Welcome to Dana-Farber's Research News
September 1, 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 August 1 - August 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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Blood Singh AK, Mejia L Hematopoietic stem cells (HSC) exhibit a distinctive antioxidant profile during steady-state and stress hematopoiesis. HSC and multipotential progenitors (HSC/MPP) are metabolically coupled to bone marrow (BM) mesenchymal stromal cells through mitochondrial transfer, a process dependent on hematopoietic connexin 43 (Cx43) and low AMP-activated protein kinase (AMPK) activity. However, the mechanism by which Cx43 preserves mitochondrial functionality in HSC remains elusive. Here, through integrated transcriptomic, proteomic, metabolomic, phenotypic, and functional analyses of HSC and their isolated mitochondria, we identified that Cx43 is present on inner and outer mitochondrial membranes of HSC/MPP, where it primarily regulates mitochondrial metabolism and ATP synthesis by preserving the mitochondrial cristae, activation of mitochondrial AMPK and 2-oxoglutarate dehydrogenase (OGDH)-a rate liming enzyme in TCA cycle and electron transfer chain. During replicative stress, Cx43 deficient HSC/MPP fail to adapt metabolically, accumulate mitochondrial Ca2+, increase mitochondrial AMPK activity, mitochondrial fission, mitophagy, and production of reactive oxygen species, thereby limiting HSC/MPP regeneration potential. Disruption of hyper mitochondrial fragmentation and mitophagy by Drp1 dominant negative mutant (Drp1K38A) or restoration of mitochondrial function through ex vivo heteroplasmy prevent the harmful effects of Cx43 deficiency on mitochondrial metabolism and restore HSC activity in serial transplantation experiments. Re-expression analysis of Cx43 structure function mutants indicate that Cx43 hemichannels are sufficient to reset HSC mitochondrial metabolism, dynamics, Ca2+ levels, and regeneration capacity. This report defines the cell-autonomous mechanism of action behind the role of Cx43 in HSC activity and opens a venue to translational applications in transplantation. |
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Cancer Discovery Baldacci S, Brea EJ, Facchinetti F, Li Z, Ngo K, Malhotra S, Booker MA, Tolstorukov MY, Chakravarti S, Hinchey C, Feng WW, Tsai JA, Hartley AV, Locquet MA, Saldanha A, Haller W, Zasadil LM, Zielinska M, Bui K, Tuladhar B, Lizotte PH, Ivanova EV, Sequist LV, Gokhale PC, Paweletz CP, Smith EL, Janne PA, Barbie DA EGFR tyrosine kinase inhibitors (TKIs) have dramatically improved outcomes for EGFR-mutated non-small cell lung cancer (NSCLC) patients, but relapse frequently occurs due to drug tolerant persister (DTP) cells that can evolve and develop diverse mechanisms of drug resistance. In samples from patients with EGFR-mutated NSCLC treated with EGFR-TKIs in the neoadjuvant setting, we observed enriched expression of the cell surface protein TROP2, a target of clinically active antibody drug conjugates (ADCs). We confirmed these findings across multiple EGFR-mutated NSCLC cell line and patient-derived xenograft models treated with osimertinib in vivo. Treatment with the TROP2 ADC sacituzumab govitecan at the time of osimertinib-induced minimal residual disease only modestly delayed tumor recurrence in vivo, whereas a single infusion of sacituzumab-based TROP2-directed CAR-T cells significantly prolonged relapse-free survival, with evidence of cure. These data highlight the potential of engineering TROP2 CAR-T cell therapy to eliminate EGFR DTPs in patients. |
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JAMA Reducing Drug Prices – The Most Favored Nation Policy vs Price Negotiation Kelkar AH On May 12, 2025, an executive order was issued seeking to establish a most favored nation (MFN) pricing policy for prescription drugs, an attempt to curb soaring US drug prices, which remain 2 to 3 times higher than in other high-income countries and are a key driver of health spending. An MFN policy would cap Medicare payments at the lowest price paid by a group of comparable countries; for example, a $17,000 Medicare payment for a 1-month supply of lenalidomide would be reduced to match Australia’s $900 price for the same cancer drug. Although the MFN policy correctly captures the urgency of addressing unaffordable US drug prices, it is unlikely to meaningfully reduce prices due to legal, operational, and market barriers; a more effective and sustainable solution would be to expand and accelerate drug price negotiation within (and ideally beyond) Medicare. |
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Journal of Clinical Oncology Labaki C, Saad E, Hobeika C, Bi K, Alchoueiry M, Camp S, Matar S, El Ahmar N, Priolo C, Khabibullin D, Salem S, Pimenta E, Park J, Eid M, Semaan K, Fu J, Denize T, El Hajj Chehade R, Machaalani M, Nawfal R, Khatoun WD, Saleh M, El Masri J, Xu W, McGregor BA, Hirsch MS, Xie W, McDermott DF, Signoretti S, Van Allen EM, Choueiri TK, Henske EP PURPOSE: While immune checkpoint inhibition (ICI) has transformed the management of many advanced renal cell carcinomas (RCCs), the determinants of effective antitumor immunity for chromophobe RCC (ChRCC) and renal oncocytic tumors remain an unmet clinical and scientific need. METHODS: Single-cell transcriptomic and T-cell receptor profiling was performed on tumor and adjacent normal tissue of patients with ChRCC and renal oncocytic neoplasms. Using machine learning, the cellular origin of renal oncocytic neoplasms was evaluated, with analysis of associated oncogenic pathways. Using immunohistochemistry, immune infiltration was analyzed in renal oncocytic neoplasms in comparison with clear cell RCC (ccRCC). Immune checkpoint expression, clonal expansion, and tumor specificity were compared between ChRCC and ccRCC. Using the International Metastatic RCC Database Consortium data set, clinical outcomes of patients with metastatic ChRCC (mChRCC) treated with first-line systemic regimens were compared with those of patients with ccRCC. RESULTS: We validated ?-intercalated cells as the cellular origin of renal oncocytic neoplasms. We identified a downregulation of HLA class I molecules with enrichment of potentially targetable pathways including mammalian target of rapamycin and ferroptosis in ChRCC. The tumor microenvironment of ChRCC showed markedly decreased immune infiltration, with a pronounced depletion in tumor-infiltrating CD8+ T cells. ChRCC-infiltrating CD8+ T cells demonstrated lower immune checkpoint expression, diminished clonal expansion, and decreased tumor specificity. Clinical analysis identified poor survival outcomes selectively among patients with mChRCC treated with immune-based therapies. CONCLUSION: Immunogenomic analysis of ChRCC revealed profound depletion of T cells, with an immune phenotype marked by a lack of expression of immune checkpoints and poor tumor specificity, suggesting that the few T cells in these tumor types are likely nonspecific bystanders. This immune-cold environment hinders an effective response to immunotherapy and underscores the need for ChRCC-tailored treatments designed to improve tumor-specific T-cell infiltration into the microenvironment. |
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Journal of the National Cancer Institute Lynce F, Niman SM, Ryan S, Troll E, Overmoyer BA, Nakhlis F, Harrison BT, Yeh ED, Bellon JR, Warren LE, Regan MM BACKGROUND: Susan G. Komen, the Inflammatory Breast Cancer (IBC) Research Foundation, and the Milburn Foundation convened patient advocates, clinicians, and researchers to propose novel quantitative scoring rubrics for IBC diagnosis. In this study, we developed a multi-institutional clinical dataset to test and validate the proposed scoring system. METHODS: IBC (N?=?988) and non-IBC (N?=?332) cases were identified at 2 institutions with dedicated multidisciplinary IBC programs. The non-IBC cohort included consecutive cT4b and cT4c patients. Standard operating procedures (SOPs) were developed for all ambiguous findings and languages. Three different methods were used for the imputation of missing data, resulting in 3 separate datasets. The sensitivity, specificity, and area under the receiver operator characteristic curve (AUC-ROC) were used to assess the discrimination of the proposed scoring rubric. RESULTS: The distribution of "true IBC" cases was 19.7% very likely IBC, 49.1% strong possibility of IBC, 0.4% weak possibility of IBC, 0.1% very unlikely IBC, and 30.7% unknown; corresponding groupings for true non-IBC cases were 0.6% very likely IBC, 51.8% strong possibility of IBC, 9.9% weak possibility of IBC, 2.1% very unlikely IBC, and 35.5% unknown. The AUC-ROC values for missing data imputation methods were similar (0.83-0.84); exploratory score refinement improved the AUC-ROC to 0.88-0.89. CONCLUSION: Using the largest multi-institutional IBC clinical database to date, the score has been validated and is available for clinical use at https://www.komen.org/ibc-calc to assist health-care providers and their patients in IBC diagnosis. Exploratory score refinement demonstrates the potential to increase specificity; however, any change requires separate validation. |
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Journal of the National Cancer Institute Tarantino P, O'Meara T, Morganti S, Waks AG, Lin NU, Tolaney SM, Sammons S BACKGROUND: Most patients with metastatic breast cancer (MBC) are eligible for treatment with trastuzumab deruxtecan (T-DXd). No data are available to guide treatment after exposure to T-DXd. METHODS: We utilized a nationwide electronic health record-derived, deidentified database to review data of patients with MBC who initiated T-DXd between 12/2019 and 9/2023 and who received an additional line of treatment after T-DXd. Tumors were categorized as HER2-positive if ever positive before T-DXd, HER2-negative if never HER2-positive before T-DXd. We compared real-world progression-free survival (rwPFS) and overall survival for post-T-DXd treatments using the Kaplan-Meier method and the log-rank test. RESULTS: We identified 793 patients receiving a post-T-DXd treatment. Post-T-DXd treatment outcomes differed significantly by MBC subtype: median rwPFS was 4.6?months for HER2-positive, 3.4?months for hormone receptor- (HR)-positive/HER2-negative and 2.8?months for triple-negative MBC (p?<?.001). Outcomes with post-T-DXd treatments also varied significantly according to treatment regimen (p?<?.001). Among patients with HER2-positive MBC, median rwPFS ranged from 6.7?months with endocrine treatment regimens to 2.3?months with sacituzumab govitecan (SG). Among patients with HR-positive/HER2-negative MBC, rwPFS ranged from 5.9?months with eribulin to 2.5?months with SG. Among patients with triple-negative MBC, poor outcomes (rwPFS ?3?months) were observed with most treatment regimens, including SG (3?months), eribulin (2?months) and multiagent chemotherapy (2.5?months). CONCLUSIONS: Outcomes of post-T-DXd treatments differ significantly by MBC subtype and type of regimen administered. The use of SG immediately after T-DXd was associated with relatively short rwPFS across subtypes, highlighting some degree of cross-resistance with T-DXd. TRIAL REGISTRATION: N/A. |
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Journal of the National Cancer Institute Prevalence by Therapy Line and Incidence of Breast Cancer Brain Metastases in 18?075 Patients Sammons SL, Leone JP, Erick TK, Tolaney SM, Lin NU IMPORTANCE: Brain metastases portend poor prognosis in patients with metastatic breast cancer (MBC). Designing treatment and prevention clinical trials requires knowledge of brain metastases incidence with each line of therapy. OBJECTIVES: We assessed the prevalence and cumulative incidence of brain metastases in a large MBC patient cohort by subtype and line of therapy, and the impact of HER2-low expression on prevalence. DESIGN, SETTING AND OUTCOMES: We analyzed brain metastases prevalence in patients with MBC in a nationwide electronic health record-derived de-identified database. The primary outcome was first diagnosis of brain metastases. We estimated prevalence and incidence of brain metastases by MBC subtype, including HER2-low and therapy line. We used the cumulative incidence function to estimate brain metastases risk in patients without brain metastases at initiation of systemic therapy. All P-values are 2-sided, and a P-value ?.05 indicates statistical significance. RESULTS: Among 18?075 patients with MBC, 1102 (6.1%) had at least 1 brain metastasis at first-line therapy initiation. For the remaining 16?973 patients, cumulative incidence of brain metastases at 60?months was 10% in patients with hormone receptor-positive (HR+)/HER2- disease, 23% for HR+/HER2+ disease, 34% for HR-/HER2+ disease, and 22% for triple-negative breast cancer (TNBC). HER2-low expression within HR+/HER2- and TNBC subtypes had no impact on brain metastases incidence. Brain metastases prevalence increased per line of therapy for patients with all breast cancer subtypes. CONCLUSIONS: Brain metastases incidence increases per line of therapy for every MBC subtype. The HER2-low biomarker does not impact brain metastases incidence within historical subtypes. |
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Journal of the National Cancer Institute Stereotactic MRI Guided Adaptive Radiotherapy: A Pooled Analysis of a Master Prospective Trial Leeman JE, Shin KY, Droznin A, Catalano P, Cagney DN, Singer L, Oniyangi RD, Zhai K, Benham G, Chirmade S, Campbell J, Boyle S, Saranteas A, Williams CL, Huynh E, Han Z, Sudhyadhom A, Hu YH, Ferguson D, Singhrao K, Hsu SH, Bredfeldt J, Martin NE, Mancias JD, Mamon HJ, Van Dams R, Venkatachalam V, Tanguturi SK, Huynh MA, Fitzgerald KJ, Elhalawani H, Bitterman DS, Schoenfeld JD, Nguyen P, Haas-Kogan DA, Mak R BACKGROUND: Master clinical trial protocol structures offer administrative, procedural and statistical advantages but have not been applied in assessing new radiotherapy devices. Herein, we report on a pooled analysis from a first-of-kind master trial evaluating stereotactic MRI-guided adaptive radiotherapy (SMART). METHODS: Subjects were enrolled on a prospective master protocol evaluating SMART for multiple oncologic indications. CTCAE v5 toxicities, patient reported outcome measures (PROMs), and treatment efficiency metrics were assessed across the entire cohort and in anatomic subsets. RESULTS: 193 subjects were enrolled into 20 sub-protocols for different SMART indications. Data were analyzed from the first 161 subjects. The median time from subprotocol amendment submission to activation was 70.5?days (range 63-93). All completed phase I sub-protocols (n?=?9) met the primary endpoints of safety and feasibility. The risk of grade 3+ toxicity was 1.9% (95%CI 0.4-5.3%), 7.1% (95%CI 0.9-23.5%), 1.8% (95%CI 0.05-9.6%) and 0% (95%CI 0.0-4.7%) in the overall cohort and thoracic, abdominal and pelvic subsets, respectively. PROMs (PROMIS-10) during and after SMART were unchanged from baseline in all subsets. SMART delivery efficiency improved over the study period (first vs final 3?months: 78.5 vs 48.2?minutes, p?<?.001). Adaptive planning performed for 771 fractions resulted in clinically significant plan improvements in 93.0% of fractions (52.7% for organ-at-risk sparing, 20.5% for target coverage and 19.8% for both). CONCLUSIONS: SMART is feasible and safe for multiple thoracic, abdominal and pelvic radiotherapy indications. The master protocol platform offers an adaptable approach for assessment of new oncologic treatment technologies applicable to multiple indications. CLINICAL TRIAL: NCT04115254 |
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Lancet Oncology Tarantino P, Mancino M, Waks AG, Polyak K, Filho OM, Tung NM, Tolaney SM BACKGROUND: HER2-positive breast cancer accounts for 15-20% of all breast cancers and is characterised by HER2 (also known as ERBB2) amplification. Although HER2-targeted therapies have markedly improved outcomes, current clinical-pathological variables and pathological complete response after neoadjuvant therapy are insufficient to fully capture biological heterogeneity and guide personalised treatment. HER2DX is a genomic test that integrates tumour biology and clinical data to stratify risk. Here, we conducted an individual patient-level meta-analysis to evaluate the association between the HER2DX risk score and survival outcomes in early-stage HER2-positive breast cancer. METHODS: We conducted a systematic review and individual patient-level meta-analysis using data from studies of stage 1-3 HER2-positive breast cancer, incorporating HER2DX risk scores, clinical information, and survival outcomes. A systematic literature search was conducted in PubMed on Dec 15, 2024, and complemented by a review of in-house databases to identify eligible studies with HER2DX testing and patient-level data. Eligible studies were required to include more than 50 patients with HER2-positive early breast cancer treated with anti-HER2 therapy, with available survival outcomes, and HER2DX testing performed. Individual-level data were requested from study investigators or accessed through public repositories. HER2DX risk score was evaluated as continuous score and as a risk group using pre-established cutoffs (low vs high). The primary endpoint of the study was event-free survival, estimated using the Kaplan-Meier method. Univariable and multivariable stratified Cox models were used to estimate stratified hazard ratios (HRs). The study was registered in PROSPERO (CRD42025634137). FINDINGS: 11 studies met the inclusion criteria (APT, ATEMPT, CALGB40601, DAPHNe, GOM-HGUGM-2018-05, NEOHER, SOLTI-PAMELA, PHERGain, HUAC, SCAN-B, and DFCI-14-409) and were selected for the meta-analysis. Of 3244 patients identified across the selected studies, 2518 were included in the analysis (those with available HER2DX clinical data and survival outcomes). The median follow-up was 6·1 years (95% CI 6·0-6·3). Of 2518 patients, 891 (35·4%) had stage 1 disease, 1133 (45·0%) stage 2 disease, and 494 (19·6%) stage 3 disease. Hormone receptor-positive disease was present in 1660 (65·9%) of 2518 patients and 1259 (50·0%) of 2518 patients had a high HER2DX risk score. In the multivariable analysis, HER2DX as a continuous variable was independently associated with event-free survival (stratified HR per 10-unit increment 1·25, 95% CI 1·14-1·38; p<0·0001). Patients classified as HER2DX low risk had a 6-year event-free survival rate of 93·6% (95% CI 92·0-95·2), compared with 82·9% (80·0-85·5) for the HER2DX high-risk group, representing a 10·7% absolute difference (stratified HR 2·72, 95% CI 1·97-3·76; p<0·0001). This association was consistent across subgroups, regardless of tumour stage, nodal stage, pathological complete response, or hormone receptor status. INTERPRETATION: HER2DX provides clinically meaningful prognostic stratification in early-stage HER2-positive breast cancer, beyond standard clinical-pathological variables and pathological response. These results support its use in tailoring treatment intensity and guiding clinical decision making. FUNDING: Reveal Genomics. |
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Nature Biotechnology Yang S, Sheffer M, Kaplan IE, Tarannum M, Dinh K, Abdulhamid Y, Bobilev E, Shapiro R, Porter R, Soiffer R, Ritz J, Koreth J, Liu F, Wu CJ, Barbie D, Romee R The tumor microenvironment can inhibit the efficacy of cancer therapies through mechanisms such as poor trafficking and exhaustion of immune cells. Here, to address this challenge, we exploited the safety, tumor tropism and ease of genetic manipulation of non-pathogenic Escherichia coli (E. coli) to deliver key immune-activating cytokines to tumors via surface display on the outer membrane of E. coli K-12 DH5?. Non-pathogenic E. coli expressing murine decoy-resistant IL18 mutein (DR18) induced robust CD8+ T and natural killer (NK) cell-dependent immune responses and suppressed tumor progression in immune-competent colorectal carcinoma and melanoma mouse models. E. coli K-12 DH5? engineered to display human DR18 potently activated mesothelin-targeting chimeric antigen receptor (CAR) NK cells and enhance their trafficking into tumors, which extended survival in an NK cell treatment-resistant mesothelioma xenograft model by enhancing TNF signaling and upregulating NK activation markers. Our live bacteria-based immunotherapeutic system safely and effectively induces potent anti-tumor responses in treatment-resistant solid tumors, motivating further evaluation of this approach in the clinic. |
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Nature Cancer Lightbody ED, Sklavenitis-Pistofidis R, Wu T, Tsuji J, Firer DT, Agius MP, Dutta AK, Barr H, Kim S, Alberge JB, Coorens T, Haradhvala NJ, Su NK, Boehner CJ, Aranha MP, Rahmat M, Konishi Y, Hevenor L, Towle K, Horowitz E, Perry J, Davis M, Walsh KA, Cea-Curry CJ, Fleming G, Vinyard ME, Heilpern-Mallory D, El-Khoury H, Cowan A, Ready JE, Marinac CR, Getz G, Ghobrial IM Multiple myeloma is a bone marrow (BM) plasma cell malignancy preceded by precursor conditions. BM biopsies are conducted infrequently and can yield inconclusive results due to technical limitations. Profiling circulating tumor cells (CTCs) may enable noninvasive routine clinical assessments but remains challenging. Here, to address this, we describe a single-cell sequencing workflow to interrogate few tumor cells (SWIFT-seq), and employ single-cell RNA sequencing and B cell receptor sequencing on paired BM and CTCs from 101 patients and healthy donors. We establish a sequencing-based CTC enumeration strategy and develop a CTC classifier to infer cytogenetic abnormalities. Additionally, we leverage expression profiling to measure tumor proliferative index in CTCs, and demonstrate that clonal dynamics can be captured in CTCs. Last, we propose a circulatory dynamics model whereby tumor burden, proliferation, cytogenetics and a circulatory capacity signature influence CTC burden. Overall, SWIFT-seq may advance blood-based myeloma diagnostics, surveillance and prognostication, and reveal biological mechanisms of tumor dissemination. |
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Nature Communications A Clonally Expanded Nodal T-Cell Population Diagnosed as T-Cell Lymphoma After CAR-T Therapy Maurer K, Weir JA, Nagler A, Haradhvala NJ, Bharadwaj H, Shapiro J, Alakwe S, Kumar V, Waller B, McDonough M, Dela Cruz J, Luna L, Lin E, Gong L, Gong Q, Borji M, Michaels PD, Laubach JP, Pinkus G, Getz G, Wu CJ, Chen F, Jacobson C Reports of secondary malignancies after chimeric antigen receptor (CAR)-T and possible CAR-T derived malignant transformation necessitate caution. Here we describe a patient with diffuse large B-cell lymphoma who developed new lymphadenopathy 2.5 years after CAR-T in the context of COVID-19 infection with histopathologic features consistent with T-cell lymphoma (TCL). Deep molecular interrogation with genomic sequencing and single-cell spatial transcriptomics reveals a highly proliferative clonal T-cell population co-expressing CD4 and CD8 with biallelic TCR rearrangement and no evidence of the CAR construct. The expanded clonotype displayed T follicular helper (TFH) cell transcriptomic programs and occupies immune-excluded spatial niches within the lymph node, supportive of TFH-like neoplastic T cell behavior. Remarkably, the lymphadenopathy spontaneously resolved on interval imaging. Our data underscore the need for better understanding of post-CAR-T clonal T-cell lymphoproliferative disorders to avoid unnecessary treatment and higher specificity in diagnostic methods for TCL. |
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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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American Journal of Hematology Shimony S, Luskin MR, LeBoeuf NR, Feraco AM, Lane AA |
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American Journal of Hospice and Palliative Care Zupanc SN, Volandes A, Penumarthy A, Lakin JR |
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Annals of Surgery Kawamura H, Ugai T, Takashima Y, Okadome K, Shimizu T, Mima K, Akimoto N, Haruki K, Arima K, Zhao M, Väyrynen JP, Wu K, Zhang X, Ng K, Nowak JA, Meyerhardt JA, Giovannucci EL, Giannakis M, Chan AT, Huttenhower C, Garrett WS, Song M, Ogino S |
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Blood Advances Shimamura A, Williams DA |
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Blood Advances Ethical Considerations for Hematologic Precursor Conditions Blackstone EC, Weeks LD, Abel GA |
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Blood Advances Saunders B, Boullt S, Evans B, Bianchi G |
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Blood Advances O'Donnell E, Belsky G, Hsieh YG, Herrick C, Murphy SN |
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Blood Neoplasia Real-World Performance of the CALGB 10403 Regimen in Young Adults in the United States Luskin MR |
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Blood Neoplasia Javidi-Sharifi N, Davids MS |
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Breast Cancer Research and Treatment Lloyd K, Ogayo ER, Mayer EL, Freedman RA, King TA, Mittendorf EA, Kantor O |
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Breast Cancer Research and Treatment Wehbe A, Katlin F, Sharma E, Hans M, Graichen MK, Bychkovsky BL, Scheib R, Garber JE, Pace LE, King TA, Laws A |
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Breast Cancer Research and Treatment Gonzalo-Encabo P, Giobbie-Hurder A, Mayer EL, Partridge AH, Poorvu PD, Waks AG, Tanasijevic AM, Dieli-Conwright CM, Ligibel JA |
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Breast Cancer Research and Treatment Ream M, Yi-Frazier JP, Junkins CC, Rosenberg AR |
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Cancer Medicine Fattahi S, Smart AC, D'Amico AV |
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Cancer Prevention Research Marinac CR |
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Cancers Medication Adherence in Patients Undergoing Allogeneic Hematopoietic Stem Cell Transplantation Amonoo HL, Wolfe ED, Keane EP, Larizza IS, Boardman AC, Healy BC, Cutler C, Greer JA, El-Jawahri A |
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Clinical Breast Cancer Morganti S, Chu X, Pereslete AM, Lange P, Tayob N, Lin NU, Leone JP, Krop IE, Tolaney SM, Parsons HA |
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Clinical Genitourinary Cancer Comorbidity Burden and Effectiveness of Immunotherapy in Metastatic Renal Cell Carcinoma Yekedüz E, Saad E, Chehade REH, Eid M, Saliby RM, Steiner C, Machaalani M, Nawfal R, Semaan K, Heng DYC, Choueiri TK |
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Contemporary Clinical Trials Kang DW, Ficarra S, Wilson RL, Morgans AK, Nguyen PL, Rebbeck TR, Einstein DJ, Uno H, Mossanen M, Hill DM, Gonzalo-Encabo P, Norris MK, Gardiner J, Greer J, Dieli-Conwright CM |
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Current Opinion in Neurology Neuroimaging Endpoints for Clinical Trials in Gliomas: The Neuro-Oncologist Perspective Nakhate V, Youssef G, Lasica AB, Wen PY |
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Fertility and Sterility Fertility Preservation and Mental Health Among Cancer Patients of Reproductive Age Stal J, Partridge AH, Pozo-Kaderman C, Mack JW |
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Gynecologic Oncology Reports Phase 2 Study of Wee1 Inhibitor Adavosertib in Recurrent Uterine Carcinosarcoma Xiong N, Tayob N, Krasner C, Wright AA, Lee EK, Sawyer H, Konstantinopoulos PA, Matulonis UA, Liu JF |
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Head and Neck Hanna GJ, Margalit DN |
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Health Services Research Uno H, Tramontano AC, Punglia RS, Hassett MJ |
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Hematology/Oncology Clinics of North America Emerging Role of Blood-based Biomarkers in Sarcomas Shulman DS, Crompton BD |
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Hematology/Oncology Clinics of North America Leiomyosarcoma Therapeutic Approaches and Future Directions Haddox CL, Papke DJ Jr |
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Journal of Adolescent and Young Adult Oncology Adaptive Psychosocial Outcomes in Cancer Predisposition Syndromes: A Scoping Review Hanania JW, Tsang KK, Rotman C |
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Journal of Geriatric Oncology Thompson LL, Lipson SM, Yoon J, Florissi C, Gregg AT, Amin PM, Shah S, Anabaraonye N, Jiang S, Baxter E, Saraf A, Fitzgerald K, Kann B, Kozono D, Mak RH |
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Journal of Palliative Medicine A Profound Paradox for Caregivers in Cancer Care Hanania JW, Pozo Kaderman C |
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Journal of Palliative Medicine Fenton ATHR, Charewycz N, Kanwal Z, Durieux BN, Tulsky JA, Wright AA, Lindvall CJ |
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Journal of Thoracic Oncology Nakazawa S, Pecci F, Ricciuti B, Gottlieb FH, Facchinetti F, Jiang J, Locquet MA, Makarem M, Alessi JV, Di Federico A, Aldea M, Garbo E, Gandhi MM, Saini A, Haradon D, Bahcall M, Feng WW, Awad MM, Jänne PA |
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Lancet Haematology Adverse Event Grading: The Case of Duffy Null-Associated Neutrophil Counts Merz LE, Hantel A |
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Lancet Planetary Health The Ethics of Climate Change and Health-Care Delivery: A National Survey of US-Based Physicians Hantel A, Walsh TP, Cronin A, Revette A, Nava-Coulter B, Abel GA |
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Leukemia and Lymphoma Choi S, Fay CJ, Jacobsen ED, Devlin PM, LeBoeuf NR |
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Leukemia Mutations and Translocations Associated with Venetoclax Resistance in Chronic Lymphocytic Leukemia Mashima K, Kuang Y, Fernandes SM, Xu S, Hanna B, Shupe S, Mikhaleva M, Santos RA, Predko P, Fardoun R, Bidgoli A, Martindale SP, Naeem A, Davids MS, Paweletz C, Brown JR |
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Lung Cancer Cooley ME, Xiong N, Heiling H, Mazzola E, Nayak MM, Healey MJ, Yang CJ, Lathan C, Castaldi PJ |
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Nursing Research Pozzar RA, Cooley ME, Hammer MJ |
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Oncologist Hantel A, Blackstone EC, Revette AC, Roberts JE, DeAngelo DJ, Lathan CS, Abel GA |
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Seminars in Oncology Nursing Pozzar RA, Cooley ME, Hammer MJ |
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Seminars in Oncology Nursing The Use of Biomarkers in Precision Health Symptom Science-Opportunities and Challenges Hammer MJ |
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Seminars in Oncology Nursing Cooley ME, Abrahm JL |
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Transfusion Hulspas R, Ciuculescu MF, Sasso C, Zhang B, Cancelas JA, Ritz J |
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Trends in Pharmacological Sciences Beyond G Protein and Arrestin: GRK2-Biased ??AR Signaling Ji RL, Wang Z, Zhao JJ |