Welcome to Dana-Farber's Research News
March 1, 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
Fathi AT, Stone RM, Lane AA
Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is a rare hematologic malignancy with historically poor outcomes and no worldwide consensus treatment approach. Unique among most hematologic malignancies for its frequent cutaneous involvement, BPDCN can also invade other extramedullary compartments, including the central nervous system. Generally affecting older adults, many patients are unfit to receive intensive chemotherapy, and although hematopoietic stem cell transplantation is preferred for younger, fit individuals, not all are eligible. One recent therapeutic breakthrough is that all BPDCNs express CD123 (IL3R?) and that this accessible surface marker can be pharmacologically targeted. The first-in-class agent for BPDCN, tagraxofusp, which targets CD123, was approved in December 2018 in the United States for patients with BPDCN aged ?2 years. Despite favorable response rates in the frontline setting, many patients still relapse in the setting of monotherapy, and outcomes in patients with relapsed/refractory BPDCN remain dismal. Therefore, novel approaches targeting both CD123 and other targets are actively being investigated. To begin to formally address the state of the field, we formed a new collaborative initiative, the North American BPDCN Consortium (NABC). This group of experts, which includes a multidisciplinary panel of hematologists/oncologists, hematopoietic stem cell transplant physicians, pathologists, dermatologists, and pediatric oncologists, was tasked with defining the current standard of care in the field and identifying the most important research questions and future directions in BPDCN. The position findings of the NABC's inaugural meetings are presented herein.
Cancer
What's the reality for CDK4/6 inhibitors: Clinical trials or real-world evidence?
Trapani D, Mayer EL
Clinical trials and real-world evidence (RWE) present conflicting results on the benefit of cyclin-dependent kinase 4 and 6 inhibitors for patients with advanced hormone receptor (HR)–positive and human epidermal growth factor receptor-2 overexpressing breast cancer. How can RWE be interpreted and used to help guide clinical decisions?
Cancer Discovery
Discovery of Targets for Immune-Metabolic Antitumor Drugs Identifies Estrogen-Related Receptor Alpha
Sahu A, Wang X, Munson P, Wang X, Gu SS, Qian G, Nicol P, Zeng Z, Wang C, Tokheim C, Zhang W, Fu J, Wang J, Liu JS, Juric D, Meyer CA, Liu XS, Fisher DE, Flaherty KT
Drugs that kill tumors through multiple mechanisms have the potential for broad clinical benefits. Here, we first developed an in silico multiomics approach (BipotentR) to find cancer cell-specific regulators that simultaneously modulate tumor immunity and another oncogenic pathway and then used it to identify 38 candidate immune-metabolic regulators. We show the tumor activities of these regulators stratify patients with melanoma by their response to anti-PD-1 using machine learning and deep neural approaches, which improve the predictive power of current biomarkers. The topmost identified regulator, ESRRA, is activated in immunotherapy-resistant tumors. Its inhibition killed tumors by suppressing energy metabolism and activating two immune mechanisms: (i) cytokine induction, causing proinflammatory macrophage polarization, and (ii) antigen-presentation stimulation, recruiting CD8+ T cells into tumors. We also demonstrate a wide utility of BipotentR by applying it to angiogenesis and growth suppressor evasion pathways. BipotentR (http://bipotentr.dfci.harvard.edu/) provides a resource for evaluating patient response and discovering drug targets that act simultaneously through multiple mechanisms.
SIGNIFICANCE: BipotentR presents resources for evaluating patient response and identifying targets for drugs that can kill tumors through multiple mechanisms concurrently. Inhibition of the topmost candidate target killed tumors by suppressing energy metabolism and effects on two immune mechanisms.
Cancer Discovery
Dutta AK, Alberge JB, Lightbody ED, Boehner CJ, Dunford A, Sklavenitis-Pistofidis R,
Mouhieddine TH, Cowan AN, Su NK, Horowitz EM, Barr H, Hevenor L, Beckwith JB, Perry J,
Cao A, Lin Z, Nadeem O, Stewart C, Getz G, Ghobrial IM
Multiple myeloma (MM) develops from well-defined precursor stages; however, invasive bone marrow (BM) biopsy limits screening and monitoring strategies for patients. We enumerated circulating tumor cells (CTC) from 261 patients (84 monoclonal gammopathy of undetermined significance, 155 smoldering multiple myeloma, and 22 MM), with neoplastic cells detected in 84%. We developed a novel approach, MinimuMM-seq, which enables the detection of translocations and copy-number abnormalities through whole-genome sequencing of highly pure CTCs. Application to CTCs in a cohort of 51 patients, 24 with paired BM, was able to detect 100% of clinically reported BM biopsy events and could replace molecular cytogenetics for diagnostic yield and risk classification. Longitudinal sampling of CTCs in 8 patients revealed major clones could be tracked in the blood, with clonal evolution and shifting dynamics of subclones over time. Our findings provide proof of concept that CTC detection and genomic profiling could be used clinically for monitoring and managing disease in MM.
SIGNIFICANCE: In this study, we established an approach enabling the enumeration and sequencing of CTCs to replace standard molecular cytogenetics. CTCs harbored the same pathognomonic MM abnormalities as BM plasma cells. Longitudinal sampling of serial CTCs was able to track clonal dynamics over time and detect the emergence of high-risk genetic subclones. This article is highlighted in the In This Issue feature, p. 247.
Cell
Cryo-EM Structure of the RADAR Supramolecular Anti-Phage Defense Complex
Duncan-Lowey B, Johnson AG, Rawson S, Mayer ML, Amitai G, Kranzusch PJ
RADAR is a two-protein bacterial defense system that was reported to defend against phage by "editing" messenger RNA. Here, we determine cryo-EM structures of the RADAR defense complex, revealing RdrA as a heptameric, two-layered AAA+ ATPase and RdrB as a dodecameric, hollow complex with twelve surface-exposed deaminase active sites. RdrA and RdrB join to form a giant assembly up to 10 MDa, with RdrA docked as a funnel over the RdrB active site. Surprisingly, our structures reveal an RdrB active site that targets mononucleotides. We show that RdrB catalyzes ATP-to-ITP conversion in vitro and induces the massive accumulation of inosine mononucleotides during phage infection in vivo, limiting phage replication. Our results define ATP mononucleotide deamination as a determinant of RADAR immunity and reveal supramolecular assembly of a nucleotide-modifying machine as a mechanism of anti-phage defense.
Journal of Clinical Oncology
Sattler M
The receptor tyrosine kinase MET is widely expressed in normal tissue and is typically activated by its ligand hepatocyte growth factor. Some solid tumors and particularly non–small-cell lung cancer (NSCLC) cells are frequently associated with elevated levels of MET or hepatocyte growth factor. A variety of mutations in MET are known to occur in lung cancers at a low frequency in the tyrosine kinase domain, exon 14 skipping mutations, and others. Treatment of patients with mutational activation of MET extends survival in NSCLC harboring MET exon 14 skipping alterations. Capmatinib and tepotinib are US Food and Drug Administration–approved MET-specific inhibitors available for the treatment of patients with active MET, in particular the exon 14 skipping mutation (see for review Mathieu et al), but in general, they would not be expected to be active in cancers with high MET protein expression.
Journal of Clinical Oncology
LaCasce AS, Abramson J
PURPOSE: Patients with bulky stage I/II classic Hodgkin lymphoma (cHL) are typically treated with chemotherapy followed by radiation. Late effects associated with radiotherapy include increased risk of second cancer and cardiovascular disease. We tested a positron emission tomography (PET)-adapted approach in patients with bulky, early-stage cHL, omitting radiotherapy in patients with interim PET-negative (PET-) disease and intensifying treatment in patients with PET-positive (PET+) disease.
METHODS: Eligible patients with bulky disease (mass > 10 cm or 1/3 the maximum intrathoracic diameter on chest x-ray) received two cycles of doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD) followed by interim fluorodeoxyglucose PET (PET2). Patients with PET2-, defined as 1-3 on the 5-point scale, received four additional cycles of doxorubicin, bleomycin, vinblastine, and dacarbazine. Patients with PET2+ received four cycles of escalated bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, procarbazine, and prednisone followed by 30.6 Gy involved-field radiation.
RESULTS: Of 94 evaluable patients, 53% were female with median age 30 years (range, 18-58 years). Eight-five (90%) had stage II disease, including 48 (51%) with stage IIB/IIBE. Seventy-eight (78%) were PET2- and 21 (22%) were PET2+. The predominant toxicity was neutropenia, with 9% of patients developing febrile neutropenia and one developing sepsis. The primary end point of 3-year progression-free survival (PFS) was 93.1% in PET2- and 89.7% in PET2+ patients. Three-year overall survival was 98.6% and 94.4%, respectively. The estimated hazard ratio comparing PFS of patients with PET2+ and patients with PET2- was 1.03 (85% upper bound 2.38) and was significantly less than the null hypothesis of 4.1 (one-sided P = .04).
CONCLUSION: Our study of PET-adapted therapy in bulky stage I/II cHL met its primary goal and was associated with an excellent 3-year PFS rate of 92.3% in all patients, with the majority being spared radiotherapy and exposure to intensified chemotherapy.
Journal of Clinical Oncology
Rare Germline ATM Variants Influence the Development of Chronic Lymphocytic Leukemia
Lampson BL, Gupta A, Tyekucheva S, Mashima K, Wang Z, Wojciechowska N, Shaughnessy CJ, Baker PO, Fernandes SM, Shupe S, Machado JH, Fardoun R, Kim AS, Brown JR
PURPOSE: Germline missense variants of unknown significance in cancer-related genes are increasingly being identified with the expanding use of next-generation sequencing. The ataxia telangiectasia-mutated (ATM) gene on chromosome 11 has more than 1,000 germline missense variants of unknown significance and is a tumor suppressor. We aimed to determine if rare germline ATM variants are more frequent in chronic lymphocytic leukemia (CLL) compared with other hematologic malignancies and if they influence the clinical characteristics of CLL.
METHODS: We identified 3,128 patients (including 825 patients with CLL) in our hematologic malignancy clinic who had received clinical-grade sequencing of the entire coding region of ATM. We ascertained the comparative frequencies of germline ATM variants in categories of hematologic neoplasms, and, in patients with CLL, we determined whether these variants affected CLL-associated characteristics such as somatic 11q deletion.
RESULTS: Rare germline ATM variants are present in 24% of patients with CLL, significantly greater than that in patients with other lymphoid malignancies (16% prevalence), myeloid disease (15%), or no hematologic neoplasm (14%). Patients with CLL with germline ATM variants are younger at diagnosis and twice as likely to have 11q deletion. The ATM variant p.L2307F is present in 3% of patients with CLL, is associated with a three-fold increase in rates of somatic 11q deletion, and is a hypomorph in cell-based assays.
CONCLUSION: Germline ATM variants cluster within CLL and affect the phenotype of CLL that develops, implying that some of these variants (such as ATM p.L2307F) have functional significance and should not be ignored. Further studies are needed to determine whether these variants affect the response to therapy or account for some of the inherited risk of CLL.
Journal of Clinical Oncology
McDermott DF, Lawrence DP, Hodi FS
PURPOSE: Programmed cell death 1 (PD-1) is an inhibitory receptor expressed by activated T cells that downmodulates effector functions and limits the generation of immune memory. PD-1 blockade can mediate tumor regression in a substantial proportion of patients with melanoma, but it is not known whether this is associated with extended survival or maintenance of response after treatment is discontinued.
PATIENTS AND METHODS: Patients with advanced melanoma (N = 107) enrolled between 2008 and 2012 received intravenous nivolumab in an outpatient setting every 2 weeks for up to 96 weeks and were observed for overall survival, long-term safety, and response duration after treatment discontinuation.
RESULTS: Median overall survival in nivolumab-treated patients (62% with two to five prior systemic therapies) was 16.8 months, and 1- and 2-year survival rates were 62% and 43%, respectively. Among 33 patients with objective tumor regressions (31%), the Kaplan-Meier estimated median response duration was 2 years. Seventeen patients discontinued therapy for reasons other than disease progression, and 12 (71%) of 17 maintained responses off-therapy for at least 16 weeks (range, 16 to 56+ weeks). Objective response and toxicity rates were similar to those reported previously; in an extended analysis of all 306 patients treated on this trial (including those with other cancer types), exposure-adjusted toxicity rates were not cumulative.
CONCLUSION: Overall survival following nivolumab treatment in patients with advanced treatment-refractory melanoma compares favorably with that in literature studies of similar patient populations. Responses were durable and persisted after drug discontinuation. Long-term safety was acceptable. Ongoing randomized clinical trials will further assess the impact of nivolumab therapy on overall survival in patients with metastatic melanoma.
Journal of Clinical Oncology
Art of Oncology: Yard Work
Abel GA
The lawn in Rhode Island surprises me seasonally and in-between:
JAMA Oncology
Hyaluronic Acid Spacer for Hypofractionated Prostate Radiation Therapy: A Randomized Clinical Trial
Orio PF 3rd, King MT
IMPORTANCE: Hypofractionated radiation therapy (RT) for prostate cancer has been associated with greater acute grade 2 gastrointestinal (GI) toxic effects compared with conventionally fractionated RT.
OBJECTIVE: To evaluate whether a hyaluronic acid rectal spacer could (1) improve rectal dosimetry and (2) affect acute grade 2 or higher GI toxic effects for hypofractionated RT.
DESIGN, SETTING, AND PARTICIPANTS: This randomized clinical trial was conducted from March 2020 to June 2021 among 12 centers within the US, Australia, and Spain, with a 6-month follow-up. Adult patients with biopsy-proven, T1 to T2 prostate cancer with a Gleason score 7 or less and prostate-specific antigen level of 20 ng/mL or less (to convert to ?g/L, multiply by 1) were blinded to the treatment arms. Of the 260 consented patients, 201 patients (77.3%) were randomized (2:1) to the presence or absence of the spacer. Patients were stratified by intended 4-month androgen deprivation therapy use and erectile quality.
MAIN OUTCOMES AND MEASURES: For the primary outcome, we hypothesized that more than 70% of patients in the spacer group would achieve a 25% or greater reduction in the rectal volume receiving 54 Gy (V54). For the secondary outcome, we hypothesized that the spacer group would have noninferior acute (within 3 months) grade 2 or higher GI toxic effects compared with the control group, with a margin of 10%.
RESULTS: Of the 201 randomized patients, 8 (4.0%) were Asian, 26 (12.9%) Black, 42 (20.9%) Hispanic or Latino, and 153 (76.1%) White; the mean (SD) age for the spacer group was 68.6 (7.2) years and 68.4 (7.3) years for the control group. For the primary outcome, 131 of 133 (98.5%; 95% CI, 94.7%-99.8%) patients in the spacer group experienced a 25% or greater reduction in rectum V54, which was greater than the minimally acceptable 70% (P?
CONCLUSIONS AND RELEVANCE: The trial results suggest that rectal spacing with hyaluronic acid improved rectal dosimetry and reduced acute grade 2 or higher GI toxic effects. Rectal spacing should potentially be considered for minimizing the risk of acute grade 2 or higher toxic effects for hypofractionated RT.
TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT04189913.
JAMA Oncology
Ricciuti B, Wang X, Awad MM
In Reply We thank Aslan et al and Zhang and Zhang for their interest in our cohort study on the association of tumor mutation burden (TMB) with clinical outcomes to programmed cell death–1 (PD-1) or PD-1 ligand (PD-L1) blockade across PD-L1 expression levels in non–small cell lung cancer (NSCLC). As Aslan et al noted, retrospective analyses suggest that both platinum-based chemotherapy and radiation therapy may be associated with higher PD-L1 expression levels in NSCLC. These findings, though not definitive and limited by studies with small sample sizes, raise the question about the use of archival tissue for determining PD-L1 expression levels to guide treatment decisions. Additionally, our group previously showed that PD-L1 expression tends to be higher with increasing lung cancer stage, further highlighting the importance of using recent tissue for measuring potentially dynamic biomarkers such as PD-L1. In our current study, PD-L1 was assessed in samples collected immediately prior to the start of immunotherapy in all patients who received first-line immunotherapy and for the vast majority of patients who received immunotherapy as a second or subsequent line.
Nature Cell Biology
Lu DY, Ellegast JM, Ross KN, Malone CF, Lin S, Mabe NW, Dharia NV, Meyer A, Conway A, Su AH, Seong BKA, Adane B, Gray NS, Rivera MN, Stegmaier K
Transcription factors (TFs) are frequently mutated in cancer. Paediatric cancers exhibit few mutations genome-wide but frequently harbour sentinel mutations that affect TFs, which provides a context to precisely study the transcriptional circuits that support mutant TF-driven oncogenesis. A broadly relevant mechanism that has garnered intense focus involves the ability of mutant TFs to hijack wild-type lineage-specific TFs in self-reinforcing transcriptional circuits. However, it is not known whether this specific type of circuitry is equally crucial in all mutant TF-driven cancers. Here we describe an alternative yet central transcriptional mechanism that promotes Ewing sarcoma, wherein constraint, rather than reinforcement, of the activity of the fusion TF EWS-FLI supports cancer growth. We discover that ETV6 is a crucial TF dependency that is specific to this disease because it, counter-intuitively, represses the transcriptional output of EWS-FLI. This work discovers a previously undescribed transcriptional mechanism that promotes cancer.
Nature Communications
Accelerating Inhibitor Discovery for Deubiquitinating Enzymes
Chan WC, Liu X, Magin RS, Girardi NM, Ficarro SB, Hu W, Tarazona Guzman MI, Starnbach CA,
Felix A, Adelmant G, Varca AC, Hu B, Bratt AS, DaSilva E, Schauer NJ, Jaen Maisonet I, Dolen EK, Ayala AX, Marto JA, Buhrlage SJ
Deubiquitinating enzymes (DUBs) are an emerging drug target class of ~100 proteases that cleave ubiquitin from protein substrates to regulate many cellular processes. A lack of selective chemical probes impedes pharmacologic interrogation of this important gene family. DUBs engage their cognate ligands through a myriad of interactions. We embrace this structural complexity to tailor a chemical diversification strategy for a DUB-focused covalent library. Pairing our library with activity-based protein profiling as a high-density primary screen, we identify selective hits against 23 endogenous DUBs spanning four subfamilies. Optimization of an azetidine hit yields a probe for the understudied DUB VCPIP1 with nanomolar potency and in-family selectivity. Our success in identifying good chemical starting points as well as structure-activity relationships across the gene family from a modest but purpose-build library challenges current paradigms that emphasize ultrahigh throughput in vitro or virtual screens against an ever-increasing scope of chemical space.
Proceedings of the National Academy of Sciences of the U.S.A.
Qiu Y, Shen X, Wight AE, Kim HJ, Cantor H
Alzheimer's disease (AD) is the most common form of incurable dementia and represents a critical public health issue as the world's population ages. Although microglial dysregulation is a cardinal feature of AD, the extensive heterogeneity of these immunological cells in the brain has impeded our understanding of their contribution to this disease. Here, we identify a pathogenic microglial subset which expresses the CD11c surface marker as the sole producer of Osteopontin (OPN) in the 5XFAD mouse model of AD. OPN production divides Disease-Associated Microglia (DAM) into two functionally distinct subsets, i.e., a protective CD11c+OPN- subset that robustly ingests amyloid ? (A?) in a noninflammatory fashion and a pathogenic CD11c+OPN+ subset that produces proinflammatory cytokines and fails to ingest significant amounts of A?. Genetic ablation of OPN or administration of monoclonal anti-OPN antibody to 5XFAD mice reduces proinflammatory microglia, plaque formation, and numbers of dystrophic neurites and results in improved cognitive function. Analysis of brain tissue from AD patients indicates that levels of OPN-producing CD11c+ microglia correlate strongly with the degree of cognitive deficit and AD neuropathology. These findings define an OPN-dependent pathway to disease driven by a distinct microglial subset, and identify OPN as a novel therapeutic target for potentially effective immunotherapy to treat AD.
Science
Structures of BIRC6-Client Complexes Provide a Mechanism of Smac-Mediated Release of Caspases
Hunkeler M, Jin CY, Fischer ES
Tight regulation of apoptosis is essential for metazoan development and prevents diseases such as cancer and neurodegeneration. Caspase activation is central to apoptosis and inhibitor of apoptosis (IAP) proteins are the principal actors that restrain caspase activity and are therefore attractive therapeutic targets. IAPs, in turn, are regulated by mitochondria-derived pro-apoptotic factors such as Smac and HtrA2. Through a series of cryo-electron microscopy (cryo-EM) structures of full-length human baculoviral IAP repeat-containing protein 6 (BIRC6) bound to Smac, caspases, and HtrA2, we provide a molecular understanding for BIRC6-mediated caspase inhibition and its release by Smac. The architecture of BIRC6, together with near-irreversible binding of Smac, elucidates how the IAP inhibitor Smac can effectively control a processive ubiquitin ligase to respond to apoptotic stimuli.
American Journal of Hematology
Bruton Tyrosine Kinase Inhibitors in the Management of Waldenström Macroglobulinemia
Castillo JJ, Sarosiek S, Treon SP
American Journal of Hematology
Castillo JJ
Blood Advances
Olesinski EA, Garcia JS, Letai A
Blood Advances
Stone RM
Blood Cancer Journal
Circulating Th17 T Cells at Treatment Onset Predict Autoimmune Toxicity of PI3Kd Inhibitors
Gadi D, Martindale SP, Khalsa J, Chen PH, Fernandes SM, Wang Z, Tyekucheva S, Machado JH, Fisher DC, Armand P, Davids MS, Rodig S, Brown JR
Blood Cancer Journal
Verselis SJ, O'Keefe M, Cobb J, Talluri S, Hideshima T, Dorfman DM, Anderson KC, Adamia S
British Journal of Haematology
Jing CB, Prutsch N, He S, Zimmerman MW, Look AT
Breast
How I Treat HER2-Low Advanced Breast Cancer
Tolaney SM, Tarantino P
Breast Cancer Research Treatment
Rosenberg SM, Zheng Y, Gelber S, Poorvu P, Sella T, Wassermann J, Come S, Peppercorn J, Sepucha KR, Partridge AH
Cancer Chemotherapy and Pharmacology
Parikh A, Ryan DP, Cleary JM
Cancer Research
Williams HL, Dias Costa A, Zhang J, Raghavan S, Winter PS, Kapner KS, Ginebaugh SP,
Väyrynen SA, Väyrynen JP, Yuan C, Navia AW, Wang J, Yang A, Bosse TL, Kalekar RL, Lowder KE, Lau MC, Elganainy D, Morales-Oyarvide V, Rubinson DA, Singh H, Perez K, Cleary JM, Clancy TE, Wang J, Mancias JD, Brais LK, Hill ER, Hahn WC, Shalek AK, Aguirre AJ, Nowak JA, Wolpin BM
Cancer Research
Hagel KR, Arafeh R, Gang S, Arnoff TE, Larson RC, Doench JG, Mathewson ND, Wucherpfennig KW, Maus MV, Hahn WC
Clinical Cancer Research
BRD9 Degradation Disrupts Ribosome Biogenesis in Multiple Myeloma
Kurata K, Samur MK, Liow P, Wen K, Yamamoto L, Liu J, Morelli E, Gulla A, Tai YT, Qi J, Hideshima T, Anderson KC
Clinical Gastroenterology and Hepatology
Tayob N
Digestive Diseases and Sciences
Standard Adult Gastric Emptying Scintigraphy Criteria Is Applicable for Partial Meal Ingestion
Shah H, Prado DEA, Dong JW, Chow DZ, Kuo B, Voss SD, Jacene HA, Robertson MS, Ng TSC
European Urology
Bakouny Z, El Zarif T, Ravi P, Steinharter JA, Xie W, Choueiri TK
HemaSphere
Interim Positron Emission Tomography During Frontline Chemoimmunotherapy for Follicular Lymphoma
Merryman RW, Redd R, Park H, Spilberg G, Robertson M, Chase M, Jeter E, Ahn IE, Brown JR, Crombie J, Davids MS, Fisher DC, Jacobsen E, Jacobson CA, Kim AI, LaCasce AS, Ng SY,
Odejide OO, Parry EM, Armand P, Jacene H
Hematology/Oncology Clinics of North America
Burstein HJ
Hematology/Oncology Clinics of North America
Multidisciplinary Management of Brain Metastasis from Breast Cancer
Trapani D, Aizer AA, Lin NU
Hematology/Oncology Clinics of North America
Role of Immunotherapy in Early- and Late-Stage Triple-Negative Breast Cancer
Morganti S, Tolaney SM
Hematology/Oncology Clinics of North America
Surgical Management of the Axilla for Breast Cancer
Laws A, Kantor O, King TA
JAMIA Open
Durieux BN, Zverev SR, Tarbi EC, Kwok A, Sciacca K, Tulsky JA, Lindvall C
JCI Insight
Developing SHP2-Based Combination Therapy for KRAS-Amplified Cancer
Li T, Kikuchi O, Zhou J, Wang Y, Bastl K, Gokhale P, Knott A, Zhang Y, Doench JG, Bass AJ
JCI Insight
Heterogeneity of B Cell Lymphopoiesis in Patients with Premalignant and Active Myeloma
Jakubikova J, Hideshima T, Richardson PG, Dorfman DM, Anderson KC
JCO Oncology Practice
Snaman JM, Mazzola E, Feifer D, Morris SE, Wolfe J
JCO Oncology Practice
Patel AK, Glotzbecker B, Leblebjian H, Simmons J
Journal of Adolescent and Young Adult Oncology
Phillips CS, Bockhoff J, Buchbinder E, Frazier AL, LaCasce A, Ligibel J, Luskin MR, Woods H, Knoerl R
Journal of Cancer Education
Leiter RE, Varas MTB, Miralda K, Muneton-Castano Y, Revette A, Cronin C, Lopez A, Enzinger AC
Journal of ImmunoTherapy of Cancer
MUC1-C is a Master Regulator of MICA/B NKG2D Ligand and Exosome Secretion in Human Cancer Cells
Morimoto Y, Yamashita N, Daimon T, Yamano S, Haratake N, Ishikawa S, Bhattacharya A, Fushimi A, Ahmad R, Dashevsky O, Mitsiades C, Kufe D
Journal of Music Therapy
Knoerl R, Mazzola E, Woods H, Buchbinder E, Frazier L, LaCasce A, Luskin MR, Phillips CS, Ligibel J
Journal of Pain and Symptom Management
Shared Decision Making in the Geriatric Surgery Verification Program: Assessing Baseline Performance
Streid JL, Lee KC, Bader AM, Jarman MP, Cooper Z, Lindvall C
Journal of the American Academy of Dermatology
Zhong CS, Horiguchi M, Uno H, Ukaegbu C, Chittenden A, LeBoeuf NR, Syngal S, Nambudiri VE, Yurgelun MB
Journal of Thoracic Oncology
Alessi JV, Ricciuti B, Wang X, Vaz VR, Lamberti G, Frias RL, Venkatraman D, Pecci F, Recondo G,
Di Federico A, Barrichello A, Park H, Nishino M, Hambelton GM, Digumarthy S, Johnson BE, Christiani DC, Lin X, Gainor JF, Lin JJ, Awad MM
Korean Journal of Radiology
Network Radiology: Future of Imaging Practice in the Post COVID-19 Era
Shinagare AB, Khorasani R
Leukemia
Network Radiology: Future of Imaging Practice in the Post COVID-19 Era
Shinagare AB, Khorasani R
Leukemia Research
Raman HS, Kim SE, DeAngelo DJ, Stevenson KE, Neuberg D, Winer ES, Wadleigh M, Garcia JS,
Kim AS, Stone RM, Ho VT, Luskin MR
Nature Reviews Clinical Oncology
Perioperative Immunotherapy for Renal Cell Carcinoma: Looking Beyond the Data
Labaki C, Choueiri TK
Neoplasia
Pediatric Low-Grade Glioma: Targeted Therapeutics and Clinical Trials in the Molecular Era
Liu KX, Haas-Kogan DA, Bandopadhayay P
Neuro-Oncology
Gonzalez Castro LN, Liu I, Filbin M
Oncologist
Managing Ibrutinib-Intolerant Patients with B-Cell Malignancies
Sarosiek S, Castillo JJ
Pediatric Blood and Cancer
Mack JW
Psycho-Oncology
Proxy Ratings of Psychological Well-Being in Patients with Primary Brain Tumors: A Systematic Review
Sannes TS, Yusufov M, Amonoo HL, Broden EG, Burgers DE, Bain P, Pozo-Kaderman C, Miran DM, Smith TS, Braun IM, Pirl WF
Radiology
Advances in Thoracic Imaging: Key Developments in the Past Decade and Future Directions
Nishino M
Transplantation and Cellular Therapy
Delirium and Healthcare Utilization in Patients Undergoing Hematopoietic Stem Cell Transplantation
Amonoo HL, Markovitz NH, Johnson PC, Kwok A, Dale C, Deary EC, Daskalakis E, Choe JJ, Yamin N, Gothoskar M, Cronin KG, Fernandez-Robles C, Pirl WF, Chen YB, Cutler C, Lindvall C, El-Jawahri A
Trends in Pharmacological Sciences
More Than One Route to Render Tumors Resistant to cGAS/STING Activation
Manokaran C, Roberts TM, Wang Y