Dana-Farber Research News 09.15.2026
Welcome to Dana-Farber's Research News
September 15, 2026
This twice-monthly newsletter highlights recently published research where Dana-Farber faculty are listed as first or senior authors. The information is pulled from PubMed and this issue notes papers published from August 16 - 31.
If you are a Dana-Farber faculty member and you think your paper is missing from Research News, please let us know by emailing dfciresearchnews@dfci.harvard.edu.
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Annals of Oncology Choueiri TK BACKGROUND: The randomized phase III study KEYNOTE-564 (NCT03142334) established pembrolizumab after surgery as the standard of care for patients with clear cell renal cell carcinoma (ccRCC) at increased risk of recurrence. Prior analyses showed significantly improved disease-free survival (DFS) and overall survival (OS) with adjuvant pembrolizumab versus placebo. We present results from the fourth prespecified interim analysis, with a minimum follow-up of five years. PATIENTS AND METHODS: Eligible adults with ccRCC at increased risk of recurrence were randomly assigned 1:1 to adjuvant pembrolizumab 200 mg or placebo every 3 weeks following nephrectomy or following nephrectomy and metastasectomy. Study treatment continued for ?17 cycles (?1 year), until recurrence, or until treatment discontinuation criteria were met. The primary endpoint was DFS per investigator assessment, and the key secondary endpoint was OS. Safety was a secondary endpoint. RESULTS: Overall, 994 participants were randomized to pembrolizumab (n = 496) or placebo (n = 498). Median time from randomization to data cutoff (September 25, 2024) was 70 months (range, 60-87). Pembrolizumab improved DFS versus placebo (hazard ratio [HR] 0.71, 95% CI 0.59-0.86); median DFS was not reached (NR) versus 68 months, and estimated 5-year DFS rates were 60.9% versus 52.2%, respectively. OS was improved with pembrolizumab over placebo (HR 0.66, 95% CI 0.48-0.90); median OS was NR for both arms with an estimated 5-year OS rate of 87.7% and 82.3%, respectively. DFS and OS benefits were consistent across key subgroups. Safety was largely unchanged since last analysis. CONCLUSIONS: After a median follow-up of 70 months, adjuvant pembrolizumab demonstrated sustained DFS and OS benefit and a safety profile consistent with prior analyses. These findings continue to support the use of adjuvant pembrolizumab in ccRCC at increased risk of recurrence. |
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Annals of Oncology Garber JE, Gelber RD BACKGROUND: The randomised phase III OlympiA trial (NCT02032823) compared 1 year of adjuvant olaparib (oral poly-(ADP-ribose) polymerase [PARP] inhibitor) to placebo in 1,836 patients with pathogenic/likely pathogenic BRCA1 or BRCA2 (gBRCApv) germline variants and high-risk human epidermal growth factor receptor 2 (HER2)-negative early breast cancer (BC). Previous interim analyses (IA) demonstrated statistically significant improvements in invasive disease-free survival (IDFS), distant disease-free survival (DDFS) and overall survival (OS), irrespective of hormone receptor status, prior platinum, timing of prior chemotherapy or type of gBRCApv. Herein are the results of the third pre-specified IA with a median follow-up (MFU) of 6.1 years. PATIENTS AND METHODS: Descriptive analyses are presented for the primary endpoint IDFS, and key secondary endpoints of DDFS and OS. Estimates of the hazard ratio (HR) based on the stratified Cox's Proportional Hazards Model and 95% confidence intervals (CI) are presented with yearly event rates up to 6.1 years MFU. Safety analyses included AESIs. RESULTS: Olaparib benefits were maintained in IDFS [HR=0.65 (95% CI: 0.53, 0.78)], DDFS [HR=0.65 (95% CI: 0.53, 0.81)] and OS [HR=0.72 (95% CI: 0.56, 0.93)]. The 6-year OS for olaparib vs. placebo was 87.5% vs. 83.2% [Difference 4.4% 95% CI: 0.9%, 6.7%]. Olaparib benefit was consistent across all key subgroups, including patients with high-risk hormone receptor-positive disease. There were fewer BRCA-associated new breast and ovarian/fallopian tube cancers and no increase in AESI risks (6.3% versus 9.3%), including myelodysplastic syndrome (MDS)/acute myeloid leukaemia (AML) (0.4% versus 0.7%), with olaparib versus placebo. CONCLUSIONS: At 6.1 years MFU, 1 year of adjuvant olaparib after (neo)adjuvant chemotherapy demonstrates ongoing clinically meaningful improvements in IDFS, DDFS and OS in patients with gBRCApv and high-risk, HER2-negative early BC, with acceptable toxicity and without increased risk of MDS/AML. These data continue to provide support for adjuvant olaparib in the treatment of gBRCApv-associated high-risk, HER2-negative early BC. |
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Annals of Oncology Therapeutic Targeting of RAS-Mediated Resistance in Oncogene-Driven Lung Cancer Facchinetti F, Liao L, Nakazawa S, Aldea M, Pecci F, Makarem M, Tuladhar B, Ngo K, Odintsov I, Koivu MKA, Kwiatkowski DJ, Ricciuti B, Rotow JK, Luo J, LoPiccolo J, Florez N, Awad MM, Barbie DA, Paweletz CP, Gokhale PC, Feng WW, Shaw AT, Jänne PA BACKGROUND: Despite the dramatic activity of next generation targeted therapies, most patients with oncogene-driven lung cancers eventually relapse. Novel inhibitors are particularly active against on-target resistance, fostering the emergence of off-target resistance mechanisms. The current clinical development of RAS inhibitors hints at their potential role in overcoming off-target resistance mediated by RAS alterations. PATIENTS AND METHODS: Using tissue and liquid biopsies, we assessed resistance mechanisms to first-line osimertinib in patients with EGFR-mutant lung cancer, and to ALK-, MET-, ROS1-, and RET- inhibitors, for a total of 590 patients. We established two patient-derived models with acquired KRAS mutations obtained at osimertinib progression, enabling in vitro and in vivo functional experiments. RESULTS: Among 312 patients progressing on first-line osimertinib, we observed a major complementary role of tissue and liquid biopsies in identifying resistance mechanisms. We identified RAS alterations in 35 of 312 patients (11.2%), with an enrichment in KRAS G12D (n = 10) and a paucity of KRAS G12C (n = 1) mutations. In patients with ALK-positive disease (n = 148), RAS alterations were more common at resistance to lorlatinib compared to second-generation inhibitors (14.7% vs 5%, p = 0.0444). Across MET-, ROS1-, and RET-driven lung cancers at progression to targeted agents, RAS alterations were detected in 7-16% of the cases. In the two patient-derived models established at osimertinib resistance with acquired KRAS mutations (G12D and G12R, respectively), we tested the combinatorial effect of osimertinib with either the selective KRAS G12D inhibitor zoldonrasib or the pan-RAS inhibitor daraxonrasib. Both combinations demonstrated marked synergistic activity in vitro and in vivo. CONCLUSIONS: RAS alterations mediate resistance to targeted agents in approximately 10% of oncogene-driven lung cancer. Rational combinations with novel RAS inhibitors are effective in preclinical models, providing the basis for their clinical investigation and extending the paradigm of precision oncology. |
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Blood Bone Marrow Stem Cell Connexins: Misconceptions and New Insights Singh AK, Rallis KS, Cancelas JA Hematopoietic regeneration requires coordinated activation of hematopoietic stem and progenitor cells (HSPCs) and adaptive remodeling of the bone marrow microenvironment to meet extreme metabolic and oxidative demands imposed by cytotoxic injury, transplantation, and inflammation. Although soluble factors and cytokine signaling are central to this process, emerging evidence identifies direct intercellular communication as a critical regulatory layer in stress hematopoiesis. Connexins, particularly connexin-43 (Cx43), form an evolutionarily conserved communication network that integrates metabolic coupling, redox buffering, and organelle dynamics across hematopoietic and stromal compartments. Beyond canonical gap junction channel activity, connexins exert nonjunctional, compartment-specific functions through cytoplasmic, nuclear, and mitochondrial pools that regulate signaling scaffolds, transcriptional programs, cytoskeletal organization, mitochondrial dynamics, calcium homeostasis, and bioenergetics. In HSPCs, mitochondrial Cx43 functions as a metabolic checkpoint that preserves regenerative capacity by supporting oxidative phosphorylation, limiting chronic adenosine monophosphate-activated protein kinase activation, maintaining fusion-fission balance, and preventing mitochondrial Ca2+ overload. In parallel, Cx43 enables mitochondrial transfer from donor HSPCs to stromal niche cells, restoring stromal metabolic competence and promoting effective niche repair and engraftment. Dysregulation of connexin networks contributes to marrow failure, clonal evolution, leukemic niche remodeling, and chemoresistance, highlighting their context-dependent roles in health and disease. This review synthesizes advances in connexin biology in hematopoiesis, reframes connexins as integrators of metabolic and regenerative signaling rather than passive conduits, and defines emerging translational opportunities. Isoform- and compartment-specific targeting of connexin pathways offers a therapeutic strategy to enhance hematopoietic recovery, preserve long-term stem cell function, and disrupt pathological niche support in hematologic malignancies. |
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Blood Esrick EB, Lehmann L, Federico A, Vincon H, Liu B, Daley H, Dansereau C, Kao PC, Morris E, Negre H, Shaw KL, Ritz J, Silva O, Grant PE, London WB, Justus DG, Armant M, Manis J, Williams DA Sickle cell disease (SCD) is characterized by chronic hemolysis, and painful vaso-occlusive episodes (VOE). High levels of fetal hemoglobin (HbF) attenuate the disease phenotype. We used a lentivirus vector (LVV) expressing a short hairpin RNA embedded in a microRNA (shmiR) that targets BCL11A in erythrocytes to induce HbF in a first-in-human study in SCD. The purpose of the study was to assess hematopoietic stem/progenitor cells collection, transduction parameters, safety, HbF induction, and durability. Eleven eligible patients with SCD underwent hematopoietic stem cell (HSC) collection. Plerixafor-mobilized peripheral blood HSCs required for manufacturing were obtained in 1 mobilization cycle for 10 of 11 participants, and 11 of 11 patient products were successfully manufactured with a median time to release of product of 39 days. Ten patients were infused with HSCs transduced with the shmiR vector. Engraftment occurred in all 10 patients. At a median follow-up of 58 months (range, 35-82) after infusion, there were no adverse events attributed to the vector. The transduction efficiency was 93.1%. One patient demonstrated low engraftment of the transduced cells and had suboptimal HbF induction. In the remaining 9 patients, at 2 years after treatment, the peripheral blood demonstrated 71% F cells with 11.9 pg HbF per F cells, and both parameters remained stable in 9 patients with ?48 months follow-up. All patients who had VOEs before gene therapy demonstrated sustained mitigation of pain events. These data demonstrate excellent manufacturing efficiency, efficacy and safety of targeting BCL11A using a shmiR LVV, and long-term durability of the shmiR vector, leading to a pivotal, multisite, phase 2 trial that is currently underway (NCT05353647). This trial was registered at www.clinicaltrials.gov as NCT03282656. |
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Cell Genomics Defining and Cataloging Variants in Pangenome Graphs Salehi Nowbandegani P, Zhang S, Hu H, Li H, O'Connor LJ Structural variation causes some human haplotypes to align poorly with the linear reference genome, and this leads to "reference bias." A pangenome reference graph could ameliorate this bias by relating a sample to multiple reference assemblies. However, this approach requires a new definition of a "genetic variant." We define pangenome variants against a reference tree that includes all nodes (sequences) of the pangenome graph but only a subset of its edges; non-reference edges are variant edges. Analyzing the Minigraph-Cactus draft human pangenome reference graph, we identified 29.6 million genetic variants. 3.5 million variants (11.7%) have a reference allele that is not on GRCh38; these variants are difficult to detect without a pangenome reference and are found within tangled, multiallelic regions. We analyze the HLA-A and RHD gene regions and identify thousands of small variants entangled with several structural variants. We release the open-source pantree and a variant call format (VCF) variant catalog. |
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JAMA Oncology Systemic Therapy Considerations in Older Adults with Early-Stage Breast Cancer: A Review Smith CE, Sammons SL, Minami CA, Hshieh TT, Smith S, Ruderman K, Bak K, Lin NU, Freedman RA IMPORTANCE: The treatment of older adults with chemotherapy for early-stage breast cancer involves a complex decision-making process that weighs the competing risks of disease recurrence against the potential harms of treatment. While older adults continue to be underrepresented in therapeutic clinical trials, there is a growing body of evidence to support optimal management of each subtype of early-stage breast cancer, including novel strategies like adjuvant cyclin-dependent kinase 4/6 inhibitors in hormone receptor-positive disease, and the neoadjuvant use of pembrolizumab in triple-negative breast cancer. OBSERVATIONS: The available evidence to support the systemic management of early-stage breast cancer in older adults with consideration of the data gaps for cytotoxic chemotherapy, de-escalated regimens, and targeted therapies is reviewed, and tools to optimize decision-making and supportive care for older adults with early breast cancer are presented. Clinicians should aim to avoid overtreatment when available evidence suggests a less intensive approach may suffice for a lower-risk cancer, and/or the patient is at high risk of serious toxic effects from chemotherapy treatment. On the other hand, undertreatment without consideration of the potential downsides may increase breast cancer-related mortality in older patients with higher-risk cancers. CONCLUSIONS AND RELEVANCE: This review will help clinicians best use the available data and decision-making tools to support best practice for treating older adults with early-stage breast cancer and will highlight ongoing clinical trials aimed at optimizing medical care for this patient population. |
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Journal of Clinical Oncology Beltran H, Berg S, Choudhury AD, Jacene HA, McGregor B, Choueiri TK PURPOSE: Bone metastases (BM) occur in approximately 30% of patients with metastatic renal cell carcinoma (mRCC) and are associated with poor survival and symptomatic skeletal events (SSEs). Radium-223, an alpha-emitting bone-seeking radioisotope, and cabozantinib, a tyrosine kinase inhibitor, have demonstrated activity in BM. RADICAL (Alliance A031801; ClinicalTrials.gov identifier: NCT04071223) evaluated cabozantinib ± radium-223 in mRCC with BM. METHODS: This phase II trial enrolled patients with mRCC of any histology with ?1 BM. Patients were randomly assigned 1:1 to cabozantinib ± radium-223, stratified by osteoclast-targeted therapy (OTT), prior therapy, opioid use, and International mRCC Database Consortium (IMDC) risk. The primary end point was SSE-free survival (SSE-FS). Secondary end points included safety, objective response rate (ORR), progression-free survival, and overall survival (OS). A target of 124 evaluable patients was planned, with a prespecified interim futility analysis at 50% of expected SSE-FS events; the trial would stop if the stratified hazard ratio (sHR) > 1.0. RESULTS: The prespecified interim futility analysis was conducted after 90 patients were enrolled and crossed the futility boundary, leading to closure at 98 patients. The final analysis included all 98 patients. Median age was 63 years, 82.7% had clear cell histology, and 79.6% were using an OTT. IMDC risk was favorable (18.4%), intermediate (67.3%), and poor (14.3%). Median follow-up was 13.1 months. Median SSE-FS for cabozantinib with radium-223 versus cabozantinib was 16.7 versus 17.6 months (sHR, 1.46 [90% CI, 0.86 to 2.51]). Median OS was 28.3 versus 19.7 months (sHR, 1.40 [95% CI, 0.70 to 2.79]). ORR was 19.4% versus 25.0% (P = .78). Grade ?3 adverse events were similar across arms (69.6% v 75.5%). CONCLUSION: Radium-223 did not improve SSE-FS when added to cabozantinib. The combination demonstrated a manageable safety profile. |
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Journal of Clinical Oncology Hassett MJ PURPOSE: To provide recommendations on use of medical therapies for patients with stage I-III hormone receptor-positive, HER2-negative breast cancer. METHODS: An Expert Panel including patient representation completed a systematic review of the evidence and formulated recommendations for practice. Eligible studies included patients with stage I-III hormone receptor-positive, HER2-negative breast cancer and evaluated neoadjuvant or adjuvant chemotherapy, endocrine therapy, immunotherapy, or targeted therapy. Outcomes of interest included pathologic complete response, disease-free survival, distant recurrence-free survival, overall survival, health-related quality of life, and treatment-related adverse effects. RESULTS: Forty-five randomized clinical trials (68 references) published from 2018-2026 were identified by the broad literature search. Supplemental searches identified six individual patient data meta-analyses and 21 retrospective studies that, combined with the primary clinical trials, informed guidance on which patients should receive treatment, which treatments should be selected, optimal treatment timing, duration of treatment, and approaches to support adherence. A final section addresses estimation of prognosis and treatment benefit to inform decisions across all phases of treatment. RECOMMENDATIONS: The recommendations are organized to follow the longitudinal care of patients with stage I-III hormone receptor-positive, HER2-negative breast cancer, reflecting the sequence of decisions faced by clinicians from diagnosis through completion of systemic therapy. Endocrine therapy remains the foundation of treatment for stage I-III hormone receptor-positive, HER2-negative breast cancer. For selected patients, chemotherapy and targeted therapies can further reduce the risk of recurrence and breast cancer death. Treatment recommendations should integrate clinicopathologic features, genomic assays, patient preferences, treatment tolerability, and estimated recurrence risk. The guideline provides evidence-based recommendations to support individualized treatment selection and sequencing across the continuum of care. Additional information is available on the ASCO Publications website. |
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Molecular Cell BRAF and MEK Caught in Flagrante Delicto Jang DM, Eck MJ The RAF/MEK/ERK kinase cascade is a central signaling axis governing cell proliferation and survival. This cascade is activated downstream of receptor tyrosine kinases on the cell surface that activate RAS, which in turn binds and activates RAF. Mutations in BRAF, one of three RAF isoforms, and other components of this pathway drive many common cancers. Regulation of RAFs is famously complex, but structural studies over the past dozen years have brought many aspects of its activation and inhibition into focus. RAFs are maintained in a monomeric, autoinhibited state by binding of a 14-3-3 dimer to two serine-phosphorylated sites that flank the kinase domain. RAS-driven recruitment of RAFs to the plasma membrane releases these autoinhibitory constraints, thereby allowing the 14-3-3 dimer to rearrange to bind the C-terminal phosphosites of two RAFs, a process that ultimately drives the side-by-side dimerization of the RAF kinase domain that is crucial for its activation. Prior work has also revealed how RAF binds MEK and forms a stable complex even prior to activation. Despite this wealth of structural information, important questions remained to be answered. Available structures with MEK show it in a conformation in which its activating phosphorylation sites are inaccessible to RAF. How does it rearrange to allow phosphotransfer? And how does the N-terminal acidic (NtA) motif, a four-residue segment just N-terminal to the kinase domain that is differentially phosphorylated across RAF isoforms, participate in RAF activation? This segment has been disordered in prior RAF structures, with its regulatory effects left as a mystery. In this issue of Molecular Cell, Kondo and colleagues describe new crystal structures that address both questions by capturing BRAF in the act of phosphorylating MEK. |
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Molecular Cell Disruption of Microhomology-Mediated End Joining in Ewing Sarcoma Asada S, Zhu G, Abeykoon JP, Tanaka Y, Nguyen H, Hirohashi Y, Iyer DR, Ashton NW, Mukkavalli S, Velazquez M, Jiang L, Parmar K, Van Allen EM, Gillani R, Shapiro GI, D'Andrea AD Ewing sarcoma (EwS) is a group of bone and soft-tissue cancers in children and young adults. Because EwS cells have pronounced sensitivity to radiation and chemotherapy-induced DNA damage, the oncoprotein EWS-FLI1 is likely to be involved in DNA repair. Here, we demonstrate that EWS-FLI1 causes a defect in microhomology-mediated end joining (MMEJ) repair. EWSR1 is a splicing factor that promotes the faithful splicing of the POLQ pre-mRNA, required for the expression of Pol?, a critical protein in the MMEJ pathway. Expression of EWS-FLI1 or depletion of EWSR1 causes increased POLQ exon 25 skipping, decreased Pol? expression, impaired MMEJ, and enhanced cellular sensitivity to inhibitors of the Fanconi anemia (FA), homologous recombination (HR), or non-homologous end joining (NHEJ) pathways, through the mechanism of synthetic lethality. Correction of POLQ exon 25 skipping restored Pol? expression and MMEJ activity in EwS. Inhibitors of the FA, HR, or NHEJ pathways may therefore provide a targeted therapy for EwS patients. |
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Nature Chemical Biology An Enantioselective Covalent Inhibitor of BAX Confers Cytoprotection in Vivo Shi P, McHenry MW, Camara CM, Yang K, Godes M, Pazyra-Murphy MF, Branch MR, Tesar B, Segal RA, Rubin LL, Bird GH, Gygi SP, Walensky LD No therapies directly block apoptosis in tissue injury or the many diseases driven by cell loss. The BCL-2 family protein BAX is a central mediator of this pathway and C126 resides within a key regulatory region where physiologic or pharmacologic ligands can activate or inhibit its function. Here, we report enantioselective covalent BAX inhibitors that site-specifically react with C126 and confer cytoprotection across multiple cell types. These ligands constrain BAX conformation and suppress apoptosis in a strictly BAX-dependent manner. Medicinal chemistry optimization yielded covalent BAX inhibitor 3 (CBI-3), an analog with pharmacokinetics suitable for in vivo studies. In a murine model of Fas-induced fulminant hepatic failure, CBI-3 reduced hepatocyte apoptosis and preserved liver histology and survival. CBI-3 also conferred cytoprotection of motor neurons derived from human induced pluripotent stem cells of healthy and amyotrophic lateral sclerosis donors. These findings establish covalent BAX inhibition as a therapeutic strategy to directly block pathologic cell death. |
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ACS Chemical Biology Evaluation of HDAC8 as a Druggable Target in STAG2-Mutant Ewing Sarcoma Olaoye O, Xiong Y, Rillahan CD, Adane B, DiGiovanni G, Ross KN, Alexe G, Howard B, Kirmani N, Nowak RP, Donovan KA, Fischer ES, Stegmaier K |
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American Journal of Hematology Rolles B, Brunner AM, Barua S, Harris AC, Shimony S, Lindsley RC, Stahl M |
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Bone Marrow Transplantation Dulery R |
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Cancer Research Communications Choudhury AD, Zhong C, Xie W, Kochupurakkal BS, Liu R, Yang DD, Einstein DJ, Pace A, Mouw KW, Adalsteinsson VA, Van Allen EM, D'Andrea A, Taplin ME, Shapiro GI |
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Cancer Research Communications Vitronectin Enrichment in Prostate Cancer Liver Metastases Promotes Adhesion and Survival Egelberg J, Kim R, Kim MJ, Dsouza JM, Molania R, Venkadakrishnan VB, Chen J, Bakht MK, Beltran H |
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Cell Reports Medicine Biomarker-Guided Responses in Patient-Derived Organoids Predict Effective Therapies in Breast Cancer Moore K, Dillon D, Overmoyer B, Lynce F, Rosenbluth JM |
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Cell Reports Medicine PARP Inhibition Enhances the Antitumor Activity of HER3-DXd in Non-Small Cell Lung Cancer Lopez T, Knott A, Soroko KM, Gokhale PC, Jänne PA, Haikala HM |
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Cell Systems Cheng YC, McDonald TO, Wu W, Guarducci C, Russo D, Abravanel DL, Bailey M, Jeselsohn R, Michor F |
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Clinical Cancer Research Schlechter BL, Bullock AJ, Bockorny B |
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Clinical Cancer Research Rhoades J, Patel A, Xiong K, Li R, Walsh L, Crnjac A, Hannigan A, Remland J, Brais L, Jain P, Sridhar S, Gilligan K, Carnes M, Shin KY, Catalano P, Wiener D, Papke DJ, Makrigiorgos GM, Adalsteinsson VA, Enzinger P, Mamon H |
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Current Biology Evolution of a Core Ribosomal Innovation in Octopus Mitra R, Han R, Scott TJ, Grearson AG, Liu CG, Kim H, Bellono NW, Lee ASY |
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International Journal of Radiation Oncology, Biology, Physics Stawiski K, Mouw KW, Fendler W |
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International Journal of Radiation Oncology, Biology, Physics Leeman JE, Droznin AD, Dwyer CD, Shin KY, Roth DF, Chirmade S, Han Z, Boyle S, Margalit DN, Tishler RB, Sethi RK, Annino DJ, Goguen LA, Rettig EM, Haddad RI, Uppaluri R, Mak RH, Carroll TL, Singhrao K, Schoenfeld JD |
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Journal of Clinical Investigation Li Y, Laimon YN, Cho H, Vivero M, de Oliveira GR, Seager MD, Delcea A, Savla V, Durmaz YT, Qiu X, Kukreja S, Li R, El Zarif T, Lu W, Van Orden M, Bronson RT, Li S, Barbie DA, Freedman ML, Long HW, Signoretti S, Oser MG |
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Journal of Clinical Investigation Hao J, Kochupurakkal B, Branigan TB, Somuncu OS, Liu R, Jadhav H, da Costa AABA, Jiao Y, Yu JZ, Martignetti DB, Sadatrezaei G, Mukkavalli S, Gokhale PC, Cheng SC, Skates SJ, Konstantinopoulos PA, Liu JF, Parmar K, D'Andrea AD, Shapiro GI |
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Journal of Clinical Pathology Paediatric B-Lymphoblastic Leukaemia with Low Peripheral Blasts: A Potential Diagnostic Pitfall Harris EM, Heeney MM, Place AE, Harris MH, Fleming MD, Bledsoe JR |
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Journal of Neuro-Oncology Rahman R, Tanguturi S, Catalano PJ, Haas-Kogan DA, Meredith D, Bi WL, Guenette JP, Lamba N, Aizer AA |
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Journal of Pain and Symptom Management Impact of Satisfactory Family Coping on the Mental Health of Parents Whose Children Died of Cancer Rosenbaum ARP, Pearson G, Chen L, Ream M, Rosenberg AR, McCarthy S, Snaman J |
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Journal of Thrombosis and Haemostasis Connors JM |
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Leukemia and Lymphoma DeAngelo DJ |
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MedEdPORTAL What You Need to Know About Sports Psychiatry: An Introductory Curriculum for Psychiatry Residents Watson J, Desir M, Twark C, Amonoo HL |
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Pediatric Blood and Cancer Mullen EA |
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Philosophical Transactions of the Royal Society B: Biological Sciences Eck MJ, Scott DA |
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Physics in Medicine and Biology From Optimization of Radiation Dose Distributions to Optimal Cancer Treatments Bortfeld T |
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Transplantation and Cellular Therapy Murdock HM, Hebert K, Gooptu M, Shapiro R, Abel G, Cutler C, Kelkar A, Ho VT, Koreth J, O'Connor TP, Brock J, Auriemma E, Bat-Erdene D, Panaro K, Ritz J, Lindsley RC, Antin JH, Soiffer RJ, Garcia JS |
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