Welcome to Dana-Farber's Research News
August 15, 2025
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 July 16 through July 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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Blood A BCMA-mRNA Vaccine is a Promising Therapeutic for Multiple Myeloma Dutta D, Liu J, Wen K, Ray A, Salatino A, Liu X, Hideshima T, Song Y, Anderson KC Cancer vaccines are emerging as promising therapies to not only prevent cancer but to treat cancer. Here, we developed a therapeutic vaccine for multiple myeloma (MM) using BCMA protein as a target. Given the remarkable efficacy of COVID 19 mRNA vaccines, we first packaged sequence- and base- optimized BCMA mRNA into lipid nanoparticles (LNPs) using next-generation ionizable lipid enhancing their accumulation in the spleen. A TLR3 agonist, polyinosinic:polycytidylic acid (Poly(I:C)), was also encapsulated in LNPs to further elicit BCMA-specific immune response. BCMA-mRNA LNPs were internalized by dendritic cells (DCs) in vitro, triggering proliferation and activation of BCMA-specific CD8+ cytolytic T cells (CTLs). Importantly, these CTLs lysed BCMA+ U266 MM cells and CD138+ patient MM cells, without affecting BCMA-knockout (KO) U266 or CD138- patient derived bone marrow cells. Vaccination of C57BL/6J mice with BCMA-mRNA LNPs activated splenic DCs and induced BCMA-specific CTLs, assessed by tetramer staining, which selectively killed murine 5TGM1 BCMA overexpressing (5TGM1-BCMA-OE) MM cells. Finally, vaccination of C57BL/KaLwRijHsd mice bearing BCMA-overexpressing 5TGM1 cells inhibited tumor growth associated with BCMA-specific CD8+ T cell responses. The combination treatment with Poly(I:C) further triggered the immune response induced by BCMA-mRNA LNPs in all instances. Our findings provide the framework for clinical evaluation of BCMA-mRNA LNP vaccines to improve patient outcome in MM. |
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Blood Davids MS The treatment landscape for chronic lymphocytic leukemia (CLL) has been revolutionized by the advent of novel agents, particularly covalent BTK inhibitors (cBTKis) and BCL-2 inhibitors (BCL-2is). This has resulted in significant improvement in outcome of patients with CLL many of whom experience a life expectancy comparable to general population. However, patients who are double-refractory, having progressed following exposure to both classes face limited options and poor outcomes. This manuscript presents a practical approach to managing double-exposed or double-refractory CLL, integrating clinical case discussions, trial data, and expert insights. For patients with intolerance to cBTKis, second-generation agents may remain effective. Similarly, re-treatment with venetoclax can be considered after prior fixed-duration use. In double-refractory disease, the non-covalent BTK inhibitor (e.g., pirtobrutinib) and CD19-directed CAR-T therapy (lisocabtagene maraleucel) are available standard-of-care options. Pirtobrutinib provides rapid disease control but often with limited durability, emphasizing the importance of early planning for consolidation with CAR-T or allogeneic stem cell transplant. Persistent disease after CAR-T warrants close follow-up and timely referral for transplant evaluation in eligible patients. While PI3K inhibitors are also available, their role is limited due to toxicity and modest efficacy. Investigational agents-including BTK degraders, bispecific antibodies, and novel cellular therapies-offer promise for the future. A nuanced, individualized treatment strategy that incorporates current therapies and emerging options is essential to optimize outcomes in double-refractory CLL. |
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Blood Vianna P, Hossain S, Miller S, Rossi A, Cuddy SA, Falk RH, Laubach J, Bianchi G Immunoglobulin light chain (AL) amyloidosis is a plasma cell disorder characterized by progressive organ dysfunction secondary to deposition of organized immunoglobulin light chain aggregates. Achievement of rapid and deep normalization of involved immunoglobulin free light chains is necessary to maximize chances of reversibility of organ dysfunction, which in turn results in improved quality and length of life. There are no FDA-approved therapies for patients with relapsed and/or refractory immunoglobulin light chain (AL) amyloidosis. B cell maturation antigen (BCMA)-targeting bispecific T cell engagers teclistimab and elranatamab have shown high activity and acceptable safety profile in relapsed and/or refractory multiple myeloma patients, leading to their FDA approval. Herein we report on safety and efficacy of elranatamab for patients with relapsed and/or refractory AL amyloidosis. We treated 9 consecutive, advanced-stage AL amyloidosis patients with Elranatamab single agent, observing a 100% overall response and 67% complete response rate, including minimal residual disease (MRD)-negativity, with expected toxicities. Median time to hematological response was 9 days (6-24), with deep suppression in involved free light chains observed within one cycle of therapy, translating in cardiac and renal responses at 3-6 months. These data support prospective studies exploring Elranatamab in relapsed and/or refractory AL amyloidosis patients. |
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Blood Two Clones, One Niche: How CH Shapes the MM Microenvironment Sperling AS In this issue of Blood, Lionetti et al describe their in-depth analysis of a cohort of 106 patients with newly diagnosed multiple myeloma (MM), finding concurrent clonal hematopoiesis (CH) in 22.6% of patients and noting that the presence of CH is associated with an altered tumor-promoting bone marrow microenvironment despite the CH and MM having distinct clonal origins. MM, an incurable blood cancer arising from neoplastic plasma cells, is preceded in almost all cases by a premalignant phase known as monoclonal gammopathy (MG). The factors that promote the progression from MG to overt MM are multifactorial and incompletely understood but include somatic genetic evolution and the development of an altered tumor microenvironment (TME) that favors progression. The altered TME that supports growth of neoplastic plasma cells is also believed to contribute to a dysfunctional immune system in patients with MM, leading to abnormal tumor cell surveillance and increased infectious complications. Whether this abnormal TME is a cause or consequence of MM progression remains an open question. |
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JAMA Early-Onset Gastrointestinal Cancers: A Review Jayakrishnan T, Ng K IMPORTANCE: Early-onset gastrointestinal (GI) cancer is typically defined as GI cancer diagnosed in individuals younger than 50 years. The incidence of early-onset GI cancer is rising globally, and early-onset GI cancers represent the most rapidly increasing early-onset cancer in the US. OBSERVATIONS: Worldwide, among early-onset GI cancers reported in 2022, colorectal cancer (CRC) was the most common (54.3%; 184?709 cases), followed by gastric cancer (23.8%; 80?885 cases), esophageal cancer (13.2%; 45?056 cases), and pancreatic cancer (8.6%; 29?402 cases). In the US, among early-onset GI cancers reported in 2022, 20?805 individuals were diagnosed with early-onset CRC, 2689 with early-onset gastric, 2657 with early-onset pancreatic, and 875 with early-onset esophageal cancer. Most early-onset GI cancers are associated with modifiable risk factors including obesity, poor-quality diet (eg, sugar-sweetened beverages, ultraprocessed foods), sedentary lifestyle, cigarette smoking, and alcohol consumption. Nonmodifiable risk factors include family history, hereditary syndromes (eg, Lynch syndrome), and inflammatory bowel disease for patients with early-onset CRC. Approximately 15% to 30% of early-onset GI cancers have pathogenic germline variants in genes such as DNA mismatch repair genes and BRCA1/2. All patients with early-onset GI cancers should undergo germline and somatic genetic testing to guide treatment, screen for other cancers (eg, endometrial cancer in Lynch syndrome), and assess familial risk. Treatment for early-onset GI cancers are similar to later-onset GI cancers and may include chemotherapy, surgery, radiation, and therapies such as poly-adenosine diphosphate ribose polymerase inhibitors for BRCA-associated pancreatic cancer. Compared with GI cancers diagnosed after age 50 years, patients with early-onset GI cancers typically receive more treatments but often have similar or shorter survival. Specialized centers and multidisciplinary teams can support patients with challenges around fertility preservation, parenting with cancer, financial difficulty, and psychosocial distress. Currently, screening is not recommended for most early-onset GI cancers, although in the US, screening for CRC is recommended for average-risk individuals starting at age 45 years. High-risk individuals (eg, those with Lynch syndrome, a first-degree relative with CRC, or advanced colorectal adenoma) should begin CRC screening earlier, at an age determined by the specific risk factor. CONCLUSIONS AND RELEVANCE: Early-onset GI cancers, typically defined as cancer diagnosed in individuals younger than 50 years, are among the largest subset of early-onset cancers globally. Treatment is similar to later-onset GI cancers and typically involves a combination of chemotherapy, surgery, and radiation, depending on the cancer type and stage. The prognosis for patients with early-onset GI cancers is similar to or worse than that for patients with later-onset GI cancers, highlighting the need for improved methods of prevention and early detection. |
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Journal of Clinical Oncology Konstantinopoulos PA, Matulonis UA PURPOSE: Patients with platinum-resistant/platinum-refractory high-grade serous ovarian cancer (HGSOC) without a BRCA mutation have poor prognosis and limited treatment options. We report efficacy and biomarker data from EPIK-O, which investigated alpelisib + olaparib versus single-agent chemotherapy in these patients. PATIENTS AND METHODS: EPIK-O was an open-label, phase III trial that randomly assigned patients with platinum-resistant/platinum-refractory HGSOC with no germline or known somatic BRCA mutation 1:1 to alpelisib 200 mg once daily + olaparib 200 mg twice daily or treatment of physician's choice (TPC; paclitaxel 80 mg/m2 once weekly or pegylated liposomal doxorubicin 40-50 mg/m2 once every 28 days). Patients had 1-3 previous systemic therapies. Previous bevacizumab was required (unless contraindicated); previous poly(adenosine diphosphate-ribose) polymerase inhibitors were allowed. Primary end point was progression-free survival (PFS) per RECIST 1.1 (blinded independent review committee [BIRC]). Secondary efficacy end points included overall response rate (ORR; per BIRC), duration of response (per BIRC), and overall survival (OS; key secondary end point). RESULTS: A total of 358 patients (alpelisib + olaparib [n = 180], TPC [n = 178]) were included. The median follow-up time was 9.3 months. At data cutoff (April 21, 2023), 33 (18.3%) and 30 (16.9%) patients remained on treatment with alpelisib + olaparib and TPC, respectively. The median PFS (BIRC) was 3.6 versus 3.9 months (hazard ratio [HR], 1.14 [95% CI, 0.88 to 1.48]; one-sided P = .84) for alpelisib + olaparib versus TPC. The ORR was 15.6% (95% CI, 10.6% to 21.7%) versus 13.5% (95% CI, 8.8% to 19.4%). The median OS was 10.0 versus 10.6 months (HR, 1.22; 95% CI, 0.87 to 1.71). The safety profile of alpelisib + olaparib was consistent with that observed for the individual agents. CONCLUSION: The primary objective, PFS improvement, was not met in EPIK-O. No new or unexpected adverse events were observed. Biomarker analyses provided new insights for responders to alpelisib + olaparib. |
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Nature Communications Apfelbaum AA, Morin E, Ayoub G, DiGiacomo J, Bahadur S, Power PC, Cusick MM, Novikov D, Prabhakar P, Jones RE, Vogelzang J, Bossi CC, Malinowski S, Jeang J, Lamson SW, Collins J, Cai KY, Jones JS, Oh S, Jeon H, Wang J, Cameron A, Rechter P, De Leon A, Yeo KK, Rosenberg T, Chi SN, Wright KD, Buhrlage SJ, Fischer ES, Eck MJ, Baird L, Alexandrescu S, Ligon KL, Bandopadhayay P Oncogenic alterations in fibroblast growth factor receptor (FGFR)-family proteins occur across cancers, including pediatric gliomas. Our genomic analysis of 11,635 gliomas across ages finds that 5.3% of all gliomas harbor FGFR alterations, with an incidence of almost 9% in pediatric gliomas. Alterations in FGFR proteins are differentially enriched by age, tumor grade, and histology, with FGFR1 alterations associated with glioneuronal histologies. Leveraging isogenic systems, we confirm FGFR1 alterations to induce downstream Mitogen Activated Protein Kinase (MAPK) and mTOR signaling pathways, drive gliomagenesis, activate neuronal transcriptional programs and exhibit sensitivity to MAPK pathway and pan-FGFR inhibitors. Finally, we perform a retrospective analysis of clinical responses in children diagnosed with FGFR-altered gliomas and find that treatment with currently available inhibitors is largely associated with stability of disease. This study provides key insights into the biology of FGFR1-altered gliomas, therapeutic strategies to target them and associated challenges that still need to be overcome. |
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Nature Communications De Novo Pyrimidine Biosynthesis Inhibition Synergizes with BCL-X(L) Targeting in Pancreatic Cancer Zhang H, Santana-Codina N, Yu Q, Poupault C, Campos C, Qin X, Sindoni N, Padhye A, Kuljanin M, Wang J, Dorman MJ, Aguirre AJ, Dougan SK, Sarosiek KA, Mancias JD Oncogenic KRAS induces metabolic rewiring in pancreatic ductal adenocarcinoma (PDAC) characterized, in part, by dependency on de novo pyrimidine biosynthesis. Pharmacologic inhibition of dihydroorotate dehydrogenase (DHODH), an enzyme in the de novo pyrimidine synthesis pathway, delays pancreatic tumor growth; however, limited monotherapy efficacy suggests that compensatory pathways may drive resistance. Here, we use an integrated metabolomic, proteomic and in vitro and in vivo DHODH inhibitor-anchored genetic screening approach to identify compensatory pathways to DHODH inhibition (DHODHi) and targets for combination therapy strategies. We demonstrate that DHODHi alters the apoptotic regulatory proteome thereby enhancing sensitivity to inhibitors of the anti-apoptotic BCL2L1 (BCL-XL) protein. Co-targeting DHODH and BCL-XL synergistically induces apoptosis in PDAC cells and patient-derived organoids. The combination of DHODH inhibition with Brequinar and BCL-XL degradation by DT2216, a proteolysis targeting chimera (PROTAC), significantly inhibits PDAC tumor growth. These data define mechanisms of adaptation to DHODHi and support combination therapy targeting BCL-XL in PDAC. |
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Nature Communications Specific Oncogene Activation of the Cell of Origin in Mucosal Melanoma Babu S, Chen J, Baron CS, Sun K, Robitschek E, McConnell AM, Wu C, Dedeilia A, Sade-Feldman M, Modhurima R, Manos MP, Chen KY, Cox AM, Ludwig CG, Kellis M, Buchbinder EI, Hacohen N, Yang J, Boland GM, Liu D, Zon LI, Insco ML Mucosal melanoma (MM) is a deadly cancer derived from mucosal melanocytes. To test the consequences of MM genetics, we develop a zebrafish model in which all melanocytes experience CCND1 expression and loss of PTEN and TP53. Surprisingly, melanoma only develops from melanocytes lining internal organs, analogous to the location of patient MM. We find that zebrafish MMs have a unique chromatin landscape from cutaneous melanomas. Internal melanocytes are labeled using a MM-specific transcriptional enhancer. Normal zebrafish internal melanocytes share a gene expression signature with MMs. Patient and zebrafish MMs show increased migratory neural crest and decreased antigen presentation gene expression, consistent with the increased metastatic behavior and decreased immunotherapy sensitivity of MM. Our work suggests that the cell state of the originating melanocyte influences the behavior of derived melanomas. Our animal model phenotypically and transcriptionally mimics patient tumors, allowing this model to be used for MM therapeutic discovery. As this is a non-MAPK driven genetically engineered model of melanoma, our work also has implications for the 15% of cutaneous melanoma patients who lack MAPK-driving mutations. |
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Nature Communications Unveiling the Hidden Interactome of CRBN Molecular Glues Baek K, Metivier RJ, Roy Burman SS, Bushman JW, Yoon H, Lumpkin RJ, Ryan JK, Abeja DM, Lakshminarayan M, Yue H, Ojeda S, Xiong Y, Che J, Verano AL, Schmoker AM, Donovan KA, Fischer ES Induced proximity by molecular glues refers to strategies that leverage the recruitment of proteins to facilitate their modification, regulation or degradation. As prospective design of molecular glues remains challenging, unbiased discovery methods are necessary to discover new chemical targets. Here we establish a high throughput affinity proteomics workflow leveraging E3 ligase activity-impaired CRBN-DDB1?B in cell lysates for the unbiased identification of molecular glue targets. By mapping the interaction landscape of CRBN-binding molecular glues, we unveil 298 protein targets and demonstrate the utility of enrichment methods for identifying targets overlooked by established methods. We use a computational workflow to estimate target confidence and perform biochemical and structural validation of uncharacterized neo-substrates. We further identify a lead compound for the previously untargeted non-zinc finger PPIL4 through a biochemical screen. Our study provides a comprehensive inventory of targets chemically recruited to CRBN and delivers a robust and scalable workflow for identifying drug-induced protein interactions in cell lysates. |
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Nature Genetics Lu Z, Gusev A Multiancestry statistical fine-mapping of cis-molecular quantitative trait loci (cis-molQTL) aims to improve the precision of distinguishing causal cis-molQTLs from tagging variants. Here we present the sum of shared single effects (SuShiE) model, which leverages linkage disequilibrium heterogeneity to improve fine-mapping precision, infer cross-ancestry effect size correlations and estimate ancestry-specific expression prediction weights. Through extensive simulations, we find that SuShiE consistently outperforms existing methods. We apply SuShiE to 36,907 molecular phenotypes including mRNA expression and protein levels from individuals of diverse ancestries in the TOPMed-MESA and GENOA studies. SuShiE fine-maps cis-molQTLs for 18.2% more genes compared with existing methods while prioritizing fewer variants and exhibiting greater functional enrichment. While SuShiE infers highly consistent cis-molQTL architectures across ancestries, it finds evidence of heterogeneity at genes with predicted loss-of-function intolerance. Lastly, using SuShiE-derived cis-molQTL effect sizes, we perform transcriptome- and proteome-wide association studies on six white blood cell-related traits in the All of Us biobank and identify 25.4% more genes compared with existing methods. Overall, SuShiE provides new insights into the cis-genetic architecture of molecular traits. |
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New England Journal of Medicine Opening the Door to Tailored Treatment in Newly Diagnosed Multiple Myeloma Richardson PG, Munshi NC, Longo DL How much is enough in the treatment of newly diagnosed multiple myeloma? As clinicians, we want to provide efficacious treatments for our patients to avoid undertreating them. However, we also want to avoid overtreatment with intensive therapy that has limited extra benefit but an increased risk of toxic effects that are potentially life-altering and sometimes fatal. The introduction of highly active induction regimens has focused attention on the evolving role of high-dose melphalan plus autologous stem-cell transplantation (ASCT). Are these newer regimens active enough to obviate the need for high-dose melphalan–ASCT, or does high-dose melphalan–ASCT further improve the already impressive efficacy of the newer regimens? And how do we determine when patients have received sufficient initial treatment to maximize long-term outcomes? |
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ACS Chemical Biology High-Throughput Screening Tool to Identify Small Molecule Inhibitors of Telomerase Aquilanti E, Barkho S, Bozinov V, Kageler L, Garrity-Janger M, Mesleh MF, Horner S, Ranaghan MJ, Meyerson M |
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American Journal of Hematology Practical Guidance on Clinical Management of Belantamab Mafodotin-Associated Ocular Events Richardson P |
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Annals of Surgical Oncology Patient-reported Outcomes After Routine Treatment of In Situ/Atypical Lesions: The PORTAL Study Rosenberg SM, Schreiber KL, Hughes KS, Frank ES, Darai S, Lanahan C, Partridge AH |
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Blood Advances Guijosa A, Sarosiek S, Branagan AR, von Keudell G, Treon SP, Castillo JJ |
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Blood Advances Castillo JJ, Guijosa A, Flynn C, Meid KE, Budano N, Nguyen J, Tsakmaklis N, Hunter ZR, Patterson CJ, Treon SP, Sarosiek S |
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Blood Advances Krasnow N, Maurer K, Song CJ, Rhoades J, Xiong K, Crnjac A, Blewett T, Gao L, Jacene H, Merryman RW, Gohil SH, Duffy C, Guerrero LI, Dela Cruz J, McDonough M, Wolff JO, Redd RA, Makrigiorgos GM, Neuberg DS, Rodig SJ, Armand P, Jacobson CA, Adalsteinsson VA, Wu CJ |
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Blood Advances Zon RL, Pozdnyakova O, Neuberg DS, Battinelli EM, Luskin MR, Tothova Z, Morgan EA, Ebert BL |
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BMC Medical Ethics Ethics of Overtreatment and Undertreatment in Older Adults with Cancer DuMontier C, Revette AC, Roberts J, Sanyal A, Perumal N, Blackstone EC, Uno H, Hshieh TT, Driver JA, Abel GA |
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British Journal of Haematology Hantel A, Merz LE |
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Clinical Cancer Research Molecular Characterization of NUT Carcinoma: A Report from the NUT Carcinoma Registry Kim JJ, Walton SA, Haradon J, Paoloni F, Jänne PA, Barbie DA, Sholl LM, Dubois SG, Hanna GJ, Shapiro GI, French CA, Luo J |
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Clinical Journal of the American Society of Nephrology Liu A, Reich A, Kalim S, Roberts JE, Nava-Coulter B, El-Jawahri A, Ufere NN, Lakin JR |
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Current Opinion in Oncology De Placido P, Parsons HA |
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ESMO Open Jeselsohn R, Fu J, Ren Y, Burstein HJ, DeMeo M, Regan M, Tolaney SM, Mayer EL |
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ESMO Open Corti C, Chu X, Kline DM, Priedigkeit NM, Mayer EL, Waks AG, Hughes ME, Abravanel DL, Giordano A, Lin NU, King TA, Jeselsohn RM, Manning DK, Dillon DA, Mittendorf EA, Tayob N, Tolaney SM |
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Expert Opinion on Investigational Drugs Isatuximab for the Treatment of Multiple Myeloma: Current Clinical Advances and Future Directions Richardson PG, O'Donnell EK, Laubach J |
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Genes and Development Lineage Rewiring in Lung Adenocarcinoma Via HNF4? and NKX2-1 Dynamics Feng A, Yermalovich A, Meyerson M |
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Gynecologic Oncology The RAS-MEK-ERK Pathway in Low-Grade Serous Ovarian Cancer Stover EH, Lee EK, Shapiro GI, Brugge JS, Matulonis UA, Liu JF |
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Hematology/Oncology Clinics of North America The Rapidly Evolving Landscape of the Biology and Therapy of Chronic Lymphocytic Leukemia Brown JR, Davids MS |
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Hematology/Oncology Clinics of North America Triplet Therapies in Chronic Lymphocytic Leukemia Soumerai JD, Davids MS |
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International Journal of Radiation Oncology, Biology, Physics Thompson LL, Amin PM, Shah S, Lipson SM, Yoon J, Lee G, Anabaraonye N, Gregg AT, Jiang S, Baxter E, Florissi C, He J, Saraf A, Bontempi D, Haugg F, Aerts HJ, Mak RH |
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iScience Padmanabha Das KM, Charifson PS, Green J, Arthanari H, Namchuk MN |
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JAMA Otolaryngology – Head & Neck Surgery Emerging Role of Pathologic Response in Head and Neck Squamous Cell Carcinoma Immunotherapy Dahal A, Uppaluri R |
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JAMA Surgery Long-Term Locoregional Outcomes in a Contemporary Cohort of Young Women with Breast Cancer Dominici LS, Zheng Y, King TA, Wong J, Peppercorn J, Collins LC, Partridge AH |
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JCI Insight Shigeta K, Daimon T, Hongo H, Ku SY, Ozawa H, Haratake N, Fushimi A, Nakashoji A, Bhattacharya A, Takamori S, Kono M, Rokugo M, H, Kufe D |
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Journal of Controlled Release Advances in RNA Therapeutics and Its Delivery Strategies Against Multiple Myeloma Zhang Z, Anderson KC |
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Laboratory Investigation Antibody-Based Multiplex Image Analysis: Standard Analytical Workflows and Tools for Pathologists Ullanat V, Reddy Puchala S, Wen J, Chowdhury A, Marchionni L, Umeton R, Loda M |
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Leukemia Heavican-Foral TB, Korell F, Scarfò I, Wiggers CRM, B AT, Eisenbies Z, Powers F, Hegel J, Liu J, Kulp S, Silva H, Wu G, Letai A, Stegmaier K, Lohr JG, Weinstock DM, Maus MV, Knoechel B |
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Leukemia Rare Germline Variant in NFATC4 Associated with Familial CLL Itchaki G, Bai H, Tiao G, Improgo R, Oppenheimer BE, Kasar S, Tesar B, Fernandes SM, Pochet N, Machado JH, Thrash EM, Freedman AS, Getz G, Brown JR |
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Leukemia Chong SJF, Guièze R, Wu CJ, Davids MS |
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Molecular Cancer Therapeutics Targeting Transcriptional Cyclin-Dependent Kinases in Cancer Kolodziejczyk A, Sicinski P |
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Neuro-Oncology Rahman R, Redd R, Fell G, Tan Y, Orio P, Wen PY, Trippa L |
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NPJ Breast Cancer Antibody-Drug Conjugates for Treating Early-Stage Breast Cancer: Current Use, Anticipated Evolutions Patel P, Giordano A, Giordano S, Schlam I, Tolaney SM, Tarantino P |
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Seminars in Oncology Nursing Cooley ME, Abrahm JL |
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Trends in Cancer Bone Appetite: Bone-Derived Factors Feed Distant Immune Suppression Ganguly D, Agudo J |