April 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.
Blood
How I Treat Neurologic Complications in Patients with Lymphoid Cancer
Nayak L, Batchelor TT
Neurologic complications of lymphoid cancer can be challenging to recognize and treat. The nervous system can be affected directly by hematogenous or local spread of lymphoma. Indirect neurologic effects of lymphoma include paraneoplastic syndromes and vascular complications. Lymphoma treatments can also cause neurologic complications. Early identification and treatment are crucial to stabilize or reverse neurologic deficits, prevent further nervous system injury, and optimize overall oncologic therapy. This article provides an overview of the different neurologic complications of lymphoma and its treatments, in addition to presenting case studies that emphasize commonly encountered clinical scenarios.
Blood
mpact of Diagnostic Genetics on Remission MRD and Transplantation Outcomes in Older AML Patients
Murdock HM, Kim HT, Tsai HK, Ho VT, Koreth J, Soiffer RJ, Ritz J, Lindsley RC, Gibson CJ
Older patients with acute myeloid leukemia (AML) have high relapse risk and poor survival after allogeneic hematopoietic cell transplantation (HCT). Younger patients may receive myeloablative conditioning to mitigate relapse risk associated with high-risk genetics or measurable residual disease (MRD), but older adults typically receive reduced-intensity conditioning (RIC) to limit toxicity. To identify factors that drive HCT outcomes in older patients, we performed targeted mutational analysis (VAF 2%) on diagnostic samples from 295 AML patients age 60 or older who underwent HCT in first complete remission, 91% of whom received RIC, and targeted duplex sequencing at the time of remission in 192 patients. In a multivariable model for leukemia-free survival (LFS) including baseline genetic and clinical variables, we defined patients with low (3-year LFS 85%), intermediate (55%), high (35%), and very high risk (7%). Prior to HCT, 79.7% of patients had persistent baseline mutations, including 18.3% with only DNMT3A or TET2 mutations (DT) and 61.4% with other mutations (MRDpositive). In univariable analysis, MRD-positivity was associated with increased relapse and inferior LFS compared with DT and MRDnegative patients. However, in a multivariable model accounting for baseline risk, MRD-positivity had no independent impact on LFS, likely due to its significant association with diagnostic genetic characteristics including MDS-associated gene mutations, TP53 mutations, and high-risk karyotype. In conclusion, molecular associations with MRD positivity and transplant outcomes in older AML patients are driven primarily by baseline genetics, and not by mutations present in remission. In this group of patients, where high-intensity conditioning carries substantial risk of toxicity, alternative approaches to mitigating MRD-associated relapse risk are required.
Cancer Discovery
EP300 Selectively Controls the Enhancer Landscape of MYCN-Amplified Neuroblastoma
Durbin AD, Wang T, Wimalasena VK, Zimmerman MW, Li D, Dharia NV, Mariani L, Park PMC, Sigua LH, Morita K, Conway AS, Robichaud AL, Perez-Atayde AR, Bulyk ML, Stegmaier K, Look AT, Qi J
Gene expression is regulated by promoters and enhancers marked by histone H3 lysine 27 acetylation (H3K27ac), which is established by the paralogous histone acetyltransferases (HAT) EP300 and CBP. These enzymes display overlapping regulatory roles in untransformed cells, but less characterized roles in cancer cells. We demonstrate that the majority of high-risk pediatric neuroblastoma (NB) depends on EP300, whereas CBP has a limited role. EP300 controls enhancer acetylation by interacting with TFAP2?, a transcription factor member of the lineage-defining transcriptional core regulatory circuitry (CRC) in NB. To disrupt EP300, we developed a proteolysis-targeting chimera (PROTAC) compound termed "JQAD1" that selectively targets EP300 for degradation. JQAD1 treatment causes loss of H3K27ac at CRC enhancers and rapid NB apoptosis, with limited toxicity to untransformed cells where CBP may compensate. Furthermore, JQAD1 activity is critically determined by cereblon (CRBN) expression across NB cells.
SIGNIFICANCE: EP300, but not CBP, controls oncogenic CRC-driven transcription in high-risk NB by binding TFAP2?. We developed JQAD1, a CRBN-dependent PROTAC degrader with preferential activity against EP300 and demonstrated its activity in NB. JQAD1 has limited toxicity to untransformed cells and is effective in vivo in a CRBN-dependent manner. This article is highlighted in the In This Issue feature, p. 587.
Gastroenterology
Rosenthal MH, Wolpin BM, Yurgelun MB
Pancreatic cancer (PC) is the third leading cause of cancer-related death in the United States and the European Union. More than 80% of patients who develop pancreatic cancer have locally advanced or metastatic disease at diagnosis and experience median overall survival times of . Identification of early-stage PC and high-risk PC precursors is a necessary step in reducing mortality from this malignancy. An expert panel convened by the International Cancer of the Pancreas Screening (CAPS) Consortium has stated that the goal of PC surveillance should be identification and resection of PC precursor lesions with high-grade dysplasia or PCs that are confined to the pancreas, ?2 cm in maximal diameter, and without lymph node involvement (AJCC 7th Edition, pT1N0M0). Initial attempts at imaging-based PC surveillance in high-risk individuals (HRIs) with genetic or familial PC predisposition demonstrated the feasibility of annual magnetic resonance imaging (MRI) and endoscopic ultrasound (EUS) to identify asymptomatic individuals with high-grade precursor lesions. Although randomized data on PC surveillance remain lacking, recent prospective studies have suggested tumor downstaging from MRI- and EUS-based PC surveillance and longer survival times compared with historical data, leading to clinical practice guidelines that recommend surveillance be considered for certain HRIs.
Journal of Clinical Oncology
Adjuvant Therapy for Stage II Colon Cancer: ASCO Guideline Update
Meyerhardt JA
PURPOSE: To develop recommendations for adjuvant therapy for patients with resected stage II colon cancer.
METHODS: ASCO convened an Expert Panel to conduct a systematic review of relevant studies and develop recommendations for clinical practice.
RESULTS: Twenty-one observational studies and six randomized controlled trials met the systematic review inclusion criteria.
RECOMMENDATIONS: Adjuvant chemotherapy (ACT) is not routinely recommended for patients with stage II colon cancer who are not in a high-risk subgroup. Patients with T4 tumors are at higher risk of recurrence and should be offered ACT, whereas patients with other high-risk factors, including sampling of fewer than 12 lymph nodes in the surgical specimen, perineural or lymphovascular invasion, poorly or undifferentiated tumor grade, intestinal obstruction, tumor perforation, or grade BD3 tumor budding, may be offered ACT. The addition of oxaliplatin to fluoropyrimidine-based ACT is not routinely recommended, but may be offered as a result of shared decision making. Patients with mismatch repair deficiency/microsatellite instability tumors should not be routinely offered ACT; if the combination of mismatch repair deficiency/microsatellite instability and high-risk factors results in a decision to offer ACT, oxaliplatin-containing chemotherapy is recommended. Duration of oxaliplatin-containing chemotherapy is also addressed, with recommendations for 3 or 6 months of treatment with capecitabine and oxaliplatin or fluorouracil, leucovorin, and oxaliplatin, with decision making informed by key evidence of 5-year disease-free survival in each treatment subgroup and the rate of adverse events, including peripheral neuropathy.Additional information is available at www.asco.org/gastrointestinal-cancer-guidelines.
Journal of Clinical Oncology
Sweeney CJ
PURPOSE: We previously reported that enzalutamide improved overall survival when added to standard of care in metastatic, hormone-sensitive prostate cancer. Here, we report its effects on aspects of health-related quality of life (HRQL).
METHODS:HRQL was assessed with the European Organisation for Research and Treatment of Cancer core quality-of-life questionnaire and QLM-PR25 at weeks 0, 4, 12, and then every 12 weeks until progression. Scores from week 4 to 156 were analyzed with repeated measures modeling to calculate group means and differences. Deterioration-free survival was from random assignment until the earliest of death, clinical progression, discontinuation of study treatment, or a worsening of 10 points or more from baseline in fatigue, physical function, cognitive function, or overall health and quality of life (OHQL). HRQL scores range from 0 (lowest possible) to 100 (highest possible).
RESULTS: Twenty-one observational studies and six randomized controlled trials met the systematic review inclusion criteria.
RECOMMENDATIONS: HRQL was assessed in 1,042 of 1,125 participants (93%). Differences in means favored control over enzalutamide for fatigue (5.2, 95% CI, 3.6 to 6.9; P < .001), cognitive function (4.0, 95% CI, 2.5 to 5.5; P < .001), and physical function (2.6, 95% CI, 1.3 to 3.9; P < .001), but not OHQL (1.2, 95% CI, -0.2 to 2.7; P = .1). Deterioration-free survival rates at 3 years, and log-rank P values comparing the whole distributions, favored enzalutamide over control for OHQL (31% v 17%; P < .0001), cognitive function (31% v 20%; P = .001), and physical function (31% v 22%; P < .001), but not fatigue (24% v 18%; P = .16). The effects of enzalutamide on HRQL were independent of baseline characteristics.
CONCLUSION: Enzalutamide was associated with worsening of self-reported fatigue, cognitive function, and physical function, but not OHQL. Enzalutamide was associated with improved deterioration-free survival for OHQL, physical function, and cognitive function because delays in disease progression outweighed early deteriorations in these aspects of HRQL.
Journal of Clinical Oncology
Isn't Androgen Deprivation Enough? Optimal Treatment for Newly Diagnosed Metastatic Prostate Cancer
Morgans AK, Beltran H
The Oncology Grand Rounds series is designed to place original reports published in the Journal into clinical context. A case presentation is followed by a description of diagnostic and management challenges, a review of the relevant literature, and a summary of the authors' suggested management approaches. The goal of this series is to help readers better understand how to apply the results of key studies, including those published in Journal of Clinical Oncology, to patients seen in their own clinical practice.
Journal of Clinical Oncology
Hodi FS
We appreciate the thoughtful comments from Drs Olivier and Prasad regarding the primary manuscript and editorial describing the CheckMate 067 6.5-year follow-up data. In general, we agree that there is no single standard of care for all patients with metastatic melanoma. The choice of primary therapy is one that requires careful balancing of antitumor activity with toxicities and is best decided through transparent discussions between patients and oncology clinicians. We also concur that such decisions are best informed by randomized trials and that only data from such trials would address the important point made regarding combination checkpoint blockade or monotherapy. However, the choice of a control arm for such a trial is challenging given the dynamic nature of available therapies for metastatic melanoma. As noted in the editorial, given the recently published RELATIVITY-047 results,4 which demonstrated superior progression-free survival with nivolumab plus relatlimab (a LAG-3–blocking antibody) versus nivolumab monotherapy, an ethical question would emerge when comparing nivolumab plus ipilimumab with nivolumab monotherapy.
Journal of Clinical Oncology
Therapy for Muscle-Invasive Urothelial Carcinoma: Controversies and Dilemmas
Sonpavde GP, Mouw KW, Mossanen M
The Oncology Grand Rounds series is designed to place original reports published in the Journal into clinical context. A case presentation is followed by a description of diagnostic and management challenges, a review of the relevant literature, and a summary of the authors' suggested management approaches. The goal of this series is to help readers better understand how to apply the results of key studies, including those published in Journal of Clinical Oncology, to patients seen in their own clinical practice.
Journal of the National Cancer Institute
Lipsyc-Sharf M, Ma C, McCleary NJ, Mayer RJ, Meyerhardt JA, Ng K
Background: The incidence of young-onset colorectal cancer (yoCRC) is increasing. It is unknown if there are survival differences between young and older patients with metastatic colorectal cancer (mCRC).
METHODS: We studied the association of age with survival in 2326 mCRC patients enrolled in the Cancer and Leukemia Group B and SWOG 80405 trial, a multicenter, randomized trial of first-line chemotherapy plus biologics. The primary and secondary outcomes of this study were overall survival (OS) and progression-free survival (PFS), respectively, which were assessed by Kaplan-Meier method and compared among younger vs older patients with the log-rank test. Hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated based on Cox proportional hazards modeling, adjusting for known prognostic variables. All statistical tests were 2-sided.
RESULTS:Of 2326 eligible subjects, 514 (22.1%) were younger than age 50 years at study entry (yoCRC cohort). The median age of yoCRC patients was 44.3 vs 62.5 years in patients aged 50 years and older. There was no statistically significant difference in OS between yoCRC vs older-onset patients (median = 27.07 vs 26.12 months; adjusted HR = 0.98, 95% CI = 0.88 to 1.10; P = .78). The median PFS was also similar in yoCRC vs older patients (10.87 vs 10.55 months) with an adjusted hazard ratio of 1.02 (95% CI = 0.92 to 1.13; P = .67). Patients younger than age 35 years had the shortest OS with median OS of 21.95 vs 26.12 months in older-onset patients with an adjusted hazard ratio of 1.08 (95% CI = 0.81 to 1.44; Ptrend = .93).
CONCLUSION:In this large study of mCRC patients, there were no statistically significant differences in survival between patients with yoCRC and CRC patients aged 50 years and older.
Lancet Oncology
Richardson PG, Anderson KC
Background: The primary analysis of the ICARIA-MM study showed significant improvement in progression-free survival with addition of isatuximab to pomalidomide-dexamethasone in relapsed and refractory multiple myeloma. Here, we report a prespecified updated overall survival analysis at 24 months after the primary analysis.
METHODS: In this randomised, multicentre, open-label, phase 3 study adult patients (aged 18 years) with relapsed and refractory multiple myeloma who had received at least two previous lines of therapy, including lenalidomide and a proteasome inhibitor, and had an Eastern Cooperative Oncology Group performance status of 0-2 were recruited from 102 hospitals in 24 countries across Europe, North America, and the Asia-Pacific regions. Patients were excluded if they had anti-CD38 refractory disease or previously received pomalidomide. Patients were randomly assigned (1:1), using an interactive response technology with permuted blocked randomisation (block size of four) and stratified by number of previous treatment lines (2-3 vs >3) and aged (
Wen PY
We thank Osman Sütcüo?lu and colleagues for their response to our Article on treatment with dabrafenib–trametinib in patients with BRAFV600E-mutant low-grade and high-grade glioma. Their Correspondence raises two points for discussion: the difference between median progression-free survival and median overall survival and the post-progression therapies in patients with gliomas, including glioblastoma after dabrafenib–trametinib treatment.
As shown in our Article's appendix, notably the cohort of patients with high-grade glioma was separated into two subsets—those with disease that progressed quickly, often at or before the first assessment after baseline, and those with good durability of response, with only a few patients falling between these groups. These subsets provide insight into the difference between median progression-free survival and median overall survival, since the median describes the average patient, who might fall between these two subsets. Additionally, the upper limit of the 95% CI for median progression-free survival in patients with glioblastoma is 13·7 months, indicating a high degree of variation in the median estimate of 2·8 months and reflecting the subgroup of patients with longer progression-free survival.
Molecular Cell
Olsen SN, Godfrey L, Healy JP, Choi YA, Kai Y, Hatton C, Perner F, Haarer EL, Armstrong SA
MLL rearrangements produce fusion oncoproteins that drive leukemia development, but the direct effects of MLL-fusion inactivation remain poorly defined. We designed models with degradable MLL::AF9 where treatment with small molecules induces rapid degradation. We leveraged the kinetics of this system to identify a core subset of MLL::AF9 target genes where MLL::AF9 degradation induces changes in transcriptional elongation within 15 minutes. MLL::AF9 degradation subsequently causes loss of a transcriptionally active chromatin landscape. We used this insight to assess the effectiveness of small molecules that target members of the MLL::AF9 multiprotein complex, specifically DOT1L and MENIN. Combined DOT1L/MENIN inhibition resembles MLL::AF9 degradation, whereas single-agent treatment has more modest effects on MLL::AF9 occupancy and gene expression. Our data show that MLL::AF9 degradation leads to decreases in transcriptional elongation prior to changes in chromatin landscape at select loci and that combined inhibition of chromatin complexes releases the MLL::AF9 oncoprotein from chromatin globally.
Molecular Cell
Regulation of GTPase Function by Autophosphorylation
Johnson CW, Seo HS, Yang MH, Geffken EA, Lakhani J, Song K, Bashyal P, Popow O, Paulo JA, Liu A, Dhe-Paganon S, Haigis KM
A unifying feature of the RAS superfamily is a conserved GTPase cycle by which these proteins transition between active and inactive states. We demonstrate that autophosphorylation of some GTPases is an intrinsic regulatory mechanism that reduces nucleotide hydrolysis and enhances nucleotide exchange, altering the on/off switch that forms the basis for their signaling functions. Using X-ray crystallography, nuclear magnetic resonance spectroscopy, binding assays, and molecular dynamics on autophosphorylated mutants of H-RAS and K-RAS, we show that phosphoryl transfer from GTP requires dynamic movement of the switch II region and that autophosphorylation promotes nucleotide exchange by opening the active site and extracting the stabilizing Mg2+. Finally, we demonstrate that autophosphorylated K-RAS exhibits altered effector interactions, including a reduced affinity for RAF proteins in mammalian cells. Thus, autophosphorylation leads to altered active site dynamics and effector interaction properties, creating a pool of GTPases that are functionally distinct from their non-phosphorylated counterparts.
Nature
Silent Mutations Reveal Therapeutic Vulnerability in RAS Q61 Cancers
Kobayashi Y, Chhoeu C, Li J, Wei Z, Hong F, Bahcall M, Gokhale PC, Jänne PA
RAS family members are the most frequently mutated oncogenes in human cancers. Although KRAS(G12C)-specific inhibitors show clinical activity in patients with cancer1-3, there are no direct inhibitors of NRAS, HRAS or non-G12C KRAS variants. Here we uncover the requirement of the silent KRASG60G mutation for cells to produce a functional KRAS(Q61K). In the absence of this G60G mutation in KRASQ61K, a cryptic splice donor site is formed, promoting alternative splicing and premature protein termination. A G60G silent mutation eliminates the splice donor site, yielding a functional KRAS(Q61K) variant. We detected a concordance of KRASQ61K and a G60G/A59A silent mutation in three independent pan-cancer cohorts. The region around RAS Q61 is enriched in exonic splicing enhancer (ESE) motifs and we designed mutant-specific oligonucleotides to interfere with ESE-mediated splicing, rendering the RAS(Q61) protein non-functional in a mutant-selective manner. The induction of aberrant splicing by antisense oligonucleotides demonstrated therapeutic effects in vitro and in vivo. By studying the splicing necessary for a functional KRAS(Q61K), we uncover a mutant-selective treatment strategy for RASQ61 cancer and expose a mutant-specific vulnerability, which could potentially be exploited for therapy in other genetic contexts.
New England Journal of Medicine
Tumor-Infiltrating T Cells - A Portrait
Wu CJ
Immunotherapies have transformed the management of advanced cancers, yet many patients do not receive long-lasting clinical benefit from these agents. T cells are the primary mediators of antitumor immunity and play a central role in the response to immunotherapies. Despite substantial therapeutic advances, we do not fully understand the phenotype and function of tumor-infiltrating T cells in different types of cancer and how they affect clinical outcomes.
Neuron
A Functional Subdivision within the Somatosensory System and its Implications for Pain Research
Ma Q
Somatosensory afferents are traditionally classified by soma size, myelination, and their response specificity to external and internal stimuli. Here, we propose the functional subdivision of the nociceptive somatosensory system into two branches. The exteroceptive branch detects external threats and drives reflexive-defensive reactions to prevent or limit injury. The interoceptive branch senses the disruption of body integrity, produces tonic pain with strong aversive emotional components, and drives self-caring responses toward to the injured region to reduce suffering. The central thesis behind this functional subdivision comes from a reflection on the dilemma faced by the pain research field, namely, the use of reflexive-defensive behaviors as surrogate assays for interoceptive tonic pain. The interpretation of these assays is now being challenged by the discovery of distinct but interwoven circuits that drive exteroceptive versus interoceptive types of behaviors, with the conflation of these two components contributing partially to the poor translation of therapies from preclinical studies.
Advances in Radiation Oncology
Qian JM, Akama-Garren E, Shin J, Gunasti L, Bang A, Grassberger C, Schoenfeld JD
American Journal of Hematology
Davids MS, Crombie JL
American Journal of Hematology
Davids MS, Crombie JL
American Journal of Medical Quality
Jackman DM, Foster E, Hamilton JM, Tremonti C, Bunnell CA, Stuver SO, Jacobson JO
BJUI Compass
FGFR2/3 Genomic Alterations and Response to Enfortumab Vedotin in Metastatic Urothelial Carcinoma
Adib E, El Zarif T, Freeman D, Curran C, Akl E, Nassar AH, Ravi P, Mantia C, Kwiatkowski DJ, Choueiri TK, Sonpavde G
Blood Advances
A New Role for the SRC Family Kinase HCK as a Driver of SYK Activation in MYD88 Mutated Lymphomas
Munshi M, Liu X, Kofides A, Tsakmaklis N, Guerrera ML, Hunter ZR, Patterson CJ, Canning AG, Meid KE, Branagan AR, Flynn C, Sarosiek S, Castillo JJ, Wang J, Buhrlage S, Munshi NC, Anderson KC, Treon SP
Blood Cancer Discovery
Schaefer EJ, Wang HC, Karp HQ, Meyer CA, Cejas P, Fares I, Apffel A, Lim K, Xie Y, Gibson CJ, Schenone M, Murdock HM, Vedula RS, Winer ES, Garcia JS, Stone RM, Luskin MR, Carr SA, Long HW, Lindsley RC
British Journal of Cancer
Adib E, El Zarif T, Nassar AH, Akl EW, Abou Alaiwi S, Rana HQ, Choueiri TK, Kwiatkowski DJ, Sonpavde G
Cancer
Bychkovsky BL, Garber JE, Rana HQ
Cancer
Erfani P, Phelan J, Orav EJ, Figueroa JF, Lam MB
Cancer Epidemiology, Biomarkers and Prevention
Cardiometabolic Risk in Childhood Cancer Survivors: A Report from the Children's Oncology Group
Lipshultz ER, Vrooman LM
Cancer Immunology Research
Linking a Trio of Molecular Features in Clear-Cell Renal Cell Carcinoma
Labaki C, Van Allen EM, Choueiri TK
Cancer Nursing
A Systematic Review and Meta-analytic Evaluation of Moral Distress in Oncology Nursing
Eche IJ, Phillips CS, Alcindor N, Mazzola E
Cancer Nursing
Knoerl R, Wallar J, Fox E, Hong F, Salehi E, McCleary N, Ligibel JA, Reyes K
Cancer Treatment Reviews
Global Challenges and Policy Solutions in Breast Cancer Control
Trapani D, Fadelu T, Lin NU, Hassett M
Cell Research
The Hens Guarding Epithelial Cancer Fox-Houses
Gaynor LT, Shivdasani RA
Chemical Society Reviews
Small Molecule Modulation of Protein Polymerization
Fischer ES, Jones LH
Clinical Cancer Research
Choudhury AD, Shapiro GI
Clinical Cancer Research
Detecting Neuroendocrine Prostate Cancer Through Tissue-Informed Cell-Free DNA Methylation Analysis
Berchuck JE, Baca SC, McClure HM, Tsai HK, Nuzzo PV, Kelleher KM, He M, Steinharter JA, Zacharia S, Spisak S, Seo JH, Hirsch MS, Taplin ME, Choueiri TK, Pomerantz MM, Beltran H, Freedman ML
Clinical Cancer Research
Choueiri TK, Bakouny Z, Braun DA, Kaelin WG, Labaki C, McDermott DF, Pels K, Signoretti S
Clinical Nuclear Medicine
Radiation Recall Pneumonitis on FDG PET/CT Triggered by COVID-19 Vaccination
Hughes NM, Hammer MM, Awad MM, Jacene HA
Clinical Nuclear Medicine
Radiation Recall Pneumonitis on FDG PET/CT Triggered by COVID-19 Vaccination
Hughes NM, Hammer MM, Awad MM, Jacene HA
Current Opinion in Hematology
Venetoclax Combination Therapy in Acute Myeloid Leukemia and Myelodysplastic Syndromes
Shimony S, Stone RM, Stahl M
Current Opinion in Oncology
Preoperative Immunotherapy for Head and Neck Cancers: State of Art
Egloff AM, Uppaluri R
Diabetology and Metabolic Syndrome
Dieli-Conwright CM
ESMO Open
How I Treat HER2-Positive Early Breast Cancer: How Long Adjuvant Trastuzumab is Needed?
Morganti S, Giordano A
European Journal of Cancer
Sonpavde GP
European Journal of Cancer
Tyekucheva S, Regan MM
Experimental Hematology
Van Egeren D, Kamaz B, Liu S, Nguyen M, Reilly CR, DeAngelo DJ, Galinsky I, Wadleigh M, Winer ES, Luskin MR, Stone RM, Garcia JS, Hobbs GS, Michor F, Mullally A, Hormoz S
Head and Neck
Tyan K, Bae JE, Lorch JH, Margalit DN, Tishler RB, Huynh MA, Jo VY, Haddad RI, Chau NG, Hanna GJ, Schoenfeld JD
International Journal of Cancer
Rettig EM, Faden DL, Sandhu S, Wong K, Faquin WC, Warinner C, Richmon JD, Uppaluri R, Varvares M, Sethi R, Hanna GJ, Sroussi H
International Journal of Radiation Oncology, Biology, Physics
Bitterman DS, Selesnick P, Bredfeldt J, Williams CL, Guthier C, Huynh E, Kozono DE, Cormack RA, Mak RH, Atkins KM
Journal of Clinical Neuroscience
Agaronnik ND, Kwok A, Schoenfeld AJ, Lindvall C
Journal for ImmunoTherapy of Cancer
PI3K Activation Allows Immune Evasion by Promoting an Inhibitory Myeloid Tumor Microenvironment
Collins NB, Al Abosy R, Bi K, Yates KB, Manguso RT, Wadsworth M, Hughes T, Shalek AK, Boehm JS, Hahn WC, Doench JG
Journal for ImmunoTherapy of Cancer
Phase IB Study of Ziv-Aflibercept Plus Pembrolizumab in Patients with Advanced Solid Tumors
Rahma OE, Tyan K, Giobbie-Hurder A, Hathaway E, Cunningham R, Manos M, Severgnini M, Rodig S, Stephen Hodi F
Journal of Integrative and Complementary Medicine
Auricular Acupuncture During Chemotherapy Infusion in Breast Cancer Patients: A Feasibility Study
Yang E, Lu W, Giobbie-Hurder A, Chen WY, Block CC, Partridge A, Jeselsohn RM, Tolaney SM, Freedman RA, Ligibel JA
Journal of Neuroimaging
Mishra S, Bergmark RW, Jo VY, Miyawaki EK, Schoenfeld JD, Uppaluri R, Guenette JP
Journal of Pain and Symptom Management
One Size Doesn't Fit All in Early Pediatric Oncology Bereavement Support
Helton G, Beight L, Morris SE, Wolfe J, Snaman JM
Journal of Palliative Medicine
Missing Voices: Lessons Learned from Nonparticipating Caregivers in Palliative Care Research
Umaretiya PJ, Ilowite M, Fisher L, Mack JW, Bona K
Journal of Palliative Medicine
Sager Z, Ljuslin M, Tulsky JA, Beaussant Y
Journal of Palliative Medicine
Sager Z, Ljuslin M, Tulsky JA, Beaussant Y
Journal of Pediatric Hematology/Oncology
Umaretiya P, Vrooman LM
Journal of Thoracic Oncology
Ricciuti B, Lin JJ, Vajdi A, Vokes N, Tolstorukov MY, Li YY, Spurr LF, Cherniack AD, Recondo G, Lamberti G, Wang X, Venkatraman D, Alessi JV, Vaz VR, Khosrowjerdi S, Digumarthy S, Park H, Vaz N, Nishino M, Sholl LM, Barbie D, Gainor JF, Awad MM
JAMA Network Open
Achieving Global Pediatric Palliative Care Equity-What We Have Yet to Learn
Umaretiya PJ, Wolfe J
JAMA Otolaryngology – Head and Neck Surgery
Shah H, Wang Y, Cheng SC, Gunasti L, Chen YH, Lako A, Guenette J, Rodig S, Jo VY, Uppaluri R, Haddad R, Schoenfeld JD, Jacene HA
JCI Insight
Li MM, Chen N, Duncan CN, Margossian SP, Lehmann LE, Birbrayer O, Silverstein S, Kim S, Ritz J, London WB, Whangbo JS
JCO Oncology Practice
Optimal Endocrine Therapy in Premenopausal Women: A Pragmatic Approach to Unanswered Questions
Sella T, Partridge AH
JCO Oncology Practice
Refining Patient-Centered Measures of End-of-Life Care Quality for Children with Cancer
Wolfe J
Leukemia and Lymphoma
Targeting Mitochondrial Metabolism in Acute Myeloid Leukemia
Stahl M
Leukemia
Gadi D, Griffith A, Tyekucheva S, Wang Z, Rai V, Vartanov A, Thrash E, Fernandes SM, Lehmberg TZ, Lee B, Martindale SP, Machado JH, Odejide O, Armand P, Fisher DC, Arnason J, Davids MS, Lederer JA, Brown JR
Medical Physics
Huynh E, Boyle S, Campbell J, Penney J, Mak RH, Schoenfeld JD, Leeman JE, Williams CL
Neuro-Oncology
Nayak L, Batchelor TT, Huang RY, Guenette JP
Neuro-Oncology
Predictors of Long-Term Survival Among Patients with Brain Metastases
Lamba N, Catalano PJ, Bi WL, Wen PY, Haas-Kogan DA, Aizer AA
NPJ Breast Cancer
Impact of a Randomized Weight Loss Trial on Breast Tissue Markers in Breast Cancer Survivors
Dieli-Conwright CM
Pediatric Blood and Cancer
Pediatric Palliative Care has a Place Everywhere
Feraco AM
Pediatric Critical Care Medicine
Duncan C, Randolph AG, Lehmann L
Radiology
Nishino M
Supportive Care in Cancer
Knoerl R, Giobbie-Hurder A, Sannes TS, Dillon D, Dominici LS, Frank ES, Rhei E, Tolaney SM, Winer EP, Ligibel JA
Urologic Oncology
Nassar AH, Abou Alaiwi S, Adib E, Akl EW, Sonpavde GP
World Neurosurgery
Incidence and Predictors of Neurologic Death in Patients with Brain Metastases
Lamba N, Catalano PJ, Cagney DN, Wen PY, Aizer AA