Deaths due to treatment-emergent adverse events occurred in ten (20%) patients in cohort 1 (disease progression in six (12%) patients and bronchospasm, hydrocephalus, respiratory failure, and pneumonitis in one [2%] patient each), and in seven (17%) patients in cohort 1A (due to disease progression in four (10%) patients and dyspnoea, malignant neoplasm, and sepsis in one (2%) patient each). One death due to a treatment-emergent adverse event was determined to be due to study treatment by the investigator, which was in cohort 1 (pneumonitis). Independent adjudication of interstitial lung disease or pneumonitis found that drug-related interstitial lung disease or pneumonitis occurred in ten (20%) patients in cohort 1 (two [4%] grade 1, five [10%] grade 2, and three [6%] grade 5) and two (5%) patients in cohort 1A (one [2%] grade 2 and one [2%] grade 5). An additional patient in cohort 1A had grade 4 pneumonitis after the data cutoff, which was subsequently adjudicated as drug-related grade 5 interstitial lung disease or pneumonitis.
INTERPRETATION: Given the low antitumour activity of existing treatment options in this patient population, trastuzumab deruxtecan might have the potential to fill a large unmet need in HER2-overexpressing NSCLC. Our findings support further investigation of trastuzumab deruxtecan in patients with HER2-overexpressing NSCLC.
FUNDING: Daiichi Sankyo and AstraZeneca.
Molecular Cell
Dissection of a CTCF Topological Boundary Uncovers Principles of Enhancer-Oncogene Regulation
Kim KL, Rahme GJ, Goel VY, El Farran CA, Hansen AS, Bernstein BE
Enhancer-gene communication is dependent on topologically associating domains (TADs) and boundaries enforced by the CCCTC-binding factor (CTCF) insulator, but the underlying structures and mechanisms remain controversial. Here, we investigate a boundary that typically insulates fibroblast growth factor (FGF) oncogenes but is disrupted by DNA hypermethylation in gastrointestinal stromal tumors (GISTs). The boundary contains an array of CTCF sites that enforce adjacent TADs, one containing FGF genes and the other containing ANO1 and its putative enhancers, which are specifically active in GIST and its likely cell of origin. We show that coordinate disruption of four CTCF motifs in the boundary fuses the adjacent TADs, allows the ANO1 enhancer to contact FGF3, and causes its robust induction. High-resolution micro-C maps reveal specific contact between transcription initiation sites in the ANO1 enhancer and FGF3 promoter that quantitatively scales with FGF3 induction such that modest changes in contact frequency result in strong changes in expression, consistent with a causal relationship.
Nature Communications
Cold-Induced FOXO1 Nuclear Transport Aids Cold Survival and Tissue Storage
Zhang X
Cold-induced injuries severely limit opportunities and outcomes of hypothermic therapies and organ preservation, calling for better understanding of cold adaptation. Here, by surveying cold-altered chromatin accessibility and integrated CUT&Tag/RNA-seq analyses in human stem cells, we reveal forkhead box O1 (FOXO1) as a key transcription factor for autonomous cold adaptation. Accordingly, we find a nonconventional, temperature-sensitive FOXO1 transport mechanism involving the nuclear pore complex protein RANBP2, SUMO-modification of transporter proteins Importin-7 and Exportin-1, and a SUMO-interacting motif on FOXO1. Our conclusions are supported by cold survival experiments with human cell models and zebrafish larvae. Promoting FOXO1 nuclear entry by the Exportin-1 inhibitor KPT-330 enhances cold tolerance in pre-diabetic obese mice, and greatly prolongs the shelf-life of human and mouse pancreatic tissues and islets. Transplantation of mouse islets cold-stored for 14 days reestablishes normoglycemia in diabetic mice. Our findings uncover a regulatory network and potential therapeutic targets to boost spontaneous cold adaptation.
Nature Communications
Spisak S, Chen D, Likasitwatanakul P, Doan P, Li Z, Bala P, De Silva P, Giannakis M, Wolpin B, Qi J, Sethi NS
Aberrant stem cell-like activity and impaired differentiation are central to the development of colorectal cancer (CRC). To identify functional mediators of these key cellular programs, we engineer a dual endogenous reporter system by genome-editing the SOX9 and KRT20 loci of human CRC cell lines to express fluorescent reporters, broadcasting aberrant stem cell-like and differentiation activity, respectively. By applying a CRISPR screen targeting 78 epigenetic regulators with 542 sgRNAs to this platform, we identify factors that contribute to stem cell-like activity and differentiation in CRC. Perturbation single cell RNA sequencing (Perturb-seq) of validated hits nominate SMARCB1 of the BAF complex (also known as SWI/SNF) as a negative regulator of differentiation across an array of neoplastic colon models. SMARCB1 is a dependency and required for in vivo growth of human CRC models. These studies highlight the utility of biologically designed endogenous reporter platforms to uncover regulators with therapeutic potential.
Advances in Radiation Oncology
Lee JH, Shi DD, Shin KY, Buckley E, Gunasti L, Hall E, Mann E, Spicer B, Chen YH, Huynh MA, Spektor A, Krishnan MS, Balboni TA, Hertan LM
Advances in Radiation Oncology
Kwan C, Chen YH, Killoran JH, Ferrone M, Marcus KJ, Tanguturi S, Balboni TA, Spektor A, Huynh MA
AJNR American Journal of Neuroradiology
Guenette JP, Qin L
Annals of Surgical Oncology
Defining the Biology of Estrogen Receptor-Low-Positive Breast Cancer
Higgins T, Kantor O, Harrison B, Giordano J, McGrath M, Burstein HJ, Schnitt SJ, Rahman T, Vora H, Garrido-Castro A, Tolaney SM, King TA, Mittendorf EA
Blood Advances
Davids MS
Blood Advances
Hernandez-Lopez P, Vijaykumar T, Anand P, Frede J, Knoechel B, Lohr JG
Blood Advances
Lee DJ, El-Khoury H, Tramontano AC, Alberge JB, Perry J, Davis MI, Horowitz E, Redd R, Mucci L, Rebbeck TR, Ghobrial IM, Marinac CR
Blood Advances
Shimony S, Keating JH, Fay CJ, Luskin MR, Neuberg DS, LeBoeuf NR, Lane AA
Blood Cancer Journal
A Novel Small Molecule Inhibitor of CD73 Triggers Immune-Mediated Multiple Myeloma Cell Death
Ray A, Du T, Wan X, Song Y, Pillai SC, Musa MA, Fang T, Chauhan D, Anderson KC
Breast
2023 Year in Review: Early Breast Cancer
Nader-Marta G, Partridge AH
Breast Cancer Research and Treatment
Nakhlis F, Niman SM, Troll E, Ryan S, Yeh E, Warren L, Bellon J, Harrison B, Overmoyer B, Tolaney SM, Regan M, Lynce F
Cancer
Beaussant Y, Tarbi E, Nigam K, Sager Z, Ljuslin M, Tulsky JA
Cancer
Diller LR, Rosenberg AR, Shusterman S, Mack JW
Cancer
Snaman JM, Chen L, Mazzola E, Helton G, Feifer D, Rosenberg AR, Wolfe J
Cancer
Rosenberg AR
Cancer
Resilience in Adolescent and Young Adult Oncology: Problems and Prospects
Rosenberg AR
Cancer Research Communications
Nakashoji A, Haratake N, Bhattacharya A, Mao W, Wang K, Daimon T, Ozawa H, Shigeta K, Fushimi A, Yamashita N, Morimoto Y, Saito S, Egloff AM, Uppaluri R, Kufe D
Cancers
Precision Immuno-Oncology in NSCLC through Gender Equity Lenses
Kiel L, Kaufman R, Abioye O, Mantz C, Florez N
Cellular and Molecular Immunology
Synthetic Biology Approaches for Improving the Specificity and Efficacy of Cancer Immunotherapy
Yin H, Scimeca L, Wu MR
Chem
Bioorthogonally Activated Reactive Species for Target Identification
Siriwongsup S, Schmoker AM, Ficarro SB, Marto JA, Kim J
Clinical Cancer Research
Clinical and Genomic Predictors of Adverse Events in Newly Diagnosed Glioblastoma
Rahman R, Bhave V, Muzikansky A, Woodward E, Whorral S, Allen M, Patel J, Gerstner ER, Kalpathy-Cramer J, Youssef G, Chukwueke U, McFaline-Figueroa JR, Nayak L, Lee EQ, Reardon DA, Beroukhim R, Huang RY, Bi WL, Ligon KL, Wen PY
Clinical Cancer Research
From Serendipity to Intention: Development of Brain-Penetrant PARP1-Selective Inhibitors
Lynce F, Lin NU
Clinical Cancer Research
Haddox CL, Nathenson MJ, Mazzola E, Lin JR, Baginska J, Nau A, Weirather JL, Choy E, Marino-Enriquez A, Morgan JA, Cote GM, Merriam P, Wagner AJ, Sorger PK, Santagata S, George S
Clinical Cancer Research
Singh H, Sahgal P, Kapner K, Gupta H, Li YY, Cherniack AD, El Alam R, Kerfoot J, Andrews E, Lee A, Nambiar C, Hannigan AM, Remland J, Brais L, Leahy ME, Rubinson DA, Schlechter BL, Meyerson M, Kuang Y, Paweletz CP, Aguirre AJ, Perez KJ, Huffman BM, Rossi H, Abrams TA, Kabraji S, Sicinska ET, Parikh AR, Wolpin BM, Giannakis M, Ng K, Meyerhardt JA, Hornick JL, Sethi NS, Cleary JM
Clinical Cancer Research
Update on Cancer Predisposition Syndromes and Surveillance Guidelines for Childhood Brain Tumors
Schienda J, Kamihara J
Clinical Genitourinary Cancer
Gulhan DC, Savignano H, Lakshminarayanan G, McClure HM, Silver R, Hirsch MS, Sholl LM, Choudhury AD, Ananda G, Park PJ, Tewari AK, Berchuck JE
Current Treatment Options in Oncology
Role of Metastasis-Directed Therapy in Genitourinary Cancers
Lee KN, Huynh MA
European Journal of Cancer
Tarantino P, Ajari O, Graham N, Vincuilla J, Parker T, Hughes ME, Tayob N, Garrido-Castro AC, Morganti S, King TA, Mittendorf EA, Lin NU, Tolaney SM
European Urology Open Science
Integrative Analysis of Germline Rare Variants in Clear and Non-clear Cell Renal Cell Carcinoma
Han SH, Camp SY, Chu H, Collins R, Gillani R, Park J, Bakouny Z, Ricker CA, Reardon B, Labaki C, Choueiri TK, AlDubayan SH, Van Allen EM
Future Oncology
Bardia A, Tolaney SM
Genome Biology
Evaluating and Improving the Representation of Bacterial Contents in Long-Read Metagenome Assemblies
Feng X, Li H
Gut
Zhang F, Peng K, Wang Y, Bala P, Aitymbayev D, Sahgal P, Sethi N, Zhang H
Gynecologic Oncology Reports
Konstantinopoulos PA, Xiong N, Krasner C, Liu JF, Sawyer H, Polak M, Needham H, Geddes M, Koppermann L, Shea M, Castro C, Cheng SC, Matulonis UA, Lee EK
Haematologica
BH3 Profiling as Pharmacodynamic Biomarker for the Activity of BH3 Mimetics
Pan RA, Villalobos-Ortiz M, Ryan J, Letai A
Haematologica
Hantel A, Luskin MR, Warner E, Walsh TP, DeAngelo DJ, Lathan CS, Abel GA
HemaSphere
Merryman RW, Rhoades J, Xiong K, Redd RA, Antel K, An HH, McDonough M, Guerrero L, Crnjac A, Sridhar S, Blewett T, Cheng J, Joyce RM, Chen YB, Armand P, Murakami M, Adalsteinsson VA
Hematology/Oncology Clinics of North America
Mitsiades CS
International Journal of Radiation Oncology, Biology, Physics
The Next Chapter in Immunotherapy and Radiation Combination Therapy: Cancer-Specific Perspectives
Wisdom AJ, Marciscano AE, Mouw KW, Schoenfeld JD
Journal of Adolescent and Young Adult Oncology
Morris SE, Ryan AK, Malinowski P, Pozo-Kaderman C, Fasciano KM
Journal of the American Academy of Dermatology
Risk Factors and Outcomes of Melanoma in Children and Adolescents: A Retrospective Multicenter Study
Hawryluk EB, Moustafa D, Reusch DB, Kao PC, Schmidt B, London WB, Huang J
Journal of the American Chemical Society
Branching Crisscross Polymerization of Single-Stranded DNA Slats
Deng J, Minev D, Ershova A, Shih WM
Journal of the American College Surgeons
Mullen EA
Journal of the American Geriatrics Society
Agaronnik ND, Streid JL, Kwok A, Schoenfeld AJ, Cooper Z, Lindvall C
Journal of the American Medical Informatics Association
Evaluating the ChatGPT Family of Models for Biomedical Reasoning and Classification
Chen S, Li Y, Van H, Aerts HJWL, Savova GK, Bitterman DS
Journal of Biological Chemistry
Wachter F, Nowak RP, Ficarro S, Marto J, Fischer ES
Journal of Cancer Education
Bao T
Journal of Cancer Survivorship
Chevalier LL, Blackmon JE, Bober SL, Roman A, Chang G, Recklitis CJ
Journal of Hospital Medicine
Things We Do for No Reason™: Opioid Infusions as Initial Therapy for Symptoms at the End of Life
Gelfand SL, Drutchas A, Rosenberg LB
Journal for ImmunoTherapy of Cancer
Jegede OA, Mcdermott DF, Einstein D, Catalano PJ, Regan MM
Journal of Palliative Medicine
Bolstering Advance Care Planning Measurement Using Natural Language Processing
Zupanc SN, Durieux BN, Lindvall C
Journal of Palliative Medicine
Lally K, Macip-Rodriquez P, Wu C, McGuire H, Pirl W
JAMA Network Open
Incidence and Presenting Characteristics of Angiosarcoma in the US, 2001-2020
Wagner MJ, Hassett MJ
JAMA Network Open
Briercheck EL, Wagner MJ
JAMA Otolaryngology – Head and Neck Surgery
Patient Experience of Head and Neck Surgery with Free Flap Reconstruction
Dattilo LW, Russell TI, Warinner CB, Annino DJ Jr, Goguen LA, Sethi RKV, Uppaluri R, Bergmark RW, Rettig EM
JCO Precision Oncology
Luo J, Florez N
JCO Oncology Practice
Jacobson JO, Rompelman G, Morrison-Ma S, Murray L, Ferzoco M, Bunnell C, Wagner AJ, Roberts D, Chan J, Block C, Rubinson D
Leukemia
Shimony S, Liu Y, Schaefer EJ, Lindsley RC, Chen EC, DeAngelo DJ, Neuberg DS, Stone RM, Stahl M
Molecular Cancer Research
Omar M, Xu Z, Rand SB
Neuro-Oncology
Liquid Biopsy for Improving Diagnosis and Monitoring of CNS Lymphomas: A RANO Review
Nayak L, Wen PY
NPJ Breast Cancer
Prognosis and Treatment Outcomes for Patients with Stage IA Triple-Negative Breast Cancer
Tarantino P, Freedman RA, Waks AG, Martínez-Sáez O, Garrido-Castro A, Lynce F, Tayob N, Lin NU, Tolaney SM, Leone JP
NPJ Precision Oncology
Sahgal P, Huffman BM, Sztupinszki Z, Morris CX, Chen D, Diossy M, Likasitwatanakul P, Enzinger P, Singh H, Ubellaker J, Lazaro JB, Cleary JM, Szallasi Z, Sethi NS
Oncologist
Xie W, Jegede O, Choueiri TK
Oncologist
Kozono DE
Oral Oncology
Kono M, Saito S, Rokugo M, Egloff AM, Uppaluri R
Pediatric Blood and Cancer
Bhasin S, Brown J, Dorste A, Samsel C, Vrooman LM, Muriel AC
Pediatrics
A Communication and Decision-Making Framework for Pediatric Precision Medicine
Rosenberg AR, Marron JM
Pediatrics
Meaning-Making Among Parents of Children with Severe Neurologic Impairment in the PICU
Rosenberg AR
Protein Science
Mallis RJ, Lee JJ, Brazin KN, Viennet T, Reinherz EL, Arthanari H
Science Signaling
Loda M
Seminars in Radiation Oncology
Baldini EH
Transplantation and Cellular Therapy
Amonoo HL, Guo M, Boardman AC, Acharya N, Daskalakis E, Deary EC, Waldman LP, Joffe H, Huffman JC, El-Jawahri A
Transplantation and Cellular Therapy
Takahashi T, Bratrude B, Neuberg D, Hebert K, Betz K, Yu A, Duncan C, Horan JT, Kean LS
