Dana-Farber Research News 04.15.2026
Welcome to Dana-Farber's Research News
April 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 March 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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Cancer Cell A Tumor-Associated Photoreceptor Signature Unifies Distinct Central Nervous System Malignancies Englinger B, Meredith D, Alexandrescu S, Filbin MG Pineoblastoma is a clinically aggressive childhood brain tumor composed of distinct molecular subgroups with divergent driver genes, demographics, and clinical outcomes. To identify developmental origins and mechanisms governing disease pathogenesis, we derive single-cell transcriptomes from pineal parenchymal tumors, aligning malignant cells with developmental counterparts to retrace cellular origins. Integrative computational analyses map pineoblastoma origins to transient, cycling pinealocyte progenitors during development. Lineage-specific perturbation of suspected drivers in the early pineal gland yields preclinical models representative of consensus molecular subgroups. Multi-omic characterization of patient tumors and these models uncover a tumor-associated photoreceptor signature (TAPS) common to pineoblastoma, retinoblastoma, and Group 3 medulloblastoma. Transcriptional activity of this signature within respective cellular origins establishes a developmental basis for molecular similarities between entities. Photoreceptor signature constituents are selective dependencies across these anatomically distinct central nervous system malignancies, motivating future studies evaluating developmentally encoded programs of malignancy as potential therapeutic liabilities. |
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Journal of Clinical Oncology Ethical Design and Implementation of Monetary Transfer Interventions in Clinical Cancer Research Hantel A, Hanson E, Abel GA, Bona K Monetary transfer interventions (MTIs) are payments provided to recipients to meet specific needs. MTIs originated in the 1980s to combat the impacts of several South and Central American debt crises. Since that time, MTIs have been designed, implemented, and evaluated as a public health or welfare mechanism to improve social and economic outcomes driven by poverty or related vulnerabilities. Monetary incentives have also been studied in cancer control research to promote specific health behaviors, such as smoking cessation. Now, however, MTIs are being tested in clinical research as therapeutic interventions intended to modify the economic conditions that may causally contribute to health outcomes. The first oncology studies using this approach are now emerging, such as one evaluating the impact of an MTI on childhood cancer survival. Unlike reimbursement, compensation, or appreciation payments for participating in research testing other interventions, payments in MTIs are the intervention. This raises a distinct set of ethical and practical challenges with which cancer researchers and institutional review boards may be less familiar. In this article, we assess the types, purposes, and challenges of MTIs in clinical cancer research and provide guidance on their ethical design and practical conduct. |
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Journal of Clinical Oncology Sentana-Lledo D, Morgans AK Vasomotor symptoms (VMS), including hot flashes, plague many patients with prostate cancer receiving androgen deprivation therapy (ADT). A majority of patients report VMS to be the most bothersome ADT-related symptom, which can ultimately affect adherence to a cornerstone of systemic therapy in prostate cancer. Perhaps due to decades with a lack of precise understanding of the biologic mechanism underlying VMS, a paucity of readily available efficacious treatment options, and a general disinterest by patients in taking more medications, the search for effective therapies against VMS for the prostate cancer population has lagged behind that of other patient groups. |
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Journal of the National Cancer Institute Survival and Treatment Among Older Patients with Brain Metastases: A Population-Based Study Grobman B, Lamba N, Catalano PJ, Tanguturi SK, Rahman R, Haas-Kogan DA, Wen PY, Aizer AA BACKGROUND: Generalizable, large-scale data describing outcomes and treatment approaches for older adults with brain metastases remain limited. In this investigation, we evaluated prognosis and patterns of care in this population over time, with particular attention to the potential impact of social determinants of health. METHODS: We used the SEER-Medicare database to delineate survival, treatment patterns, and disparities among patients aged ?65?years with brain metastases diagnosed between 2010 to 2020. Survival was assessed with Kaplan-Meier methods and multivariable Cox regression. RESULTS: This study included 67,832 patients (51% female). The median survival from diagnosis of brain metastases was 3.42?months, improving modestly from 2.99?months in 2010 to 3.88?months in 2019. Higher zip-code-level annual income (HR 0.98 per $10,000 increase, 95% CI: 0.97 to 0.98, p?<?0.001) and higher rates of high school graduation (HR 0.98 per 10% increase, 95% CI: 0.97 to 0.99, p?=?0.001) were associated with lower mortality. Among patients managed with brain-directed radiation, 62% and 38% received non-stereotactic (inclusive of whole brain radiation) and stereotactic approaches, respectively. Use of stereotactic radiation increased from 22% in 2010 to 54% in 2019. Compared to White patients, Black patients (HR 0.79, 95% CI: 0.73 to 0.86, p?<?0.001) and Hispanic patients (HR 0.87, 95% CI: 0.79 to 0.95, p?=?0.002) were less likely to receive stereotactic radiation. CONCLUSIONS: The prognosis among older patients with brain metastases remains poor. Many patients continue to receive non-stereotactic approaches. Further work to improve the prognosis of older patients with brain metastases and optimize patterns of care is needed. |
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Nature Thymic Health and Immunotherapy Outcomes in Patients with Cancer Bernatz S, Prudente V, Pai S, Attermann AK, Di Federico A, Nürnberg L, Alessi JV, Ott PA, Sharon E, Mak RH, Bitterman D, Awad M, Ricciuti B, Aerts HJWL Although immunotherapy has revolutionized cancer treatment, many patients still experience limited benefit, highlighting the urgent need for improved biomarkers1. Although immunotherapy is founded on unleashing T?cells2, most existing biomarkers remain tumour-centric and mainly overlook host immune competence. The thymus is a key immune organ that is crucial for T?cell maturation, and we hypothesized that thymic functionality is associated with immunotherapy outcomes3. Here we show that thymic health, a radiographic measure of thymic functionality, is strongly associated with immunotherapy outcomes across several cancer types. Using a deep-learning framework applied to routine computed tomography images, we quantified thymic health in a pan-cancer cohort of 3,476 patients receiving immune checkpoint inhibitors. In patients with non-small cell lung cancer, higher thymic health was associated with reduced risks of progression and all-cause mortality. These associations remained significant across clinically relevant levels of programmed death ligand?1 (PD-L1) and tumour mutation burden. In the prospective TRACERx lung cancer study, thymic health was positively associated with T cell receptor diversity and T cell receptor excision circles, and correlated with immune-system signalling pathways, supporting radiographic thymic health as a proxy for thymic activity and adaptive immune competence. Analysis across patients with melanoma, breast cancer or renal cancer demonstrated pan-cancer relevance. Together, these findings identify thymic health as a previously unrecognized, tumour-agnostic determinant of immunotherapy efficacy, with potential implications for patient stratification, treatment timing and the development of immune-rejuvenating strategies in precision immuno-oncology. |
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Nature Thymic Health Consequences in Adults Bernatz S, Prudente V, Pai S, Attermann AK, Foldyna B, Nürnberg L, Bressem K, Lu MT, Aerts HJWL The thymus is essential for establishing T cell diversity early in life, but undergoes profound involution with age and has therefore traditionally been regarded as largely nonfunctional in adults1,2. Here we propose that preserving thymic functionality is integral to adult health and longevity. We developed a deep learning framework to quantify thymic health from routine radiographic images and evaluated its association with longevity and risk of major age-associated diseases in two large prospective cohorts of asymptomatic adults: the National Lung Screening Trial (n?=?25,031) and the Framingham Heart Study (n?=?2,581). In both cohorts, thymic health varied markedly across the population. In the National Lung Screening Trial, higher thymic health was consistently associated with lower all-cause mortality, reduced lung cancer incidence and lower cardiovascular mortality over 12 years of follow-up after adjustment for age, sex, smoking and comorbidities. In the independent Framingham Heart Study cohort, higher thymic health was significantly associated with reduced cardiovascular mortality, independent of age, sex and smoking. Thymic health was further linked to systemic inflammation and metabolic dysregulation, and associated with modifiable lifestyle factors including smoking, obesity and physical activity. Together, these findings reposition the thymus as a central regulator of immune-mediated ageing and disease susceptibility in adulthood, highlighting its potential as a target for preventive and regenerative strategies to promote healthy ageing and longevity. |
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Nature Biotechnology High-Resolution Metagenome Assembly for Modern Long Reads with Myloasm Shaw J, Marin MG, Li H Long-read metagenome assembly promises complete genomic recovery from microbiomes. However, the complexity of metagenomes poses challenges. Here we present myloasm, a metagenome assembler for modern long reads such as PacBio HiFi and Oxford Nanopore Technologies (ONT) R10.4 long reads. Myloasm uses polymorphic k-mers to construct a high-resolution string graph and then leverages differential abundance for graph simplification. On real-world ONT metagenomes, myloasm assembled three times more complete circular contigs than the next-best assembler. Myloasm can make ONT and HiFi assemblies comparable. For example, on a jointly sequenced gut metagenome, myloasm with ONT assembled more complete circular genomes than any assembler with HiFi. Myloasm also recovers previously inaccessible within-species diversity. Here, we recovered six complete Prevotella copri single-contig genomes from a gut metagenome and eight complete TM7 (Saccharibacteria) contigs with >93% similarity from an oral metagenome. Overall, we show that myloasm outperforms existing long-read metagenome assemblers across a range of environments and modern sequencing technologies. |
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Nature Communications Porter RL, Zhou Y, Eskndir N, Hayes M, Polak M, Lee EK, Krasner C, Campos S, Wright AA, Liu JF, Stover EH, Sawyer H, Xiong N, Pfaff KL, Rodig SJ, Tayob N, Veneris J, Matulonis UA, Konstantinopoulos PA Immune checkpoint inhibitors (ICI) synergize preclinically with antibody drug conjugates (ADC), harboring anti-tubulin maytansinoid payloads. We conducted an investigator-initiated, single-arm, phase 2 trial of mirvetuximab soravtansine (MIRV), a folate receptor alpha (FOLR1/FR?)-targeting ADC with the maytansinoid payload, DM4, combined with pembrolizumab in female patients with recurrent FOLR1-expressing serous endometrial cancer (EC, NCT03835819). Co-primary objectives include objective response rate (ORR) and rate of progression-free survival at 6 months (PFS6); secondary objectives include PFS, overall survival, duration of response and safety. Exploratory objectives include correlation of tumor genomics and immunoprofiling with clinical activity. Eighteen patients initiated protocol therapy [MIRV 6?mg/kg adjusted ideal body weight IV and pembrolizumab 200?mg IV every 3 weeks]. Confirmed ORR is 28% (1 complete and 4 partial responses, 95% CI:10-53%), Kaplan Meier estimate of PFS6 is 24.4% (95% CI:7.7-46.1%) with 4 patients progression free at 6 months; trial was closed early for feasibility (planned sample size of 35 patients not reached) and hence these results are considered preliminary. G3 treatment-related adverse effects were rare with no grade ?4 toxicities. We report a population of high FOLR1-expressing tumor-associated macrophages (CD163?+?FOLR1?+?), suggesting potential on-target, off-tumor immune editing by MIRV. A composite biomarker score derived in this cohort correlates with objective response to MIRV and pembrolizumab. |
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Nature Communications Gutierrez C, Kwok M, Ruthen N, Waddicor P, Curran C, Ouspenskaia T, Fu D, Smalec B, Sedor S, Knisbacher BA, Biran A, Nagler A, Garbicz F, Sewastianik T, Penailillo J, Lucas F, Yin S, Liani A, Chen S, Lazarian G, Witten E, Dangle N, Brunsting EL, Zheng M, Lin ES, Lee MJ, Wells B, Pomerance L, Li S, Lin Z, Al'Khafaji A, Thakurela S, Livak KJ, Neuberg D, Getz G, Regev A, Churchman S, Ten Hacken E, Carrasco R, Shao S, Wu CJ Ribosomal protein mutations are increasingly associated with cancer risk and thought to perturb ribosome function. At the same time, they reportedly activate p53, a critical anti-cancer barrier. To determine how these mutations overcome this protective block to enable tumorigenesis, we generate an in vivo model of the hotspot ribosomal protein RPS15-S138F mutation identified as a putative driver of chronic lymphocytic leukemia. Under pre-leukemic conditions, this mutation induces ribosome biogenesis defects and altered translation resulting in oxidative stress, DNA damage and induction of a p53-dependent response that promote initial cellular hypo-proliferation. However, a subset of aged mice with mutated Rps15 eventually develop B-cell leukemia (37% penetrance), which exhibits increased Myc activity with strong pro-survival and proliferation signatures. Mutant RPS15 thus induces both hypo- and hyper-proliferative signals, initially weighted towards cell cycle arrest; and that through translational rewiring, oxidative stress, DNA damage response defects and genomic instability set the stage for the acquisition of additional driving mutations, such as TP53 deletion, that can overcome this cell cycle block to trigger tumorigenesis. |
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Nature Medicine Enhanced Dynamic Risk Stratification of Smoldering Multiple Myeloma Chabrun F, Schwartz DE, Gupta TR, Perry J, Cordas Dos Santos DM, Timonian MA, Alberge JB, Patel V, Costello P, Tobia C, Phan S, Lamb J, Silverio MT, Davis M, O'Donnell EK, Marinac CR, Nadeem O, Trippa L, Ghobrial IM Accurate prediction of risk of progression from smoldering multiple myeloma (SMM) to active multiple myeloma (MM) is paramount to individualized early therapeutic strategies with minimum risk of overtreatment. Current risk stratification models do not account for evolving biomarker trajectories. We assembled a cohort of 2,344 patients with SMM from seven international centers with longitudinal clinical and biological data to train and validate the Precursor Asymptomatic Neoplasms by Group Effort Analysis (PANGEA)-SMM risk models. Four evolving biomarkers were significantly associated with shorter time to progression: M-protein increase ?0.2?g?dl-1, involved/uninvolved serum free light chain ratio increase ?20, creatinine increase >25% and hemoglobin decrease ?1.5?g?dl-1. PANGEA-SMM outperforms established models, including the 20/2/20 and IMWG models, by more accurately predicting progression (C-statistic?=?0.79), even without biomarker history (C-statistic?=?0.78) or recent bone marrow biopsy (C-statistic?=?0.78). We present PANGEA-SMM to the community as an easy-to-use, open-access tool for risk stratification in SMM. Validation tools are available to compare PANGEA-SMM to established models. |
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New England Journal of Medicine Atezolizumab Plus FOLFOX for Stage III Mismatch Repair-Deficient Colon Cancer Meyerhardt JA BACKGROUND: Standard adjuvant chemotherapy for stage III colon cancer consists of a fluoropyrimidine-plus-oxaliplatin regimen. Whether the addition of atezolizumab (an anti-programmed death ligand 1 agent) to a modified FOLFOX6 regimen (fluorouracil, oxaliplatin, and leucovorin; called mFOLFOX6) would improve outcomes in patients with stage III colon cancer with mismatch repair-deficient (dMMR) status is unclear. METHODS: In a phase 3 trial, we randomly assigned, in a 1:1 ratio, patients with resected stage III dMMR tumors to receive either adjuvant atezolizumab plus mFOLFOX6 for 6 months, with atezolizumab continued as monotherapy (for a total of 12 months of therapy), or mFOLFOX6 alone for 6 months. The primary end point was disease-free survival. Secondary end points were overall survival and the adverse-event profile. RESULTS: A total of 355 patients were assigned to receive atezolizumab plus mFOLFOX6 and 357 to receive mFOLFOX6 alone. The median age of the patients was 64 years, 55.1% were women, and 53.9% had tumors that were T4, N2, or both (indicating high risk). At a median follow-up of 40.9 months, the 3-year disease-free survival was 86.3% (95% confidence interval [CI], 81.8 to 89.8) in the atezolizumab-mFOLFOX6 group, as compared with 76.2% (95% CI, 70.9 to 80.6) in the mFOLFOX6 group (hazard ratio for disease recurrence or death, 0.50; 95% CI, 0.35 to 0.73; P<0.001). Adverse events of grade 3 or 4 occurred in 84.1% of the patients who received atezolizumab plus mFOLFOX6 and in 71.9% of those who received mFOLFOX6 alone. CONCLUSIONS: The addition of atezolizumab to mFOLFOX6 significantly improved disease-free survival among patients with stage III dMMR colon cancer. (Funded by the National Cancer Institute of the National Institutes of Health and Genentech; ATOMIC ClinicalTrials.gov number, NCT02912559.). |
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New England Journal of Medicine Genetic Medicine - Primed and Ready Bauer DE, Orkin SH Immunodeficiency chronic granulomatous disease (CGD) is a rare disorder characterized by defects in a multiprotein complex that generates superoxide in phagocytic cells. Recurrent infections and formation of granulomas are hallmarks of X-linked and autosomal-recessive CGD, which is caused by variants in genes encoding individual subunits. As a monogenic disorder with a functional defect in hematopoietic-derived cells, CGD has been successfully treated by allogeneic bone marrow transplantation. Ex vivo somatic genetic approaches involving either gene addition with a viral vector or clustered regularly interspaced short palindromic repeats (CRISPR) gene editing may also be used to restore oxidase activity in hematopoietic stem-cell–derived cells in patients with X-linked gp91phox CGD and in those with autosomal recessive p47phox disease. The recent history of clinical trials in CGD mirrors the evolution of gene-modifying approaches for other blood disorders, most notably hemoglobinopathies. |
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Proceedings of the National Academy of Sciences of the U.S.A. Regulation of the Immune CD155-CD226-TIGIT Axis by Cyclin D-CDK4/6 Fassl A, Palacios Espinoza M, Butter D, Kolodziejczyk A, Seehawer M, Hill C, Ning X, Branigan TB, Peñailillo J, Saengboonmee C, Jadhav H, Charbonnier LM, Waks AG, Shapiro GI, Tolaney SM, Polyak K, Sammons S, Wucherpfennig KW, Sicinski P Cyclin D-CDK4/6 is a component of mammalian cell-cycle machinery that drives cell proliferation. Small-molecule inhibitors of CDK4/6 have been approved for treatment of breast cancer patients. In addition to halting cell-cycle progression, inhibition of CDK4/6 can affect other tumor cell-intrinsic and -extrinsic functions. Here, we examined the impact of CDK4/6 inhibition on the CD155-CD226-TIGIT pathway that operates at the interface of tumor cells and the immune environment. We demonstrate that inhibition of CDK4/6 upregulates the expression of surface CD155 protein in cancer cells and downregulates an immuno-inhibitory receptor TIGIT in tumor-infiltrating lymphocytes. We observed these effects in human breast cancer cell lines, in mouse mammary carcinoma allograft models, in freshly resected human breast tumors and in paired pre-/on-treatment biopsies of breast cancers from patients undergoing monotherapy with a CDK4/6 inhibitor. We propose that inhibition of CDK4/6, through its tumor cell-intrinsic and -extrinsic effects, may shift the balance from the immunoinhibitory CD155-TIGIT to the immunostimulatory CD155-CD226 interaction, and through this mechanism may augment the antitumor immunity. Our results suggest that coadministration of CDK4/6 inhibitors and anti-TIGIT antibodies may further promote CD155-CD226-signaling and may have a strong synergistic antitumor effect. |
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ACS Chemical Biology O'Donohue E, Haigis KM |
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Blood Advances Crombie JL, Ryan CE, Ren Y, Tyekucheva S, Carey C, Zou A, Normilus S, Montegaard J, Soumerai JD, Arnason JE, Kim AI, Parry EM, Armand P, Fisher DC, Brown JR, Davids MS |
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Blood Advances Nishitani M, DeFilipp Z, Takahashi T, Duncan CN |
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Blood Advances Redd R, Armand P, Merryman RW |
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Blood Advances Xu R, Booker M, Weekes JC, Bell HL, Nirmal AJ, Liu H, Luo Q, Fortune AL, Whalen K, Guanci TM, Wan Y, Louissaint A Jr, Lin JR, Manalis SR, Armand P, Smith EL, Jacobson CA, Tolstorukov M, Murakami MA, Sorger PK, Weinstock DM, Lane AA |
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Blood Advances Tsakmaklis N, Hunter ZR, Liu X, Kofides A, Liu S, Guerrera ML, Guijosa A, Sun H, Hatcher JM, Peachey A, Patterson CJ, Meid K, Gustine J, Branagan AR, Sarosiek SR, Castillo JJ, Treon SP |
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Blood Advances Stratifying Survival: The Role of Social Determinants of Health on AML Outcomes by ELN 2022 Criteria Shimony S, Wang Y, Cronin A, Walsh TP, Charles A, Slopen N, Cho HL, Luskin MR, Abel GA, DeAngelo DJ, Stone RM, Lindsley RC, Hantel A |
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Blood Cancer Discovery Incorporating ALL Biology into Treatment Decisions: Next Steps toward Targeted Therapy in Adult ALL Luskin MR |
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Breast Corti C, Li T, Martin AR, Hughes ME, Parker T, Duporte TS, King TA, Mittendorf EA, Lin NU, Tayob N, Tolaney SM |
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Cancers A Mitochondrial Plasma Proteomic Signature Identifies Metastatic Chromophobe Renal Cell Carcinoma Steiner C, Han T, Safi S, Bzeih W, Mansour H, Saad E, Williams JF, Hirsch MS, Giri VK, Ascione L, Tang Y, Choueiri TK, Henske EP, Xu W |
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Cancer Science Nakazawa N, Ugai S, Kondo A, Matsuda K, Zhang X, Chan AT, Ogino S, Ugai T |
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Cell Systems Haplotype-Resolved Reconstruction and Functional Interrogation of Cancer Karyotypes Brunette GJ, Tourdot RW, Wang J, Pellman D, Zhang CZ |
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Clinical Cancer Research Yekedüz E, Bian W, Siegmund SE, Machaalani M, El Masri J, Saleh M, Saad E, Ascione L, El Hajj Chehade R, Steiner C, Barrios PM, Berg SA, McGregor B, Mantia C, Ravi P, Xu W, Hirsch MS, Choueiri TK, Serzan M |
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Clinical Cancer Research Khaddour K, Mooradian MJ, Sullivan RJ |
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Expert Opinion on Biological Therapy Liu Y, Mo CC, Salman TJ, Hossain S, Midha S, Nadeem O, Nicholson T, Croteau J, Kazierad N, Mouhieddine TH, Theprungsirikul P, Laubach JP, Richardson PG |
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Expert Opinion on Investigational Drugs Targeting the CD47/SIRP? Interaction in Cancer: Opportunities in Non-Hodgkin Lymphoma Pagès-Geli C, Weiskopf K |
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Hepatology Clinical Guideline for the Diagnosis and Treatment of Fibrolamellar Carcinoma O'Neill AF, Church A, Fitzgerald M, Kim HB, Liu KX, Rosenberg AR |
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Journal of Geriatric Oncology Thompson LL, Shah SB, Gregg AT, Yoon J, Florissi C, Amin PM, Lipson S, Jiang S, Saeed N, Saraf A, Guthier C, Warrington A, Jimenez R, Mak RH |
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Journal of the Academy of Consultation-Liaison Psychiatry Samsel C, Luccarelli J |
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Journal of the National Comprehensive Cancer Network Updates on the Perioperative Management of Resectable Non-Small Cell Lung Cancer Frumm SM, Florez N, Rotow JK |
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Leukemia and Lymphoma Merrill M, Kim HT, Kelkar AH, Panaro K, Tamada R, Au C, Singh S, Vicks A, Jain S, Ritz J, Ho VT, Jacobsen E |
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Molecular Therapy Oncology Rallis KS, Dionisio LM, Tarannum M, Romee R, Cancelas JA |
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Molecular Cancer Therapeutics Tesar B, Cathcart AM, Bird GH, Godes M, Wu R, Filbin MG, Walensky LD |
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Nature Methods SNP Calling, Haplotype Phasing and Allele-Specific Analysis with Long RNA-Seq Reads Huang N, Li H |
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Scientific Reports Wollborn L, Mishra S, Alimena S, Testino B, Fendler W, Chowdhury D, Elias KM |
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Transplantation and Cellular Therapy Impact of Post-Transplant Cyclophosphamide on the Prognostic Value of HCT-CI Mehta A, Kim HT, Pramudita A, Liney DJ, Dulery R, Ho VT, Cutler CS, Koreth J, Gooptu M, Antin JH, Kelkar AH, Nikiforow S, Wu CJ, Ritz J, Romee R, Soiffer RJ, Shapiro RM |