Welcome to Dana-Farber's Research News
May 01, 2023
This twice-monthly newsletter highlights the research endeavors at Dana-Farber Cancer Institute, noting recently published papers available from PubMed where Dana-Farber faculty are listed as first or senior authors. If you are a Dana-Farber faculty member and you think your paper is missing from Research News, please let us know at: Michael_buller@dfci.harvard.edu.
Blood
Samur MK, Aktas Samur A, Fulciniti M, Shammas MA, Sperling AS, Richardson PG, Parmigiani G, Anderson KC, Munshi NC
High-dose melphalan (HDM) improves progression-free survival in multiple myeloma (MM), yet melphalan is a DNA-damaging alkylating agent; therefore, we assessed its mutational effect on surviving myeloma cells by analyzing paired MM samples collected at diagnosis and relapse in the IFM 2009 study. We performed deep whole-genome sequencing on samples from 68 patients, 43 of whom were treated with RVD (lenalidomide, bortezomib, and dexamethasone) and 25 with RVD + HDM. Although the number of mutations was similar at diagnosis in both groups (7137 vs 7230; P = .67), the HDM group had significantly more mutations at relapse (9242 vs 13?383, P = .005). No change in the frequency of copy number alterations or structural variants was observed. The newly acquired mutations were typically associated with DNA damage and double-stranded breaks and were predominantly on the transcribed strand. A machine learning model, using this unique pattern, predicted patients who would receive HDM with high sensitivity, specificity, and positive prediction value. Clonal evolution analysis showed that all patients treated with HDM had clonal selection, whereas a static progression was observed with RVD. A significantly higher percentage of mutations were subclonal in the HDM cohort. Intriguingly, patients treated with HDM who achieved complete remission (CR) had significantly more mutations at relapse yet had similar survival rates as those treated with RVD who achieved CR. This similarity could have been due to HDM relapse samples having significantly more neoantigens. Overall, our study identifies increased genomic changes associated with HDM and provides rationale to further understand clonal complexity.
Blood
Garcia JS, Flamand Y, Penter L, Mendez LM, Cullen N, Arihara Y, Pfaff K, Wolff JO, Brunner AM, Galinsky I, Antin JH, Cutler C, Ho V, Luskin MR, Wadleigh M, Winer ES, Savell A, Leonard R, Robertson T, Davids MS, Rodig SJ, Ritz J, Wu CJ, DeAngelo DJ, Neuberg D, Stone RM, Soiffer RJ
Two articles in this week’s issue focus on the use of ipilimumab and decitabine for patients with myelodysplasia (MDS) and acute myeloid leukemia (AML) before and after hematopoietic stem cell transplantation (HSCT) for high-risk disease. In the first article, Garcia et al report on the results of a phase 1 trial of the combination in 54 patients, demonstrating overall response rate of 52% in patients who are HSCT-naïve and 20% in patients post-HSCT; responses are usually short-lived. In the second article, Penter and colleagues characterize gene expression responses to therapy and conclude that decitabine acts directly to clear leukemic cells while ipilimumab acts on infiltrating lymphocytes in marrow and extramedullary sites. Responses are determined by leukemic cell burden and by the frequency and phenotype of infiltrating lymphocytes. Increasing bone marrow regulatory T cells is identified as a potential contributor to checkpoint inhibitor escape.
Blood
Penter L, Liu Y, Wolff JO, Yang L, Taing L, Jhaveri A, Southard J, Cullen NM, Pfaff KL, Cieri N, Oliveira G, Ranasinghe S, Leonard R, Robertson T, Morgan EA, Li S, Rodig SJ, Cibulskis C,
Gabriel S, Ritz J, Neuberg DS, Hodi FS, Davids MS, Livak KJ, Altreuter J, Michor F, Soiffer RJ,
Garcia JS, Wu CJ
The challenge of eradicating leukemia in patients with acute myelogenous leukemia (AML) after initial cytoreduction has motivated modern efforts to combine synergistic active modalities including immunotherapy. Recently, the ETCTN/CTEP 10026 study tested the combination of the DNA methyltransferase inhibitor decitabine together with the immune checkpoint inhibitor ipilimumab for AML/myelodysplastic syndrome (MDS) either after allogeneic hematopoietic stem cell transplantation (HSCT) or in the HSCT-naïve setting. Integrative transcriptome-based analysis of 304 961 individual marrow-infiltrating cells for 18 of 48 subjects treated on study revealed the strong association of response with a high baseline ratio of T to AML cells. Clinical responses were predominantly driven by decitabine-induced cytoreduction. Evidence of immune activation was only apparent after ipilimumab exposure, which altered CD4+ T-cell gene expression, in line with ongoing T-cell differentiation and increased frequency of marrow-infiltrating regulatory T cells. For post-HSCT samples, relapse could be attributed to insufficient clearing of malignant clones in progenitor cell populations. In contrast to AML/MDS bone marrow, the transcriptomes of leukemia cutis samples from patients with durable remission after ipilimumab monotherapy showed evidence of increased infiltration with antigen-experienced resident memory T cells and higher expression of CTLA-4 and FOXP3. Altogether, activity of combined decitabine and ipilimumab is impacted by cellular expression states within the microenvironmental niche of leukemic cells. The inadequate elimination of leukemic progenitors mandates urgent development of novel approaches for targeting these cell populations to generate long-lasting responses. This trial was registered at www.clinicaltrials.gov as #NCT02890329.
Cell Stem Cell
Kraiczy J, McCarthy N, Tie G, Madha S, Shivdasani RA
Signals from the surrounding niche drive proliferation and suppress differentiation of intestinal stem cells (ISCs) at the bottom of intestinal crypts. Among sub-epithelial support cells, deep sub-cryptal CD81+ PDGFRAlo trophocytes capably sustain ISC functions ex vivo. Here, we show that mRNA and chromatin profiles of abundant CD81- PDGFRAlo mouse stromal cells resemble those of trophocytes and that both populations provide crucial canonical Wnt ligands. Mesenchymal expression of key ISC-supportive factors extends along a spatial and molecular continuum from trophocytes into peri-cryptal CD81- CD55hi cells, which mimic trophocyte activity in organoid co-cultures. Graded expression of essential niche factors is not cell-autonomous but dictated by the distance from bone morphogenetic protein (BMP)-secreting PDGFRAhi myofibroblast aggregates. BMP signaling inhibits ISC-trophic genes in PDGFRAlo cells near high crypt tiers; that suppression is relieved in stromal cells near and below the crypt base, including trophocytes. Cell distances thus underlie a self-organized and polar ISC niche.
Journal of Clinical Oncology
Youssef G, Rahman R, Bay C, Wang W, Arnaout O, Bi WL, Chang YS, DeSalvo M, Flood TF,
Gerstner ER, Gonzalez Castro LN, Guenette JP, Kim AE, Lee EQ, McFaline-Figueroa JR, Potter CA, Reardon DA, Huang RY, Wen PY
PURPOSE: The Response Assessment in Neuro-Oncology (RANO) criteria are widely used in high-grade glioma clinical trials. We compared the RANO criteria with updated modifications (modified RANO [mRANO] and immunotherapy RANO [iRANO] criteria) in patients with newly diagnosed glioblastoma (nGBM) and recurrent GBM (rGBM) to evaluate the performance of each set of criteria and inform the development of the planned RANO 2.0 update.
MATERIALS AND METHODS: Evaluation of tumor measurements and fluid-attenuated inversion recovery (FLAIR) sequences were performed by blinded readers to determine disease progression using RANO, mRANO, iRANO, and other response assessment criteria. Spearman's correlations between progression-free survival (PFS) and overall survival (OS) were calculated.
RESULTS: Five hundred twenty-six nGBM and 580 rGBM cases were included. Spearman's correlations were similar between RANO and mRANO (0.69 [95% CI, 0.62 to 0.75] v 0.67 [95% CI, 0.60 to 0.73]) in nGBM and rGBM (0.48 [95% CI, 0.40 to 0.55] v 0.50 [95% CI, 0.42 to 0.57]). In nGBM, requirement of a confirmation scan within 12 weeks of completion of radiotherapy to determine progression was associated with improved correlations. Use of the postradiation magnetic resonance imaging (MRI) as baseline scan was associated with improved correlation compared with use of the pre-radiation MRI (0.67 [95% CI, 0.60 to 0.73] v 0.53 [95% CI, 0.42 to 0.62]). Evaluation of FLAIR sequences did not improve the correlation. Among patients who received immunotherapy, Spearman's correlations were similar among RANO, mRANO, and iRANO.
CONCLUSION: RANO and mRANO demonstrated similar correlations between PFS and OS. Confirmation scans were only beneficial in nGBM within 12 weeks of completion of radiotherapy, and there was a trend in favor of the use of postradiation MRI as the baseline scan in nGBM. Evaluation of FLAIR can be omitted. The iRANO criteria did not add significant benefit in patients who received immune checkpoint inhibitors.
Journal of the National Cancer Institute
Survival in Male Breast Cancer Over the Past 3 Decades
Leone JP, Freedman RA, Tolaney SM, Winer EP, Lin NU, Hassett MJ
BACKGROUND: Breast cancer mortality in women has declined statistically significantly over the past several years. In men, it is unclear whether survival has changed over time. We evaluated changes in breast cancer-specific survival (BCSS) and overall survival (OS) in male breast cancer over the past 3 decades.
METHODS: We evaluated men diagnosed with breast cancer between 1988 and 2017, reported in the Surveillance, Epidemiology, and End Results registry. Patients were categorized into 3 groups by year of diagnosis: 1988-1997, 1998-2007, and 2008-2017. BCSS and OS were estimated by Kaplan-Meier, and differences between groups were compared by log-rank test. Multivariable Cox regression evaluated the independent association of year of diagnosis with BCSS and OS. All tests were 2-sided.
RESULTS: We included 8481 men. Overall, BCSS at 5?years was 83.69%, 83.78%, and 84.41% in groups 1988-1997, 1998-2007, and 2008-2017, respectively (P?=?.86). There was no statistically significant difference in BCSS between the 3 groups within each stage of disease. Among all patients, OS at 5?years was 64.61%, 67.31%, and 69.05% in groups 1988-1997, 1998-2007, and 2008-2017, respectively (P?=?.01). In adjusted Cox models, each additional year of diagnosis had no statistically significant association with BCSS (hazard ratio = 1.00, 95% confidence interval = 0.99 to 1.01, P?=?.75), but there was statistically significant improvement in OS (hazard ratio = 0.99, 95% CI = 0.98 to 0.99, P?=?.009).
CONCLUSIONS: Over the past 3 decades, there has been no statistically significant improvement in BCSS in male breast cancer. Changes in OS over time are consistent with increasing life expectancy. Efforts to improve BCSS in male breast cancer are warranted.
JAMA Oncology
Haddad R
IMPORTANCE: There remains an unmet need to improve clinical outcomes in patients with recurrent or metastatic squamous cell carcinoma of the head and neck (R/M SCCHN).
OBJECTIVE: To evaluate clinical benefit of first-line nivolumab plus ipilimumab vs nivolumab alone in patients with R/M SCCHN.
DESIGN, SETTING, AND PARTICIPANTS: The CheckMate 714, double-blind, phase 2 randomized clinical trial was conducted at 83 sites in 21 countries between October 20, 2016, and January 23, 2019. Eligible participants were aged 18 years or older and had platinum-refractory or platinum-eligible R/M SCCHN and no prior systemic therapy for R/M disease. Data were analyzed from October 20, 2016 (first patient, first visit), to March 8, 2019 (primary database lock), and April 6, 2020 (overall survival database lock).
INTERVENTIONS: Patients were randomized 2:1 to receive nivolumab (3 mg/kg intravenously [IV] every 2 weeks) plus ipilimumab (1 mg/kg IV every 6 weeks) or nivolumab (3 mg/kg IV every 2 weeks) plus placebo for up to 2 years or until disease progression, unacceptable toxic effects, or consent withdrawal.
MAIN OUTCOMES AND MEASURES: The primary end points were objective response rate (ORR) and duration of response between treatment arms by blinded independent central review in the population with platinum-refractory R/M SCCHN. Exploratory end points included safety.
RESULTS: Of 425 included patients, 241 (56.7%; median age, 59 [range, 24-82] years; 194 males [80.5%]) had platinum-refractory disease (nivolumab plus ipilimumab, n?=?159; nivolumab, n?=?82) and 184 (43.3%; median age, 62 [range, 33-88] years; 152 males [82.6%]) had platinum-eligible disease (nivolumab plus ipilimumab, n?=?123; nivolumab, n?=?61). At primary database lock, the ORR in the population with platinum-refractory disease was 13.2% (95% CI, 8.4%-19.5%) with nivolumab plus ipilimumab vs 18.3% (95% CI, 10.6%-28.4%) with nivolumab (odds ratio [OR], 0.68; 95.5% CI, 0.33-1.43; P?=?.29). Median duration of response for nivolumab plus ipilimumab was not reached (NR) (95% CI, 11.0 months to NR) vs 11.1 months (95% CI, 4.1 months to NR) for nivolumab. In the population with platinum-eligible disease, the ORR was 20.3% (95% CI, 13.6%-28.5%) with nivolumab plus ipilimumab vs 29.5% (95% CI, 18.5%-42.6%) with nivolumab. The rates of grade 3 or 4 treatment-related adverse events with nivolumab plus ipilimumab vs nivolumab were 15.8% (25 of 158) vs 14.6% (12 of 82) in the population with platinum-refractory disease and 24.6% (30 of 122) vs 13.1% (8 of 61) in the population with platinum-eligible disease.
CONCLUSIONS AND RELEVANCE: The CheckMate 714 randomized clinical trial did not meet its primary end point of ORR benefit with first-line nivolumab plus ipilimumab vs nivolumab alone in platinum-refractory R/M SCCHN. Nivolumab plus ipilimumab was associated with an acceptable safety profile. Research to identify patient subpopulations in R/M SCCHN that would benefit from nivolumab plus ipilimumab over nivolumab monotherapy is warranted.
TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT02823574.
Lancet Oncology
Rahman R, Brastianos PK, Wen PY, Piantadosi S
Successful drug development for people with cancers of the CNS has been challenging. There are multiple barriers to successful drug development including biological factors, rarity of the disease, and ineffective use of clinical trials. Based upon a series of presentations at the First Central Nervous System Clinical Trials Conference hosted by the American Society of Clinical Oncology and the Society for Neuro-Oncology, we provide an overview on drug development and novel trial designs in neuro-oncology. This Review discusses the challenges of therapeutic development in neuro-oncology and proposes strategies to improve the drug discovery process by enriching the pipeline of promising therapies, optimising trial design, incorporating biomarkers, using external data, and maximising efficacy and reproducibility of clinical trials.
Molecular Cell
Otto JE, Ursu O, Wu AP, Winter EB, Cuoco MS, Ma S, Qian K, Michel BC, Buenrostro JD, Berger B, Regev A, Kadoch C
The mammalian SWI/SNF (mSWI/SNF or BAF) family of chromatin remodeling complexes play critical roles in regulating DNA accessibility and gene expression. The three final-form subcomplexes-cBAF, PBAF, and ncBAF-are distinct in biochemical componentry, chromatin targeting, and roles in disease; however, the contributions of their constituent subunits to gene expression remain incompletely defined. Here, we performed Perturb-seq-based CRISPR-Cas9 knockout screens targeting mSWI/SNF subunits individually and in select combinations, followed by single-cell RNA-seq and SHARE-seq. We uncovered complex-, module-, and subunit-specific contributions to distinct regulatory networks and defined paralog subunit relationships and shifted subcomplex functions upon perturbations. Synergistic, intra-complex genetic interactions between subunits reveal functional redundancy and modularity. Importantly, single-cell subunit perturbation signatures mapped across bulk primary human tumor expression profiles both mirror and predict cBAF loss-of-function status in cancer. Our findings highlight the utility of Perturb-seq to dissect disease-relevant gene regulatory impacts of heterogeneous, multi-component master regulatory complexes.
Nature
Clonal Haematopoiesis and Risk of Chronic Liver Disease
Wong WJ, Emdin C, Bick AG, Zekavat SM, Niroula A, Pirruccello JP, Dichtel L, Griffin G, Uddin MM, Gibson CJ, Kovalcik V, Lin AE, McConkey ME, Vromman A, Sellar RS, Kim PG, Agrawal M, Loh PR, McCarroll S, Chung RT, Corey K, Ebert BL, Natarajan P
Chronic liver disease is a major public health burden worldwide1. Although different aetiologies and mechanisms of liver injury exist, progression of chronic liver disease follows a common pathway of liver inflammation, injury and fibrosis2. Here we examined the association between clonal haematopoiesis of indeterminate potential (CHIP) and chronic liver disease in 214,563 individuals from 4 independent cohorts with whole-exome sequencing data (Framingham Heart Study, Atherosclerosis Risk in Communities Study, UK Biobank and Mass General Brigham Biobank). CHIP was associated with an increased risk of prevalent and incident chronic liver disease (odds ratio?=?2.01, 95% confidence interval (95%?CI)?[1.46,?2.79]; P?
Nature Cancer
Bakht MK, Yamada Y, Ku SY, Venkadakrishnan VB, Mizuno K, Ahn SH, Seo JH, Garcia MM, Long HW, Freedman M, Belanger AP, Nguyen QD, Beltran H
Tumor expression of prostate-specific membrane antigen (PSMA) is lost in 15-20% of men with castration-resistant prostate cancer (CRPC), yet the underlying mechanisms remain poorly defined. In androgen receptor (AR)-positive CRPC, we observed lower PSMA expression in liver lesions versus other sites, suggesting a role of the microenvironment in modulating PSMA. PSMA suppression was associated with promoter histone 3 lysine 27 methylation and higher levels of neutral amino acid transporters, correlating with 18F-fluciclovine uptake on positron emission tomography imaging. While PSMA is regulated by AR, we identified a subset of AR-negative CRPC with high PSMA. HOXB13 and AR co-occupancy at the PSMA enhancer and knockout models point to HOXB13 as an upstream regulator of PSMA in AR-positive and AR-negative prostate cancer. These data demonstrate how PSMA expression is differentially regulated across metastatic lesions and in the context of the AR, which may inform selection for PSMA-targeted therapies and development of complementary biomarkers.
Nature Genetics
Ravi A, Arniella MB, Holton M, Freeman SS, Naranbhai V, Stewart C, Leshchiner I, Akiyama Y,
Sakhi M, Kamesan V, Ricciuti B, Digumarthy SR, Mino-Kenudson M, Jänne PA, Awad MM, Shaw AT, Hacohen N, Getz G, Gainor JF
Anti-PD-1/PD-L1 agents have transformed the treatment landscape of advanced non-small cell lung cancer (NSCLC). To expand our understanding of the molecular features underlying response to checkpoint inhibitors in NSCLC, we describe here the first joint analysis of the Stand Up To Cancer-Mark Foundation cohort, a resource of whole exome and/or RNA sequencing from 393 patients with NSCLC treated with anti-PD-(L)1 therapy, along with matched clinical response annotation. We identify a number of associations between molecular features and outcome, including (1) favorable (for example, ATM altered) and unfavorable (for example, TERT amplified) genomic subgroups, (2) a prominent association between expression of inducible components of the immunoproteasome and response and (3) a dedifferentiated tumor-intrinsic subtype with enhanced response to checkpoint blockade. Taken together, results from this cohort demonstrate the complexity of biological determinants underlying immunotherapy outcomes and reinforce the discovery potential of integrative analysis within large, well-curated, cancer-specific cohorts.
American Journal of Gastroenterology
Ugai T, Haruki K, Chan AT, Akimoto N, Fujiyoshi K, Nishihara R, Giannakis M, Song M, Nowak JA, Ogino S
Blood Advances
Amonoo HL, Johnson PC, Nelson AM, Clay MA, Daskalakis E, Newcomb RA, Deary EC, Mattera EF, Yang D, Cronin K, Boateng K, El-Jawahri A
Blood Advances
Shimony S, Liu Y, Valtis YK, Paolino JD, Place AE, Brunner AM, Weeks LD, Silverman LB,
Vrooman LM, Neuberg DS, Stone RM, DeAngelo DJ, Luskin MR
Blood Advances
Correcting the Record on Anemia of Aging — a Statistical Reanalysis
Fell GG, Nathan DG, Neuberg DS
Cancer
What's the Reality for CDK4/6 Inhibitors: Clinical Trials Real-World Evidence?
Trapani D, Mayer EL
Cancer
Ligibel JA, Zheng Y, Barry WT, Emmons KM, Partridge AH
Cancer
One Fixed Dosing of a Poly (Adenosine Diphosphate Ribose) Polymerase Inhibitor Does Not Fit All
Liu JF
Cancer Chemotherapy and Pharmacology
Parikh A, Ryan DP, Cleary JM
Cancer Letters
Morimoto Y, Yamashita N, Fushimi A, Haratake N, Daimon T, Bhattacharya A, Ahmad R, Kufe DW
Cancer Treatment Reviews
Lin NU, Tolaney SM
Cannabis and Cannabinoid Research
Nayak MM, Chai PR, Tung S, Sannes TS, Yusufov M, Braun IM
Cell Death and Disease
Quantifying Requirements for Mitochondrial Apoptosis in CAR T Killing of Cancer Cells
Pourzia AL, Olson ML, Bailey SR, Boroughs AC, Aryal A, Ryan J, Maus MV, Letai A
Cells
Copy Number Variation in Inflammatory Breast Cancer
Hazra A, Polyak K, Nakhlis F, Harrison BT, Giordano A, Overmoyer B, Lynce F
Clinical Breast Cancer
Lewinsohn R, Zheng Y, Peppercorn J, Come S, Snow C, Ginsburg ES, Partridge AH
Current Treatment Options in Oncology
Brett JO, Mayer EL
Developmental Cell
Smooth Muscle Contributes to the Development and Function of a Layered Intestinal Stem Cell Niche
McCarthy N, Tie G, Madha S, He R, Kraiczy J, Maglieri A, Shivdasani RA
Expert Review of Anticancer Therapy
Emerging Predictive Biomarkers in the Management of Bone and Soft Tissue Sarcomas
Haddox CL
Haematologica
Baumeister SHC
Hematology/Oncology Clinics of North America
Fetal Hemoglobin Regulation in Beta-Thalassemia
Lu HY, Orkin SH, Sankaran VG
Hematology/Oncology Clinics of North America
Targeted Therapy for Non-Small Cell Lung Cancer: First Line and Beyond
Brea E, Rotow J
International Journal of Radiation Oncology, Biology, Physics
Campbell K, Armant M, Pal S, Haas-Kogan DA, DuBois SG
Journal of the American College of Radiology
Frequency and Clinical Utility of Alerts for Intra-Institutional Radiologist Discrepant Opinions
DiPiro PJ, Licaros A, Zhao AH, Glazer DI, Healey MJ, Curley PJ, Giess CS, Khorasani R
Journal of the American Geriatrics Society
Evaluation of Interdisciplinary Care Pathway Implementation in Older Elective Surgery Patients
Hu FY, Rowe KA, O'Mara LM, Bulger A, Bleday R, Groff MW, Cooper Z, Bernacki RE
Journal of Cancer Survivorship
Contreras-Chavez P, Nekhlyudov L
Journal of Experimental Medicine
PD-1 Blockade and CDK4/6 Inhibition Augment Nonoverlapping Features of T Cell Activation in Cancer
Ali LR, Garrido-Castro AC, Lenehan PJ, Bollenrucher N, Stump CT, Dougan M, Shapiro GI,
Tolaney SM, Dougan SK
Journal of Immunology
cIAP1/2 Antagonism Induces Antigen-Specific T Cell-Dependent Immunity
Ventre KS, Roehle K, Bello E, Bhuiyan AM, Biary T, Crowley SJ, Bruck PT, Heckler M, Lenehan PJ,
Ali LR, Stump CT, Lippert V, Clancy-Thompson E, Conce Alberto WD, Hoffman MT, Qiang L,
Dougan M, Dougan SK
Journal of Medicinal Chemistry
Catalytic Degraders Effectively Address Kinase Site Mutations in EML4-ALK Oncogenic Fusions
Gao Y, Jiang B, Kim H, Berberich MJ, Che J, Donovan KA, Hatcher JM, Huerta F, Kwiatkowski NP,
Liu Y, Liuni PP, Metivier RJ, Murali VK, Nowak RP, Fischer ES, Gray NS, Jones LH
Journal of Pain and Symptom Management
Measuring Palliative Care Communication via Telehealth: A Pilot Study
Tarbi EC, Durieux BN, Brain JM, Kwok A, Umeton R, Samineni S, Tulsky JA, Lindvall C
Journal of Palliative Medicine
Caring for People We Know: An Unrecognized Risk for Burnout?
Morris SE, Revette AC, Brandoff DE, Leiter RE, Sannes TS, Thomas JD
Journal of Palliative Medicine
Jain N, Bernacki RE, Lee KA, Siegel JH, Yenulevich EG, Lally KM
Journal of Palliative Medicine
Cleveland RW, Ullrich CK
Journal of Surgical Oncology
Hong JH, Swami N, Lam MB
JAMA Surgery
Kantor O, King TA, Freedman RA, Mayer EL, Mittendorf EA
JAMIA Open
Durieux BN, Zverev SR, Tarbi EC, Kwok A, Sciacca K, Tulsky JA, Lindvall C
JCO Oncology Practice
Snaman JM, Mazzola E, Feifer D, Morris SE, Wolfe J
JCO Oncology Practice
The Day One Talk, 20 Years Later: What Have We Learned?
Mack JW
JCO Oncology Practice
Lynch DM, Menon S, Mazzola E, Costa J, Jabaley T
JMIR Research Protocols
Wilson R, Kang DW, Norris M, Uno H, Ligibel J, Guenette J, Christopher C, Dieli-Conwright C
Leukemia
Ryan CE, Tyekucheva S, Hackett LR, Collins MC, Fernandes SM, Ren Y, Zhou Y, McDonough MM, Walker HA, McEwan MR, Abramson JS, Jacobsen ED, LaCasce AS, Fisher DC, Brown JR, Davids MS
Molecular Cancer Research
Significance of RB Loss in Unlocking Phenotypic Plasticity in Advanced Cancers
Venkadakrishnan VB, Yamada Y, Weng K, Idahor O, Beltran H
Nature Reviews Cancer
Dynamics and Specificities of T Cells in Cancer Immunotherapy
Oliveira G, Wu CJ
Neuro-Oncology Practice
The Predictive Value of Partial MGMT Promoter Methylation for IDH-Wild-Type Glioblastoma Patients
Torre M, Wen PY, Iorgulescu JB
Oncologist
McDermott D, Choueiri TK
Oncologist
Managing Ibrutinib-Intolerant Patients With B-Cell Malignancies
Sarosiek S, Castillo JJ
Pediatric Blood and Cancer
Nekhlyudov L, Snow C, Knelson LP, Dibble KE, Partridge AH
Scandinavian Journal of Medicine and Science in Sports
Gonzalo-Encabo P, Christopher CN, Normann AJ, Yunker AG Norris MK, Dieli-Conwright CM
Science Immunology
Reyna ÁG, Griffin GK
Seminars in Radiation Oncology
Pharmacologic Pain Management: What Radiation Oncologists Should Know
Skarf LM, Jones KF, Meyerson JL, Abrahm JL
Statistics in Medicine
On Assessing Survival Benefit of Immunotherapy Using Long-Term Restricted Mean Survival Time
Horiguchi M, Uno H
Transplantation and Cellular Therapy
Nikiforow S, Frigault MJ
Transplantation and Cellular Therapy
Vergara-Cadavid J, Johnson PC, Kim HT, Yi A, Sise ME, Leaf DE, Hanna PE, Ho VT, Cutler CS,
Antin JH, Gooptu M, Kelkar A, Wells SL, Nikiforow S, Koreth J, Romee R, Soiffer RJ, Shapiro RM, Gupta S