Welcome to Dana-Farber's Research News
September 1, 2022
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.
Annals of Oncology
Deciphering Radiological Stable Disease to Immune Checkpoint Inhibitors
Luo J
BACKGROUND: 'Stable disease (SD)' as per RECIST is a common but ambiguous outcome in patients receiving immune checkpoint inhibitors (ICIs). This study aimed to characterize SD and identify the subset of patients with SD who are benefiting from treatment. Understanding SD would facilitate drug development and improve precision in correlative research.
PATIENTS AND METHODS: A systematic review was carried out to characterize SD in ICI trials. SD and objective response were compared to proliferation index using The Cancer Genome Atlas gene expression data. To identify a subgroup of SD with outcomes mirroring responders, we examined a discovery cohort of non-small-cell lung cancer (NSCLC). Serial cutpoints of two variables, % best overall response and progression-free survival (PFS), were tested to define a subgroup of patients with SD with similar survival as responders. Results were then tested in external validation cohorts.
RESULTS: Among trials of ICIs (59 studies, 14 280 patients), SD ranged from 16% to 42% in different tumor types and was associated with disease-specific proliferation index (ρ = -0.75, P = 0.03), a proxy of tumor kinetics, rather than relative response to ICIs. In a discovery cohort of NSCLC [1220 patients, 313 (26%) with SD to ICIs], PFS ranged widely in SD (0.2-49 months, median 4.9 months). The subset with PFS >6 months and no tumor growth mirrored partial response (PR) minor (overall survival hazard ratio 1.0) and was proposed as the definition of SD responder. This definition was confirmed in two validation cohorts from trials of NSCLC treated with durvalumab and found to apply in tumor types treated with immunotherapy in which depth and duration of benefit were correlated.
CONCLUSIONS: RECIST-defined SD to immunotherapy is common, heterogeneous, and may largely reflect tumor growth rate rather than ICI response. In patients with NSCLC and SD to ICIs, PFS >6 months and no tumor growth may be considered 'SD responders'. This definition may improve the efficiency of and insight derivable from clinical and translational research.
Cell
Luoma AM, Suo S, Gunasti L, Porter CBM, Chen YH, Criscitiello S, Ricker CA, Dionne D, Rozenblatt-Rosen O, Uppaluri R, Haddad RI, Ashenberg O, Regev A, Van Allen EM, Schoenfeld JD, Wucherpfennig KW
Neoadjuvant immune checkpoint blockade has shown promising clinical activity. Here, we characterized early kinetics in tumor-infiltrating and circulating immune cells in oral cancer patients treated with neoadjuvant anti-PD-1 or anti-PD-1/CTLA-4 in a clinical trial (NCT02919683). Tumor-infiltrating CD8 T cells that clonally expanded during immunotherapy expressed elevated tissue-resident memory and cytotoxicity programs, which were already active prior to therapy, supporting the capacity for rapid response. Systematic target discovery revealed that treatment-expanded tumor T cell clones in responding patients recognized several self-antigens, including the cancer-specific antigen MAGEA1. Treatment also induced a systemic immune response characterized by expansion of activated T cells enriched for tumor-infiltrating T cell clonotypes, including both pre-existing and emergent clonotypes undetectable prior to therapy. The frequency of activated blood CD8 T cells, notably pre-treatment PD-1-positive KLRG1-negative T cells, was strongly associated with intra-tumoral pathological response. These results demonstrate how neoadjuvant checkpoint blockade induces local and systemic tumor immunity.
Journal of Clinical Oncology
Lipsyc-Sharf M, Santos K, Patel A, Kirkner GJ, Hughes ME, Tolaney SM, Partridge AH, Krop IE, Winer EP, Lin NU, Parsons HA
PURPOSE: To examine the prevalence and dynamics of circulating tumor DNA (ctDNA) and its association with metastatic recurrence in patients with high-risk early-stage hormone receptor-positive breast cancer (HR+ BC) more than 5 years from diagnosis.
METHODS: We enrolled 103 patients with high-risk stage II-III HR+ BC diagnosed more than 5 years prior without clinical evidence of recurrence. We performed whole-exome sequencing (WES) on primary tumor tissue to identify somatic mutations tracked via a personalized, tumor-informed ctDNA test to detect minimal residual disease (MRD). We collected plasma at the time of consent and at routine visits every 6-12 months. Patients were followed for clinical recurrence.
RESULTS: In total, 85 of 103 patients had sufficient tumor tissue; of them, 83 of 85 (97.6%) patients had successful whole-exome sequencing. Personalized ctDNA assays were designed targeting a median of 36 variants to test 219 plasma samples. The median time from diagnosis to first sample was 8.4 years. The median follow-up was 10.4 years from diagnosis and 2.0 years from first sample. The median number of plasma samples per patient was two. Eight patients (10%) had positive MRD testing at any time point. Six patients (7.2%) developed distant metastatic recurrence, all of whom were MRD-positive before overt clinical recurrence, with median ctDNA lead time of 12.4 months. MRD was not identified in one patient (1.2%) with local recurrence. Two of eight MRD-positive patients had not had clinical recurrence at last follow-up.
CONCLUSION: In this prospective study, in patients with high-risk HR+ BC in the late adjuvant setting, ctDNA was identified a median of 1 year before all cases of distant metastasis. Future studies will determine if ctDNA-guided intervention in patients with HR+ BC can alter clinical outcomes.
Journal of Clinical Oncology
Development and Validation of the PREMMplus Model for Multigene Hereditary Cancer Risk Assessment
Yurgelun MB, Uno H, Furniss CS, Ukaegbu C, Horiguchi M, Chittenden A, Garber JE, Syngal S
PURPOSE: With the availability of multigene panel testing (MGPT) for hereditary cancer risk assessment, clinicians need to assess the likelihood of pathogenic germline variants (PGVs) across numerous genes in parallel. This study's aim was to develop and validate a clinical prediction model (PREMMplus) for MGPT risk assessment.
MATERIALS AND METHODS: PREMMplus was developed in a single-institution cohort of 7,280 individuals who had undergone MGPT. Logistic regression models with Least Absolute Shrinkage and Selection Operator regularization were used to examine candidate predictors (age, sex, ethnicity, and personal/family history of 18 cancers/neoplasms) to estimate one's likelihood of carrying PGVs in 19 genes (broadly categorized by phenotypic overlap and/or relative penetrance: 11 category A [APC, BRCA1/2, CDH1, EPCAM, MLH1, MSH2, MSH6, biallelic MUTYH, PMS2, and TP53] and eight category B genes [ATM, BRIP1, CDKN2A, CHEK2, PALB2, PTEN, RAD51C, and RAD51D]). Model performance was validated in nonoverlapping data sets of 8,691 and 14,849 individuals with prior MGPT ascertained from clinic- and laboratory-based settings, respectively.
RESULTS: PREMMplus (score 2.5%) had 93.9%, 91.7%, and 89.3% sensitivity and 98.3%, 97.5%, and 97.8% negative-predictive value (NPV) for identifying category A gene PGV carriers in the development and validation cohorts, respectively. PREMMplus assessment (score 2.5%) had 89.9%, 85.6%, and 84.2% sensitivity and 95.0%, 93.5%, and 93.5% NPV, respectively, for identifying category A/B gene PGV carriers. Decision curve analyses support MGPT for individuals predicted to have 2.5% probability of a PGV.
CONCLUSION: PREMMplus accurately identifies individuals with PGVs in a diverse spectrum of cancer susceptibility genes with high sensitivity/NPV. Individuals with PREMMplus scores 2.5% should be considered for MGPT.
Journal of Clinical Oncology
Exercise, Diet, and Weight Management During Cancer Treatment: ASCO Guideline
Ligibel JA, Meyerhardt JA
PURPOSE: To provide guidance on exercise, diet, and weight management during active cancer treatment in adults.
METHODS: A systematic review of the literature identified systematic reviews and randomized controlled trials evaluating the impact of aerobic and resistance exercise, specific diets and foods, and intentional weight loss and avoidance of weight gain in adults during cancer treatment, on quality of life, treatment toxicity, and cancer control. PubMed and the Cochrane Library were searched from January 2000 to May 2021. ASCO convened an Expert Panel to review the evidence and formulate recommendations.
RESULTS: The evidence base consisted of 52 systematic reviews (42 for exercise, nine for diet, and one for weight management), and an additional 23 randomized controlled trials. The most commonly studied types of cancer were breast, prostate, lung, and colorectal. Exercise during cancer treatment led to improvements in cardiorespiratory fitness, strength, fatigue, and other patient-reported outcomes. Preoperative exercise in patients with lung cancer led to a reduction in postoperative length of hospital stay and complications. Neutropenic diets did not decrease risk of infection during cancer treatment.
RECOMMENDATIONS: Oncology providers should recommend regular aerobic and resistance exercise during active treatment with curative intent and may recommend preoperative exercise for patients undergoing surgery for lung cancer. Neutropenic diets are not recommended to prevent infection in patients with cancer during active treatment. Evidence for other dietary and weight loss interventions during cancer treatment was very limited. The guideline discusses special considerations, such as exercise in individuals with advanced cancer, and highlights the critical need for more research in this area, particularly regarding diet and weight loss interventions during cancer treatment. Additional information is available at www.asco.org/supportive-care-guidelines.
Journal of Clinical Oncology
Yin and Yang of Psychological Health in the Cancer Experience: Does Positive Psychology Have a Role?
Amonoo HL, El-Jawahri A, Deary EC, Traeger LN, Cutler CS, Antin JA, Huffman JC
Positive psychological health is crucial to optimal clinical outcomes across the cancer care continuum, from prevention and risk reduction to palliative care and survivorship. Yet, the positive psychological factors that affect morbidity and mortality have not been extensively studied in diverse oncologic populations compared with other medical populations—although they could be extremely influential in a cancer population facing a life-threatening diagnosis. Positive psychological well-being (PPWB), a broad construct defined as “the positive cognitions, feelings, and strategies individuals use to evaluate their life favorably and function well,” includes indicators such as positive affect, gratitude, optimism, happiness, and life purpose. Although PPWB coexists with symptoms of distress, it is not simply the opposite of distress. For example, optimism and depression are only modestly inversely correlated. Many studies in medical populations have found that the beneficial effects of positive psychological health on clinical outcomes are independent of the adverse effects of negative psychological conditions like depression on clinical outcomes. Hence, the primary focus of alleviating symptoms of distress and psychiatric disorders to achieve optimal psychological health in oncology populations ignores an essential aspect of well-being: overcoming adversity and accentuating life-affirming perspectives that may enhance the positive aspects of well-being. Importantly, supporting PPWB should not be confused with the tyranny of positive thinking (ie, where patients feel pressured to think positively and may believe that failure to think positively is a character flaw that can lead to poor clinical outcomes and disease setbacks).
Journal of the National Cancer Institute
Variation in Cardiac Dose Explains a "Fraction" of the Disparities among Breast Cancer Patients
Punglia RS, Hassett MJ
Most studies on disparities in cancer have focused on differences in stage of diagnosis and access to treatment. Breast cancer death rates are highest among vulnerable populations, including African Americans, the poor, the elderly, and those living in rural settings. Few prior studies have look at differences in the characteristics of administered treatments as a potential explanation for observed disparities in outcomes. In medical oncology, an analysis of chemotherapy administered to breast cancer patients found African-Americans received 10% lower relative dose intensity compared to white patients. In this issue of the Journal, Dr. Chapman and colleagues present a novel and intricate analysis of the mediators of racial disparities among women receiving whole breast radiation therapy, using mean heart dose as the vehicle for their examination.
Lancet Oncology
PI3K Inhibitors in Haematological Malignancies
Brown JR, LaCasce AS, Davids MS
We are writing in response to the Comment by Nicholas Richardson and colleagues from the US Food and Drug Administration, which discussed the use of PI3K inhibitors in haematological malignancies. As investigators who have treated many patients with PI3K inhibitors, beginning with the phase 1 study of idelalisib in 2010, we can attest to the transformative and life-saving nature of these therapies. Many of the patients whom we have treated with PI3K inhibitors have derived great benefit for 5 years or more while on therapy. The Comment by Richardson and colleagues does not address well established approaches to patient selection, toxicity management, or the clinical benefit of PI3K inhibitors. Two of the three original idelalisib randomised registration trials in patients with relapsed chronic lymphocytic leukaemia showed both progression-free survival and overall survival benefits in patients who received idelalisib rather than placebo in combination; this was confirmed in long-term follow-up. A study published in 2021 showed improved overall response rates, progression-free survival, and overall survival in different subgroups of patients who developed autoimmune toxicity on idelalisib. PI3K inhibitors remain an important option for older patients who might not be candidates for BTK inhibitors due to cardiovascular comorbidities or anticoagulation. Comorbidities did not negatively affect outcomes in patients treated with PI3K inhibitors. The complexities of venetoclax dose ramp-up have also led to low uptake, except in academic centres. These considerations underscore the need to consider all PI3K inhibitor trials in different clinical settings and the limitations of other therapies.
Nature Cell Biology
Nucleotide Imbalance Decouples Cell Growth from Cell Proliferation
Nabel CS, Darnell Do BT, Vander Heiden MG
Nucleotide metabolism supports RNA synthesis and DNA replication to enable cell growth and division. Nucleotide depletion can inhibit cell growth and proliferation, but how cells sense and respond to changes in the relative levels of individual nucleotides is unclear. Moreover, the nucleotide requirement for biomass production changes over the course of the cell cycle, and how cells coordinate differential nucleotide demands with cell cycle progression is not well understood. Here we find that excess levels of individual nucleotides can inhibit proliferation by disrupting the relative levels of nucleotide bases needed for DNA replication and impeding DNA replication. The resulting purine and pyrimidine imbalances are not sensed by canonical growth regulatory pathways like mTORC1, Akt and AMPK signalling cascades, causing excessive cell growth despite inhibited proliferation. Instead, cells rely on replication stress signalling to survive during, and recover from, nucleotide imbalance during S phase. We find that ATR-dependent replication stress signalling is activated during unperturbed S phases and promotes nucleotide availability to support DNA replication. Together, these data reveal that imbalanced nucleotide levels are not detected until S phase, rendering cells reliant on replication stress signalling to cope with this metabolic problem and disrupting the coordination of cell growth and division.
Nature Cell Biology
Untangling the Web of Intratumour Heterogeneity
Li Z, Seehawer M, Polyak K
Intratumour heterogeneity (ITH) is a hallmark of cancer that drives tumour evolution and disease progression. Technological and computational advances have enabled us to assess ITH at unprecedented depths, yet this accumulating knowledge has not had a substantial clinical impact. This is in part due to a limited understanding of the functional relevance of ITH and the inadequacy of preclinical experimental models to reproduce it. Here, we discuss progress made in these areas and illuminate future directions.
Nature Medicine
Predicting Chronic Morbidity in Childhood Cancer Survivors
Vrooman LM, Diller LR
Approximately 85% of children diagnosed with cancer will be cured of their primary cancer, but epidemiologic and clinical studies have characterized a significant burden of morbidity, as well as excess early mortality, in survivors. This burden has largely been attributed to toxic treatment exposures during childhood cancer treatment. Excess cardiovascular-related disease is a leading cause of morbidity and mortality in survivors of childhood cancer, which is associated with exposure to cardiotoxic therapy, such as anthracyclines and therapeutic radiation to the chest. Traditional cardiometabolic risk factors, including obesity, also contribute to an increased risk of cardiovascular disease in survivors as they age, and survivors of childhood cancers have been found to have high rates of obesity.
Science
Mitochondrial Remodeling and Ischemic Protection by G Protein-Coupled Receptor 35 Agonists
Wyant GA, Yu W, Doulamis IP, Nomoto RS, Saeed MY, Duignan T, McCully JD, Kaelin WG Jr
Kynurenic acid (KynA) is tissue protective in cardiac, cerebral, renal, and retinal ischemia models, but the mechanism is unknown. KynA can bind to multiple receptors, including the aryl hydrocarbon receptor, the a7 nicotinic acetylcholine receptor (a7nAChR), multiple ionotropic glutamate receptors, and the orphan G protein-coupled receptor GPR35. Here, we show that GPR35 activation was necessary and sufficient for ischemic protection by KynA. When bound by KynA, GPR35 activated Gi- and G12/13-coupled signaling and trafficked to the outer mitochondria membrane, where it bound, apparantly indirectly, to ATP synthase inhibitory factor subunit 1 (ATPIF1). Activated GPR35, in an ATPIF1-dependent and pertussis toxin-sensitive manner, induced ATP synthase dimerization, which prevented ATP loss upon ischemia. These findings provide a rationale for the development of specific GPR35 agonists for the treatment of ischemic diseases.
American Journal of Medicine
Riaz IB, Sonpavde GP, Kehl KL, Duma N
Annals of Hematology
Richardson PG
Annals of Surgical Oncology
Tesch ME, Collins LC, Wong JS, Dominici L, Tamimi R, Come SE, Partridge AH
Annals of Surgical Oncology
Mittendorf EA, Kantor O, Weiss A, Richardson E, Garrido-Castro A, Portnow LH, Krop IE, Lin NU, Winer EP, Tolaney SM, King TA
Blood Advances
Kim HT, Koreth J, Whangbo J, Nikiforow S, Reynolds CG, Stowe P, Ho VT, Cutler C, Antin JH, Soiffer RJ, Ritz J
BMJ Open
Mack JW
Bone Marrow Transplantation
Peer Support in Patients with Hematologic Malignancies: A Systematic Review
Amonoo HL, Harnedy LE, Staton SC, Daskalakis E, El-Jawahri A, Huffman JC
Bone Marrow Transplantation
Amonoo HL, Harnedy LE, Deary EC, Traeger L, Daskalakis EP, Cutler C, Kelkar AH, Rosales R, Goldschen L, Pirl WF, Feig EH, Revette A, Huffman JC, El-Jawahri A
British Journal of Haematology
Valtis YK, Place AE, Silverman LB, Vrooman LM, DeAngelo DJ, Luskin MR
Breast Cancer Research and Treatment
Sella T, Ren S, Freret TS, Economy KE, Chen WY, Parsons HA, Lin NU, Moy B, Tung NM, Partridge AH, Tayob N, Mayer EL
Breast Cancer Research and Treatment
Sella T, Kantor O, Weiss A, Partridge AH, Metzger O, King TA
Cancer Immunology Research
Activation of Tumor-Cell STING Primes NK-Cell Therapy
Knelson EH, Ivanova EV, Tarannum M, Campisi M, Lizotte PH, Booker MA, Ozgenc I, Noureddine M, Meisenheimer B, Chen M, Piel B, Spicer N, Obua B, Messier CM, Shannon E, Mahadevan NR, Tani T, Schol PJ, Lee-Hassett AM, Zlota A, Vo HV, Ha M, Bertram AA, Han S, Thai TC, Gustafson CE, Venugopal K, Haggerty TJ, Albertson TP, Hartley AV, Eser PO, Li ZH, Vivero M, De Rienzo A, Richards WG, Abu-Yousif AO, Appleman VA, Gregory RC, Parent A, Lineberry N, Smith EL, Jänne PA, Miret JJ, Tolstorukov MY, Romee R, Paweletz CP, Bueno R, Barbie DA
Cancer Immunology Research
Alvarez-Breckenridge C, Markson SC, Stocking JH, Nayyar N, Lastrapes M, Strickland MR, Kim AE, de Sauvage M, Dahal A, Larson JM, Mora JL, Navia AW, Klein RH, Kuter BM, Gill CM, Bertalan M, Shaw B, Kaplan A, Subramanian M, Jain A, White M, Shahid O, Pauken KE, Miller BC, Frederick DT, Hebert C, Shaw M, Martinez-Lage M, Frosch M, Wang N, Gerstner E, Nahed BV, Curry WT, Carter B, Cahill DP, Boland GM, Sharpe AH, Suva ML, Sullivan RJ, Brastianos PK, Carter SL
Cancer Research
A Distinct Chromatin State Drives Therapeutic Resistance in Invasive Lobular Breast Cancer
Nardone A, Qiu X, Nagy Z, Feiglin A, Cohen Feit G, Xie Y, Font-Tello A, Guarducci C, Hermida-Prado F, Syamala S, Lim K, Munoz Gomez M, Pun M, Liu W, Cejas P, Brock JB, Freedman ML, Winer EP, Long HW, Metzger Filho O, Jeselsohn R
Cancers
Yamashita N, Fushimi A, Morimoto Y, Bhattacharya A, Hagiwara M, Yamamoto M, Hata T, Shapiro G, Kufe D
Cell Reports Methods
Jee H, Koehler AN, London WB, Lee PY, Bhatia SN, Li H
Chemical Communications
(15)N-Detected TROSY NMR Experiments to Study Large Disordered Proteins in High-Field Magnets
Dubey A, Viennet T, Chhabra S, Seo HC, Arthanari H
Clinical Cancer Research
Liu JF
Clinical Cancer Research
Improved T-cell Immunity Following Neoadjuvant Chemotherapy in Ovarian Cancer
Liu M, Tayob N, Penter L, Sellars M, Tarren A, Chea V, Carulli I, Huang T, Li S, Cheng SC, Le P, Frackiewicz L, Fasse J, Qi C, Liu JF, Stover EH, Curtis J, Livak KJ, Neuberg D, Matulonis UA, Wu CJ, Keskin DB, Konstantinopoulos PA
Clinical Genitourinary Cancer
Nuzzo PV, Adib E, Curran C, Freeman D, Nassar AH, Abou Alaiwi S, Bakouny Z, McGregor BA, Choueiri TK, Jain RK, Sonpavde G
Clinical Lymphoma, Myeloma, and Leukemia
Sermer D, Sarosiek S, Branagan AR, Treon SP, Castillo JJ
Computers, Informatics, Nursing
Knoerl R, Bockhoff J, Fox E, Giobbie-Hurder A, Berfield J, Meyerhardt J, Wright A, Ligibel J
Critical Reviews in Oncology Hematology
Kang DW, Vander Heiden MG, Dieli-Conwright CM
Current Opinion in Chemical Biology
Gorgulla C, Arthanari H
European Urology
Carvalho FLF, Mossanen M, Van Allen EM, Mouw KW
European Urology Oncology
Sweeney CJ
Future Oncology
Sonpavde GP
Gastroenterology
A Growing Hope for Earlier Detection of Pancreatic Cancer
Rosenthal M, Schawkat K, Wolpin B
Genome Biology
Differential Richness Inference for 16S rRNA Marker Gene Surveys
Kumar MS, Irizarry RA
Genome Medicine
Mäkinen N, Zhou M, Zhang Z, Perez E, Nakakura E, Meyerson M
Hematology/Oncology Clinics of North America
Gene Therapy for Pediatric Neurologic Disease
Jimenez-Kurlander L, Duncan CN
Immunotherapy
Tyan K, Abu-Shawer O, Baginska J, Severgnini M, Manos M, Vaitkevicius H, Grover S, Hodi FS, Rahma OE
International Journal of Molecular Sciences
Addiction of Cancer Stem Cells to MUC1-C in Triple-Negative Breast Cancer Progression
Yamashita N, Kufe D
Journal of the American Geriatrics Society
Hu FY, O'Mara L, Tulebaev S, Orkaby AR, Cooper Z, Bernacki RE
Journal of Cancer Survivorship
Knoerl R, Giobbie-Hurder A, Berfield J, Meyerhardt JA, Wright AA, Ligibel JA
Journal of Clinical Investigation
Sellar RS, Sperling AS, Slabicki M, Gasser JA, McConkey ME, Donovan KA, Mageed N, Adams DN, Zou C, Miller PG, Dutta RK, Boettcher S, Lin AE, Sandoval B, Quevedo Barrios VA, Kovalcik V, Koeppel J, Fink EC, Bergstrom EJ, Burt R, Udeshi ND, Carr SA, Fischer ES, Ebert BL
Journal of Clinical Investigation
Porter RL, Flores MN, Berzolla E, You E, Phillips IE, Kc N, Desai N, Tai EC, Szabolcs A, Lang ER, Pankaj A, Raabe MJ, Thapar V, Xu KH, Nieman LT, Rabe DC, Kolin DL, Stover EH, Pepin D, Stott SL, Deshpande V, Liu JF, Matulonis UA, Ting DT
Journal of Clinical Sleep Medicine
The Impact of Narcolepsy on Social Relationships in Young Adults
Davidson RD, Biddle K, Nassan M, Scammell TE, Zhou ES
Journal of Genetic Counseling
Rodgers-Fouche L, Perez K
Journal of Investigative Dermatology
Distinct Radiation Responses in Virus-Positive and Virus-Negative Merkel Cell Carcinoma
Ahmed MM, Rivas HG, Frost TC, DeCaprio JA
Journal of the National Comprehensive Cancer Network
Hshieh TT, DuMontier C, Stone RM, Soiffer RJ, Driver JA, Abel GA
Journal of the National Comprehensive Cancer Network
Impact of Genetic Counseling on Patient-Reported Electronic Cancer Family History Collection
Vanderwall RA, Schwartz A, Kipnis L, Skefos CM, Stokes SM, Bhulani N, Weitz M, Gelman R, Garber JE, Rana HQ
Journal of Palliative Medicine
Sager Z, Ljuslin M, Tulsky JA, Beaussant Y
JCI Insight
Patterns of Structural Variation Define Prostate Cancer Across Disease States
Zhou M, Carrot-Zhang J, Beroukhim R, Van Allen EM, Choudhury AD, Freedman M, Taplin ME, Meyerson M, Viswanathan SR
JCO Oncology Practice
Ethics Consultation in Oncology: The Search for Quality in Quantity
Marron JM, Hantel A, Abel GA, Peppercorn JM
JCO Oncology Practice
Sharing Decisions About Systemic Therapy for Advanced Cancers
Tarbi EC, Pirl WF
Leukemia and Lymphoma
Taranto E, Redd R, Jeter E, McHugh K, Crombie JL, Fisher DC, Jacobsen E, Jacobson CA, Kim AI, LaCasce AS, Odejide OO, Joyce RM, Chen YB, Armand P, Merryman RW
Leukemia
Galinsky IA, DeAngelo DJ
Molecular Cancer Research
Fushimi A, Moritmoto Y, Ishikawa S, Yamashita N, Bhattacharya A, Daimon T, Rajabi H, Jin C, Hagiwara M, Yasumizu Y, Luan Z, Suo W, Kufe D
Molecular Therapy
Liu B, Brendel C, Vinjamur DS, Zhou Y, Harris C, McGuinness M, Manis JP, Bauer DE, Xu H, Williams DA
Monoclonal Antibodies in Immunodiagnosis and Immunotherapy
A Comparison of Murine PD-1 and PD-L1 Monoclonal Antibodies
Bu MT, Yuan L, Klee AN, Freeman GJ
Nature Materials
Mechanical Checkpoint Regulates Monocyte Differentiation in Fibrotic Niches
Vining KH, Marneth AE, Adu-Berchie K, Grolman JM, Tringides CM, Liu Y, Wong WJ, Pozdnyakova O, Severgnini M, Stafford A, Duda GN, Hodi FS, Mullally A, Wucherpfennig KW, Mooney DJ
Neuro-Oncology
Pages M, Rotem D, Gydush G, Reed S, Rhoades J, Ha G, Lo C, Fleharty M, Duran M, Jones R, Becker S, Haller M, Sinai CE, Goumnerova L, Golub TR, Ligon KL, Wright KD, Adalsteinsson VA, Beroukhim R, Bandopadhayay P
Neuro-Oncology
Trends in Location of Death for Individuals with Primary Brain Tumors in the United States
Aizer AA, Bi WL, Haas-Kogan D, Rahman R
Neurotherapeutics
Novel Clinical Trial Designs in Neuro-Oncology
Saraf A, Trippa L, Rahman R
Pain Management Nursing
Knoerl R, Mazzola E, Hong F, Salehi E, McCleary N, Ligibel J, Reyes K, Berry DL
Pediatric Blood and Cancer
Flamand Y, Blonquist T, Stevenson KE, Harris MH, Neuberg DS, Sallan SE, Silverman LB
Prostate
Future Directions for Precision Oncology in Prostate Cancer
Mizuno K, Beltran H
Prostate
PTEN-PI3K Pathway Alterations in Advanced Prostate Cancer and Clinical Implications
Choudhury AD
Radiotherapy and Oncology
Liu KX, Milligan MG, Schoenfeld JD, Tishler RB, Ng AK, Devlin PM, Fite E, Hanna GJ, Silk AW, Yoon CH, Thakuria M, Margalit DN
Transplantation and Cellular Therapies
Liu KX, Poux N, Shin KY, Moore N, Chen YH, Margossian S, Whangbo JS, Duncan CN, Lehmann LE, Marcus KJ
Transplantation and Cellular Therapies
Little JS, Shapiro RM, Aleissa MM, Kim A, Chang JBP, Kubiak DW, Zhou G, Antin JH, Koreth J, Nikiforow S, Cutler CS, Romee R, Issa NC, Ho VT, Gooptu M, Soiffer RJ, Baden LR