Dana-Farber Research News 10.01.2026
Welcome to Dana-Farber's Research News
October 1, 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 September 1 - 15.
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 Shaw AT BACKGROUND: Due to the unprecedented progression-free survival (PFS) benefit with lorlatinib after 5 years of follow-up in the phase III CROWN study, we aimed to quantify long-term outcomes at 7 years. PATIENTS AND METHODS: Treatment-naive patients (N = 296) with advanced anaplastic lymphoma kinase (ALK)-positive non-small-cell lung cancer (NSCLC) were randomly assigned 1:1 to receive lorlatinib 100 mg once a day (n = 149) or crizotinib 250 mg twice a day (n = 147). This post hoc analysis presents investigator-assessed efficacy outcomes, safety, and biomarker analyses. RESULTS: With a median follow-up of 83.0 and 77.2 months, median PFS was not reached (NR) with lorlatinib [95% confidence interval (CI), 68.5-NR] and was 9.1 months (95% CI 7.4-10.9) with crizotinib [hazard ratio (HR) 0.19, 95% CI 0.13-0.26]; 7-year PFS was 55% and 3%, respectively. With lorlatinib, patients without a PFS event at the end of 24 months had a 79% probability of survival without progression at year 7. No new intracranial progression events occurred after the first 30 months on lorlatinib. Median time to intracranial progression was NR (95% CI NR-NR) with lorlatinib and 16.4 months (95% CI 12.7-21.9) with crizotinib (HR 0.06, 95% CI 0.03-0.12). Overall survival follow-up is ongoing; the number of events for a protocol-specified analysis has not been met. The safety profile was consistent with the 5-year results. With lorlatinib, treatment-related adverse events did not lead to discontinuations after the first 26 months. More genetic alterations were detected in circulating tumor DNA samples from early progressors than in long-term responders on lorlatinib; new potential resistance mechanisms were identified. CONCLUSIONS: With median PFS yet to be reached after 7 years of follow-up in CROWN, lorlatinib continues to show unprecedented long-term benefit in patients with advanced ALK-positive NSCLC. Patients without progression within 24 months on lorlatinib have a low risk of progression or death at year 7 and may continue long-term treatment. Findings suggest that sustained long-term disease control with first-line lorlatinib may enable advanced ALK-positive NSCLC to evolve toward a chronic condition. |
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Annals of Oncology Valenza C, Partridge AH Historically, premenopausal patients with hormone receptor (HR)-positive, early-stage breast cancer (eBC) have derived greater benefit from adjuvant chemotherapy than postmenopausal patients. Even among women with tumors classified by genomic testing as having less aggressive biology, a setting in which the cytotoxic contribution of chemotherapy would be expected to be limited or null as observed in postmenopausal patients, several trials comparing adjuvant chemoendocrine therapy (CET) with endocrine therapy (ET) alone have shown a chemotherapy benefit among premenopausal patients. This additional benefit has been attributed to not only the more aggressive disease that develops in young patients, necessitating the direct tumor-cytotoxic effects of chemotherapy, but also to its chemoendocrine effect, mediated by chemotherapy-induced ovarian toxicity and consequent estradiol suppression. Much indirect evidence supports the substantial impact of the latter mechanism, including the consistent demonstration that premenopausal patients who experience permanent chemotherapy-related amenorrhea (CRA) have lower risk of disease recurrence than those with persistent menstrual cycles or menstrual recovery after transient CRA. |
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Annals of Oncology Niman SM, Gelber RD, Partridge AH BACKGROUND: In patients with hormone receptor (HR)-positive early breast cancer (BC), the POSITIVE trial demonstrated that temporary interruption of adjuvant endocrine therapy (ET) for pregnancy is feasible and safe in early follow-up (median 41 months). In this article, we report updated results from a preplanned analysis with 2.5 years of additional follow-up. PATIENTS AND METHODS: POSITIVE, a single-arm prospective trial evaluating temporary interruption of adjuvant ET (after 18-30 months and for up to 2 years) to attempt pregnancy in young patients with BC, enrolled 518 eligible women (?42 years of age, stage I-III BC, desiring pregnancy) from December 2014 to December 2019. Using the bootstrap-matching method, 5-year breast cancer-free interval (BCFI) and distant recurrence-free interval (DRFI) event rates were compared with those of the SOFT/TEXT trials as external controls. RESULTS: At a median follow-up of 71 months in the POSITIVE cohort and 80 months in the SOFT/TEXT cohort, the 5-year cumulative incidence of BCFI events was 12.3% in POSITIVE and 13.2% in SOFT/TEXT [-0.9% difference, 95% confidence interval (CI) -4.2% to 2.6%]. The 5-year cumulative incidence of DRFI events was 6.2% and 8.3%, respectively (-2.1% difference, 95% CI -4.5% to 0.4%). Among 497 women followed for nondisease outcomes, 377 (76%) had ?1 documented pregnancy on trial, and 343 of 497 (69%) had ?1 live birth, totaling 440 offspring. In an unadjusted analysis comparing the 180 women (36%) who had pre-enrollment embryo/oocyte cryopreservation with those who did not, the 5-year cumulative incidence of BCFI events was 14.0% (95% CI 9.6% to 20.2%) and 11.5% (95% CI 8.4% to 15.7%), respectively. CONCLUSION: Longer-term follow-up of the POSITIVE trial demonstrates that temporary interruption of ET for pregnancy, including use of fertility preservation, does not increase the risk of BC events. Continued follow-up is warranted given the known risk of late recurrence in this population. |
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Cancer Discovery Borgenvik A, Misek SA, Zhang A, Boisvert M, Cai KY, Kovarzin A, Li H, Zhou KN, Gonzalez EM, Goodale A, Lazo de la Vega L, Ragnoni TJ, Persky NS, Abid T, Miglietta EA, Jones JS, Malinowski S, Elsadek LA, Parikh J, Condurat AL, Fultineer A, Choi SH, Ozdemir M, Eisenbies Z, Lee J, Novikov D, Bahadur S, Apfelbaum AA, Robinson J, Clark LM, Schulman N, Lopez G, Tang K, Maldera A, Kwon JJ, Vallurupalli M, Jeon H, Pal S, Golub TR, Hahn WC, Fischer ES, Carpenter AE, Cimini BA, Ligon KL, Janeway KA, Eck MJ, Parker Kerrigan BC, Root DE, Sharifnia T, Beroukhim R, Bandopadhayay P Fusions between protein-coding genes are common oncogenic drivers, typically pairing a proto-oncogene with a partner that does not independently drive cancer. In all therapeutically actionable fusions, the proto-oncogene is the drug target, the contributions to oncogenicity of the fusion partner have largely been ignored. We studied the role of BRAF fusion partners and found that they are necessary for transformation. In the setting of KIAA1549::BRAF, the most common fusion protein across brain tumors, we found that KIAA1549 is necessary for oncogenicity of KIAA1549::BRAF and engenders a striking and specific dependency on the protein O-mannosyltransferase complex (POMT1/2). Specifically, we show that genetic silencing or pharmacologic inhibition of POMT1/2 reverses fusion-induced transformation, thereby representing a novel and MAPK-independent therapeutic target. Furthermore, POMT1/2 is required to glycosylate and enable maturation of the K::B fusion protein. These findings represent a proof-of-concept for targeting the partners in oncogenic fusions as a potential cancer therapeutic strategy. |
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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 Ng K, Jackson NA, Kohn CG, Thalappillil JS, Meyerhardt JA IMPORTANCE: In a phase 2 randomized clinical trial, high-dose vitamin D3 added to standard treatment improved progression-free survival (PFS) compared with standard-dose vitamin D3 in patients with metastatic colorectal cancer (mCRC). OBJECTIVE: To determine if high-dose vitamin D3 added to standard chemotherapy improves outcomes in patients with previously untreated mCRC. DESIGN, SETTING, AND PARTICIPANTS: Double-blind phase 3 randomized clinical trial enrolling 455 patients with previously untreated mCRC, conducted in the US through the National Clinical Trials Network from October 2019 to December 2022 (database freeze: July 15, 2024). INTERVENTIONS: mFOLFOX6 (modified FOLFOX6 [5-fluorouracil, leucovorin, oxaliplatin]) or FOLFIRI (5-fluorouracil, leucovorin, irinotecan) plus bevacizumab every 2 weeks with either high-dose vitamin D3 (8000 IU daily?×?14 days as loading dose followed by 4000 IU daily) or standard-dose vitamin D3 (400 IU daily) until disease progression, intolerable toxicity, or withdrawal of consent. MAIN OUTCOMES AND MEASURES: The primary end point was PFS assessed by the unstratified log-rank test. Secondary end points included objective response rate, overall survival, and toxicity. Prespecified subgroup analyses of PFS were performed according to known prognostic factors. RESULTS: Among 455 randomized patients (median age, 59 years; 181 [40%] female) with median follow-up 20 months, the median PFS for high-dose vitamin D3 (n?=?228) was 11.8 months (95% CI, 10.3-13.3) vs 10.3 months (95% CI, 9.4-12.2) for standard-dose vitamin D3 (n?=?227) (1-sided log-rank P?=?.25). There were no significant differences in objective response rate between high-dose and standard-dose vitamin D3 (51% [95% CI, 44%-58%] vs 44% [95% CI, 37%-50%], respectively; P?=?.12), or in overall survival (median, 25.6 vs 27.0 months; 1-sided log-rank P?=?.66). There were no clinically meaningful differences in the most common grade 3 or greater adverse events between the high- and standard-dose groups, including neutropenia (n?=?67 [32%] vs n?=?62 [30%]) and hypertension (n?=?42 [20%] vs n?=?49 [23%]) or in incidence of vitamin D-associated toxicities. CONCLUSIONS AND RELEVANCE: Among patients with previously untreated mCRC, addition of high-dose vitamin D3, vs standard-dose vitamin D3, to standard chemotherapy plus bevacizumab did not improve PFS. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT04094688. |
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JAMA Oncology Modernizing Surrogate Decision-Making to Reflect the Complexity of Cancer Care Blackstone EC, Sontag DN, Rangachari D, Abel GA Patients with cancer are at risk of medical decisional incapacity, which poses significant challenges for goal-concordant care. Incapacity necessitates surrogate decision-making, preferably by someone selected in advance by the patient (typically a family member or close friend). The ethical standard by which surrogate decision-makers are expected to make medical decisions is substituted judgment. Rooted in respect for autonomy, this standard requires a surrogate decision-maker to choose what they believe the patient would choose if capacitated. When a patient’s wishes are unknown, the lower standard is to decide what is in the patient’s best interests following the principles of beneficence and nonmaleficence. Decades of research have shown that, in practice, surrogate decision-making does not follow this hierarchy because surrogate decision-makers do not know patient preferences, interject their own values, or do not view substituted judgment as an ideal standard.1-3 In contemporary cancer care, more nuanced, agile, and process-oriented frameworks to support surrogate decision-makers are an unmet need. |
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Journal of Clinical Oncology Shulman DS, Klega K, Chen N, Gohn E, Sexton S, Clinton C, Tanhaemami M, Cibulskis C, Choy E, London WB, Janeway KA, DuBois SG, Crompton BD PURPOSE: Identification of discrete risk groups remains a high priority for patients with Ewing sarcoma (EWS). We sought to prospectively validate circulating tumor DNA (ctDNA) as a prognostic factor and develop clinical-molecular risk groups. METHODS: We conducted a prospective investigator-initiated biology study for patients with localized EWS (LEOPARD) and embedded ctDNA analysis into the North American frontline metastatic study AEWS1221. Eligible patients were younger than 50 years with newly diagnosed EWS. All patients provided a baseline blood sample for analysis, which was subjected to ultralow-pass whole-genome sequencing and hybrid capture panel sequencing for ctDNA quantification, fusion detection, and characterization of STAG2 and TP53 alterations. Serial ctDNA sequencing was conducted on a subset of patients in each study. We tested for associations between ctDNA burden and secondary genomic events, and clinical features and outcomes. RESULTS: One hundred forty patients with localized disease and 255 with metastatic disease provided evaluable pretreatment samples for ctDNA analysis. Elevated baseline ctDNA was associated with stage, tumor size, primary site, indeterminate pulmonary nodules, and metastatic pattern. Elevated pretreatment ctDNA burden was associated with inferior outcomes in patients with localized (n = 140, hazard ratio [HR] = 2.36, P = .032) and metastatic disease (n = 255, HR = 2.15, P = .001). Patients with metastatic disease and TP53 variants and/or persistent on-therapy ctDNA had dismal outcomes. Patients with localized disease, low ctDNA, small tumors, and favorable genomics had no events and constitute a novel low-risk group. Among patients with metastatic disease, those with lung-only disease, low ctDNA, and favorable genomics represent an intermediate-risk group. CONCLUSION: This study prospectively validates pretreatment ctDNA burden as prognostic in EWS. Risk groups that integrate ctDNA burden with clinical-molecular features differentiate patients with low-, intermediate-, and high-risk disease. |
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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, 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 Surveillance, Epidemiology, and End Results-Medicare database to delineate survival, treatment patterns, and disparities among patients aged 65?years and older with brain metastases diagnosed between 2010 and 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 (hazard ratio [HR] = 0.98 per $10?000 increase, 95% confidence interval [CI] = 0.97 to 0.98; P?<?.001) and higher rates of zip-code level high school graduation (HR = 0.98 per 10% increase, 95% CI = 0.97 to 0.99; P?=?.001) were associated with lower mortality. Among patients managed with brain-directed radiation, 62% and 38% received nonstereotactic (inclusive of whole brain radiation) and stereotactic approaches, respectively. Use of stereotactic radiation increased from 22% in 2010 to 54% in 2019. Compared with White patients, Black patients (HR = 0.79, 95% CI = 0.73 to 0.86; P?<?.001) and Hispanic patients (HR = 0.87, 95% CI = 0.79 to 0.95; P?=?.002) were less likely to receive stereotactic radiation. CONCLUSIONS: The prognosis among older patients with brain metastases remains poor. Many patients continue to receive nonstereotactic approaches. Further work to improve the prognosis of older patients with brain metastases and optimize patterns of care is needed. |
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Molecular Cell Chu C, Zheng S, Mitchell N, Li Z, Zhang X, Wu X, Zhang T, Dang F, Michowski W, Kolodziejczyk A, Xu ML, Kotowski KW, Yang Z, Martinez-Alonso D, Paulo J, Sheng J, Kirby JA, Groezinger F, Zhou Y, He M, Ito Y, Gulvady AC, Cole MI, Foidart P, Nishida J, Ning X, Sharma S, Suski JM, Fassl A, Zhou Y, Geng Y, Wei W, Gygi SP, Polyak K, Wucherpfennig KW, Sicinski P The cyclin E-cyclin-dependent kinase 2 (CDK2) complex is a component of mammalian cell-cycle machinery that drives cell division. Hyperactivation of cyclin E-CDK2 is frequent in human cancers. Small-molecule CDK2 inhibitors are tested in clinical trials for cancer patients. Here, we report that cyclin E-CDK2 has a cell-cycle-independent function in regulating the global transcriptional program of cancer cells. CDK2 phosphorylates bromodomain-containing protein-4 (BRD4) and regulates its chromatin association. Overexpression of cyclin E and the resulting activation of CDK2 in cancer cells alter the cancer cell transcriptome, repress the expression of interferon-stimulated genes, and confer resistance to immunotherapy. Conversely, CDK2 inhibition has the opposite effect and augments the efficacy of immune checkpoint blockade. CDK2 inhibition also increases tumor infiltration by dendritic cells (DCs) and enhances antigen cross-presentation to CD8 T cells. These studies reveal an additional function of cyclin E-CDK2 in tumorigenesis and identify inhibition of CDK2 with clinically available compounds as a strategy for enhancing immune checkpoint blockade. |
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Nature Non-Genotoxic Transplantation and in Vivo Selection through Epitope Editing Casirati G, Cosentino A, Freschi M, Zeng J, Mucci A, Levesque S, Neri N, Drago E, Carzaniga V, Romano F, Mahmoud MS, Chávez-Navarro M, Brendel C, Manis JP, Pellin D, Bauer D, Genovese P The short-term and long-term effects of genotoxic pre-transplant conditioning remain barriers to the broader application of haematopoietic stem/progenitor cell (HSPC) transplantation and gene therapies1-4. Although monoclonal antibodies targeting KIT have been proposed as alternatives to chemotherapy or radiotherapy5-7, their pharmacokinetics hinder clinical applications owing to the risk of depleting transplanted HSPCs. Here, to address this issue, we identified amino acid changes in the extracellular domain of KIT that disrupt the binding of two therapeutic monoclonal antibodies8,9, which impair stem cell factor (SCF)-mediated signalling without affecting KIT expression or functionality. We exploited adenine base editing10 or prime editing11 to efficiently introduce these mutations in HSPCs and combined them with the disruption of the BCL11A erythroid enhancer to promote expression of fetal haemoglobin (HbF)12,13, a therapeutic approach for several haemoglobinopathies. This strategy enables in vivo co-selection of gene-engineered cells to reach the threshold required to provide therapeutic benefit in patients affected by sickle cell disease and ?-thalassaemia. We show progressive enrichment of KIT plus BCL11A multiplex-edited haematopoiesis under selective pressure with KIT monoclonal antibody, in vitro and in vivo. We report that extended treatment with anti-KIT regimens leads to superior in vivo enrichment while avoiding clonal selection, as assessed by a lentiviral barcoded library. Finally, by overcoming the limitations of monoclonal antibody pharmacokinetics, epitope editing enables novel haematopoietic replacement regimens that are not limited by on-target graft elimination, allowing prolonged immune-based conditioning that maximizes haematopoietic niche clearance without chemo-radiotherapy or monoclonal antibody wash-out. |
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Nature Medicine Nadeem O, Cordas Dos Santos DM, Magidson S, O'Donnell E, Redd RA, Liu Y, Midha S, Arters F, Davie C, Ricciardi C, Toenges R, Bidikian N, Hussein S, Alberge JB, Kim S, Pantano-Rubino L, Corrado F, Ashton H, Addonizio D, Mohamed S, Sturtevant A, Marto M, Bergeron A, Malfona F, Panaro K, Richardson PG, Ritz J, Trippa L, Ghobrial IM Teclistamab, a B cell maturation antigen-targeting bispecific antibody, has demonstrated substantial activity in relapsed multiple myeloma (MM), particularly in earlier lines of therapy, and may have higher efficacy in high-risk smoldering MM (HR-SMM) with a more functional immune system. In the randomized phase 2 ImmunoPRISM trial, we compared fixed-duration teclistamab with lenalidomide-dexamethasone (Rd) in HR-SMM. After a six-patient safety run-in, patients were randomized 2:1 to teclistamab or Rd. The primary endpoint was complete response (CR) rate. As of 26 May 2026, 59 patients were treated-45 received teclistamab and 14 received Rd. Teclistamab treatment induced a CR in 77.8% patients versus 0% with Rd, and minimal residual disease negativity at 10-5 in 82.2% patients. At a median follow-up of 24.5 months, 2-year progression-free survival was 92% with teclistamab versus 49% with Rd. Overall, response rates, duration of response and time to progression (TTP) were significantly improved in teclistamab compared to Rd. Toxicities in the teclistamab arm included grades 1-2 cytokine release syndrome, no neurotoxicity and no increase in grade 3 infections compared to Rd (20% versus 21%). No deaths occurred in either arm. Teclistamab represents a highly active immune-interception strategy for HR-SMM. ClinicalTrials.gov registration: NCT05469893. |
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New England Journal of Medicine Treatment Decisions in Multiple Myeloma Mouhieddine TH, Anderson KC Revolutions in transplantation and targeted and immune therapies have transformed multiple myeloma from a disease with an associated survival of a few years into one for which functional cure is an emerging goal. This abundance of effective therapies has created clinical complexity. Here we provide a practical framework, anchored in trial evidence and informed by emerging biologic discoveries, for the navigation of treatment decisions across the disease spectrum. We outline how cytogenetic and genomic risk stratification, functional fitness, and measurable residual disease status individualize therapy in newly diagnosed disease, in which quadruplet induction therapy is now standard and the role of autologous transplantation is being reevaluated. Regarding relapse, we address the sequencing of B-cell maturation antigen-directed chimeric antigen receptor (CAR) T cells, bispecific antibodies, and antibody-drug conjugates, emphasizing T-cell fitness and multiantigen targeting to counter exhaustion and antigen escape. We also consider early interception in high-risk smoldering myeloma. Throughout, we underscore that enrollment of patients in clinical trials should be considered in order to ensure continued progress. |
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Proceedings of the National Academy of Sciences of the U.S.A. Breast Cancer Prevention by Prophylactic Lalba mRNA-LNP Vaccination Nishida J, Seehawer M, Rojas Jimenez E, Yan P, Bui TM, Foidart P, Goyette MA, Cai X, Li Z, Polyak K Tumor-suppressive immunity is more evident in early-stage compared to advanced tumors making it the ideal point for cancer interceptive immunotherapies. We previously described that higher peripheral T cell diversity is associated with more pronounced CD8+ T cell infiltration in ductal carcinoma in situ of the breast, implying a close interaction between peripheral and intratumor immunity. Here, we developed lipid nanoparticle (LNP)-encapsulated messenger ribonucleic acid (mRNA) vaccines expressing the alpha-lactalbumin (LALBA) protein unique to mammary luminal progenitors (LPs) to test whether enhancing immune response by prophylactic vaccination against the putative cell-of-origin of breast cancer suppresses tumorigenesis. Vaccination of outbred Sprague-Dawley rats with N1- methylpseudouridine-modified or unmodified Lalba mRNA-LNP induced different degrees of LALBA-specific and nonspecific immune responses. The vaccination suppressed carcinogen-induced mammary tumorigenesis and improved tumor-free and overall survival without obvious toxicity in the normal mammary glands and other organs. Single-cell transcriptomic analysis revealed that vaccination decreases the frequency of a proliferative LP population in immunoreactive early epithelal hyperplasia. Overall, we provide proof of principle that prophylactic Lalba mRNA-LNP has the potential to suppress the initiation and progression of early breast neoplastic lesions. |
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ACS Medicinal Chemistry Letters Discovery of JH-XIII-05-01, a First-in-Class Dual IRAK1/IRAK4 Degrader for MYD88 Mutant Lymphomas Hatcher JM, Liu S, Liu X, Kofides A, Canning AG, Pizzarella D, Tsakmaklis N, Guerrera ML, Patterson CJ, Guijosa A, Gokhale P, Hunter ZR, Sarosiek SR, Castillo JJ, Wang J, Buhrlage SJ, Treon SP |
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American Journal of Hospice and Palliative Care Lindvall C, Liebowitz A, Chang Y, Lakin JR, Tulsky JA, Volandes AE |
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Annals of Internal Medicine Bereaved Caregivers: Who Is Caring for Them? Khanna GJ, Morris SE, Leiter RE, Yusufov M |
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Annals of Surgical Oncology Park KU, Delisle M, Hassett MJ, Minami CA, Punglia RS, Woodbury SR, Brindle M, Mittendorf EA, King TA |
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Annals of Surgical Oncology Park KU, Delisle M, Hassett MJ, Minami CA, Punglia RS, Woodbury SR, Brindle M, Mittendorf EA, King TA |
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Blood Advances Association Between Patient-Reported Symptoms and Clinical Outcomes in R/R CLL Brown JR |
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Blood Advances Crombie JL, Ahn IE, Ren Y, Tyekucheva S, Carey C, Kniezewski M, Normilus S, Solomon S, Montegaard J, Kim AI, Merryman RW, Armand P, Fisher DC, Brown JR, Davids MS |
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Blood Cancer Discovery Therapy-Persistent Leukemia is Selectively Vulnerable to SLC23A1 Restoration via Targeting KHSRP Luo Q, Whalen KS, Wu X, Fortune AL, Garcia JS, Marinchev K, Raulston EG, Nan Y, Booth CAG, Yan K, Root DE, Doench JG, Lane AA |
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BMJ Open Sexual Health and REhabilitation Online (SHAREonline): Study Protocol of an Optimisation Trial Miklos EM, Recklitis CJ, Medeiros-Nancarrow C, Bober SL |
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British Journal of Clinical Psychology Daniel KE, Zhou ES |
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Briefings in Bioinformatics Stawiski K, Kamran SC, Lee J, Bellmunt J, Mouw KW, De Carvalho FLF |
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Cancer Research Communications Qin Q, Heinz JM, Li H |
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Cancer Research Communications The Role of Germline Transposable Element Insertions in Pediatric Cancer Predisposition Sexton CE, Hamilton KV, Ting DT, Garber JE, Park PJ, Kamihara J |
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Cancer Treatment Reviews Immunotherapy for Locally Advanced Head and Neck Squamous Cell Carcinoma: A Review Haddad R |
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Cell Reports Atomistic TCR-pMHC Interactions Bias CD8 Memory Fate within a Single Antigen-Specific Repertoire Akitsu A, Mallis RJ, Booker MA, Duke-Cohan JS, Brazin KN, Parkins AN, Aryal S, Cinella V, Lee JJ, Uberoy KI, Koenig JK, Biddle M, Messier CM, Lizotte PH, Tolstorukov MY, Reinherz EL |
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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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Clinical Lymphoma, Myeloma, and Leukemia SOHO State-of-the-Art Updates and Next Questions: Current Approach to Waldenström Macroglobulinemia Edwards C, Castillo JJ |
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ESMO Open Tumor Genomic Landscape of Older Patients with Metastatic Breast Cancer Gupta H, Brantley KD, Freedman RA, Kodali A, Kirkner GJ, Hughes ME, Higgins A, Newman AB, Avdulla S, Files J, Suggs G, Tolaney SM, Dillon D, Sholl L, Garrido-Castro AC, Cherniack AD, Lin NU |
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European Journal of Cancer Tarantino P, Li T, Koca B, Guo R, Cunningham O, Hughes ME, Patel A, King TA, Mittendorf EA, Lin NU, Tayob N, Tolaney SM |
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Expert Opinion on Pharmacotherapy Current and New Approaches to the Treatment Landscape for Adults with Waldenström Macroglobulinemia Edwards CV, Castillo JJ, Mouhieddine TH, Sarosiek SR |
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Genes and Development Masuzawa K, Dong KD, XiaoYang Hu C, Peng T, Myung Y, Singh S, Li X, Wang T, Jin C, Paulo JA, Yang K, Schmid EW, Booker MA, Li Y, Hong D, Lazo S, Tolstorukov MY, Doench JG, Duplaquet L, Donovan KA, Iqbal S, Fischer ES, Liau BB, Gygi SP, Oser MG |
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Gynecologic Oncology Molecular Characterization of NSMP Endometrial Cancer and its Relevance for Treatment Silk T, Matulonis UA, Konstantinopoulos PA |
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Haematologica Antin JH, Shimamura A |
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JAMA Dermatology Neff H, Mortelliti C, Kassamali B, Lotter W, Hanrahan G, Solomon B, Karn E, LeBoeuf NR, Gusev A, Ready JE, Nambudiri VE, Ran NA, Silk AW, Ruiz ES |
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JCO Oncology Practice Farhat K, Paul MA, Roby L, Roberts T, Landry L, Hossaini C, Sulieman R, Lathan C, Johnson BE, Kehl KL |
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Journal of Clinical Investigation Karam J, Hoffman SE, Garza A, Gui D, Hoffman HI, Titchen BM, Tanaka Y, Pimenta E, Pappa T, Valderrabano L, Bi K, Gillani R, Brais L, Shannon E, Hornick JL, Park J, Chan J, Van Allen EM |
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Journal of Computational Biology Irizarry RA, Baharav TZ |
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Journal of Geriatric Oncology Hearing Loss: An Unmet Need in Oncology Care Zhu L, Zhang T, Lam AC, Phelan J, Orav EJ, Lam MB |
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Journal of Nursing Care Quality Reducing Nighttime Noise with Targeted Room Modifications in a Pediatric Stem Cell Transplant Unit Waitt JA, Tarquini S, Lehmann LE, Zhou ES |
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Journal of Pain and Symptom Management End-of-Life Care Patterns by Transplant Eligibility Among Patients with End Stage Kidney Disease Liu A, Kizza-Brown JFN, Jurdi AA, Malik AM, Sandhu S, Nurhussien L, Horick NK, Obiejesie OE, Bizup G, Safa K, Kalim S, Gelfand S, Lakin J, Tulsky JA, El-Jawahri A, Ufere NN |
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Journal of Palliative Medicine Chua IS, Lo YT, Succi MD, Zhang M, Yeh J, Skarf LM, Doyle K, Mazzola E, Bates DW |
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Journal of Palliative Medicine Tabata-Kelly M, Sheu C, Bulger AL, Ruan M, Gray TF, Healy BJ, Wichmann L, Bernacki RE |
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Journal of Pediatric Psychology Ream M, Amonoo HL, Rosenbaum ARP, Rosenberg AR, Yi-Frazier J |
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Journal of Surgical Oncology Wong BO, Farber ON, Reich AJ, Cooper ZR, Mack JW, Clancy TE, Raut CP, Lilley EJ |
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Journal of the European Academy of Dermatology and Venereology Ruiz ES, Silk AW |
|
|
|
Journal of the European Academy of Dermatology and Venereology O'Connell KA, Murad F, Mossanen M, Clinton TN, Schmults CD |
|
|
|
|
|
Laryngoscope Intraoperative Botulinum Toxin and Sialocele Incidence After Parotidectomy Kons ZA, Jagarlamudi R, Noyes EA, Marcus KS, Rettig EM, Annino DJ, Goguen LA, Uppaluri R, Sethi RKV |
|
|
|
Leukemia Perron N, Foster K, Mouhieddine TH, Redd RA, Magidson S, Perry J, Sturtevant A, Davie C, Ricciardi C, Arters F, Marto M, Goguen A, Liu Y, O'Donnell EK, Sperling AS, Laubach JP, Richardson PG, Getz G, Sklavenitis-Pistofidis R, Trippa L, Konishi Y, Nadeem O, Ghobrial IM |
|
|
|
Molecular Oncology Tumor B-Cell Infiltration in Platinum-Treated Advanced Muscle-Invasive Urothelial Carcinoma Stawiski K, Lee J, Michaud DE, Guerriero JL, Mouw KW, Carvalho FLF, Bellmunt J |
|
|
|
Nature Reviews Clinical Oncology Antibody-Drug Conjugates in Gynaecological Cancers: Opportunities and Challenges Yeku OO, Liu JF |
|
|
|
Neuro-Oncology Grobman B, Lamba N, Purohit S, Catalano PJ, Shin KY, Tanguturi SK, Rahman R, Haas-Kogan DA, Aizer AA |
|
|
|
Oncology and Therapy Abemaciclib in HR+, HER2- Breast Cancer: A Narrative Review of the Clinical Evidence Mayer EL |
|
|
|
Pediatric Blood and Cancer ASSIST: Refinement of a Benefits Navigator Intervention Among Low-Income Pediatric Oncology Families Kellett J, Aziz-Bose R, Kelly CA, Wolfe J, Bona K |
|
|
|
Pediatric Blood and Cancer Chevalier L, Robinson E, Weller E, Mintor R, Blacken R, Tarquini S, Warren EAH, Rosenberg AR, Lehmann LE, Zhou ES |
|
|
|
Pediatric Blood and Cancer Takahashi T, Nishitani M, Weiskopf E, Gaston L, Duncan CN |
|
|
|
Pediatric Blood and Cancer McCarthy SB, Snaman JM |
|
|
|
Radiotherapy and Oncology Adib E, Lee E, Chen YH, Menon K, Killoran JH, Stoltenberg H, Jacene H, Ravi P, Huynh MA |
|
|
|
Radiotherapy and Oncology Buti G, Ajdari A, Bridge C, Marciscano AE, Sharp GC, Oh K, Shih HA, Bortfeld T |
|
|
|
Targeted Oncology Florez N |
|
|
|
Translational Oncology Gloege HF, De Los Santos MAIC, Chakraborty A, Chadha M, Aguilar-Quintero A, Heaslip CO, Finstuen-Magro S, McDannell B, Tanhaemami M, Meyer S, Klega K, Shulman DS, DuBois SG, Blandin AF, Crompton BD |
|
|
|
Transplantation and Cellular Therapy Takahashi T, Wachter F, Keating AK |