bluuebunny/crossref_metadata_2025 huggingface dataset:
Data from Rapid Depletion of Intratumoral Regulatory T Cells Induces Synchronized CD8 T- and NK-cell Activation and IFNγ-Dependent Tumor Vessel Regression
Authors: Kurebayashi Yutaka , Olkowski Colleen P. , Lane Kelly C. , Vasalatiy Olga V. , Xu Biying C. , Okada Ryuhei , Furusawa Aki , Choyke Peter L. , Kobayashi Hisataka , Sato Noriko
Published: March 2023

Abstract
Regulatory T cells (Tregs) are known to inhibit antitumor immunity, yet the specific mechanism by which intratumoral Tregs promote tumor growth remains unclear. To better understand the roles of intratumoral Tregs, we selectively depleted tumor-infiltrating Tregs using anti-CD25-F(ab′)2 near-infrared photoimmunotherapy. Depletion of tumor-infiltrating Tregs induced transient but synchronized IFNγ expression in CD8 T and natural killer (NK) cells. Despite the small fraction of CD8 T and NK cells contained within examined tumors, IFNγ produced by these CD8 T and NK cells led to efficient and rapid tumor vessel regression, intratumoral ischemia, and tumor necrosis/apoptosis and growth suppression. IFNγ receptor expression on vascular endothelial cells was required for these effects. Similar findings were observed in the early phase of systemic Treg depletion in tumor-bearing Foxp3DTR mice; combination with IL15 therapy further inhibited tumor growth and achieved increased complete regression. These results indicate the pivotal roles of intratumoral Tregs in maintaining tumor vessels and tumor growth by suppressing CD8 T and NK cells from producing IFNγ, providing insight into the mechanism of Treg-targeting therapies.
Significance:
Intratumoral Treg depletion induces synchronized intratumoral CD8 T- and NK-cell activation, IFNγ-dependent tumor vessel regression, and ischemic tumor necrosis/apoptosis, indicating the roles of intratumoral Tregs to support the tumor vasculature.
Data from Cancer-Associated SF3B1 Mutations Confer a BRCA-Like Cellular Phenotype and Synthetic Lethality to PARP Inhibitors
Authors: Lappin Katrina M. , Barros Eliana M. , Jhujh Satpal S. , Irwin Gareth W. , McMillan Hayley , Liberante Fabio G. , Latimer Cheryl , La Bonte Melissa J. , Mills Ken I. , Harkin D. Paul , Stewart Grant S. , Savage Kienan I.
Published: March 2023

Abstract
Mutations in SF3B1 have been identified across several cancer types. This key spliceosome component promotes the efficient mRNA splicing of thousands of genes including those with crucial roles in the cellular response to DNA damage. Here, we demonstrate that depletion of SF3B1 specifically compromises homologous recombination (HR) and is epistatic with loss of BRCA1. More importantly, the most prevalent cancer-associated mutation in SF3B1, K700E, also affects HR efficiency and as a consequence, increases the cellular sensitivity to ionizing radiation and a variety of chemotherapeutic agents, including PARP inhibitors. In addition, the SF3B1 K700E mutation induced unscheduled R-loop formation, replication fork stalling, increased fork degradation, and defective replication fork restart. Taken together, these data suggest that tumor-associated mutations in SF3B1 induce a BRCA-like cellular phenotype that confers synthetic lethality to DNA-damaging agents and PARP inhibitors, which can be exploited therapeutically.
Significance:
The cancer-associated SF3B1K700E mutation induces DNA damage via generation of genotoxic R-loops and stalled replication forks, defective homologous recombination, and increased replication fork degradation, which can be targeted with PARP inhibitors.
Data from Plasticity in the Absence of NOTCH Uncovers a RUNX2-Dependent Pathway in Small Cell Lung Cancer
Authors: Hong Deli , Knelson Erik H. , Li Yixiang , Durmaz Yavuz T. , Gao Wenhua , Walton Emily , Vajdi Amir , Thai Tran , Sticco-Ivins Maura , Sabet Amin H. , Jones Kristen L. , Schinzel Anna C. , Bronson Rod T. , Nguyen Quang-De , Tolstorukov Michael Y. , Vivero Marina , Signoretti Sabina , Barbie David A. , Oser Matthew G.
Published: March 2023

Abstract
Neuroendocrine to nonneuroendocrine plasticity supports small cell lung cancer (SCLC) tumorigenesis and promotes immunogenicity. Approximately 20% to 25% of SCLCs harbor loss-of-function (LOF) NOTCH mutations. Previous studies demonstrated that NOTCH functions as a SCLC tumor suppressor, but can also drive nonneuroendocrine plasticity to support SCLC growth. Given the dual functionality of NOTCH, it is not understood why SCLCs select for LOF NOTCH mutations and how these mutations affect SCLC tumorigenesis. In a CRISPR-based genetically engineered mouse model of SCLC, genetic loss of Notch1 or Notch2 modestly accelerated SCLC tumorigenesis. Interestingly, Notch-mutant SCLCs still formed nonneuroendocrine subpopulations, and these Notch-independent, nonneuroendocrine subpopulations were driven by Runx2-mediated regulation of Rest. Notch2-mutant nonneuroendocrine cells highly express innate immune signaling genes including stimulator of interferon genes (STING) and were sensitive to STING agonists. This work identifies a Notch-independent mechanism to promote nonneuroendocrine plasticity and suggests that therapeutic approaches to activate STING could be selectively beneficial for SCLCs with NOTCH2 mutations.
Significance:
A genetically engineered mouse model of NOTCH-mutant SCLC reveals that nonneuroendocrine plasticity persists in the absence of NOTCH, driven by a RUNX2-REST–dependent pathway and innate immune signaling.
Data from Integrated Molecular Characterization of Patient-Derived Models Reveals Therapeutic Strategies for Treating CIC-DUX4 Sarcoma
Authors: Carrabotta Marianna , Laginestra Maria Antonella , Durante Giorgio , Mancarella Caterina , Landuzzi Lorena , Parra Alessandro , Ruzzi Francesca , Toracchio Lisa , De Feo Alessandra , Giusti Veronica , Pasello Michela , Righi Alberto , Lollini Pier-Luigi , Palmerini Emanuela , Donati Davide Maria , Manara Maria Cristina , Scotlandi Katia
Published: March 2023

Abstract
Capicua-double homeobox 4 (CIC-DUX4)–rearranged sarcomas (CDS) are extremely rare, highly aggressive primary sarcomas that represent a major therapeutic challenge. Patients are treated according to Ewing sarcoma protocols, but CDS-specific therapies are strongly needed. In this study, RNA sequencing was performed on patient samples to identify a selective signature that differentiates CDS from Ewing sarcoma and other fusion-driven sarcomas. This signature was used to validate the representativeness of newly generated CDS experimental models—patient-derived xenografts (PDX) and PDX-derived cell lines—and to identify specific therapeutic vulnerabilities. Annotation analysis of differentially expressed genes and molecular gene validation highlighted an HMGA2/IGF2BP/IGF2/IGF1R/AKT/mTOR axis that characterizes CDS and renders the tumors particularly sensitive to combined treatments with trabectedin and PI3K/mTOR inhibitors. Trabectedin inhibited IGF2BP/IGF2/IGF1R activity, but dual inhibition of the PI3K and mTOR pathways was required to completely dampen downstream signaling mediators. Proof-of-principle efficacy for the combination of the dual AKT/mTOR inhibitor NVP-BEZ235 (dactolisib) with trabectedin was obtained in vitro and in vivo using CDS PDX-derived cell lines, demonstrating a strong inhibition of local tumor growth and multiorgan metastasis. Overall, the development of representative experimental models (PDXs and PDX-derived cell lines) has helped to identify the unique sensitivity of the CDS to AKT/mTOR inhibitors and trabectedin, revealing a mechanism-based therapeutic strategy to fight this lethal cancer.
Significance:
This study identifies altered HMGA2/IGF2BP/IGF2 signaling in CIC-DUX4 sarcomas and provides proof of principle for combination therapy with trabectedin and AKT/mTOR dual inhibitors to specifically combat the disease.
Data from Liver Colonization by Colorectal Cancer Metastases Requires YAP-Controlled Plasticity at the Micrometastatic Stage
Authors: Heinz Maria C. , Peters Niek A. , Oost Koen C. , Lindeboom Rik G.H. , van Voorthuijsen Lisa , Fumagalli Arianna , van der Net Mirjam C. , de Medeiros Gustavo , Hageman Joris H. , Verlaan-Klink Ingrid , Borel Rinkes Inne H.M. , Liberali Prisca , Gloerich Martijn , van Rheenen Jacco , Vermeulen Michiel , Kranenburg Onno , Snippert Hugo J.G.
Published: March 2023

Abstract
Micrometastases of colorectal cancer can remain dormant for years prior to the formation of actively growing, clinically detectable lesions (i.e., colonization). A better understanding of this step in the metastatic cascade could help improve metastasis prevention and treatment. Here we analyzed liver specimens of patients with colorectal cancer and monitored real-time metastasis formation in mouse livers using intravital microscopy to reveal that micrometastatic lesions are devoid of cancer stem cells (CSC). However, lesions that grow into overt metastases demonstrated appearance of de novo CSCs through cellular plasticity at a multicellular stage. Clonal outgrowth of patient-derived colorectal cancer organoids phenocopied the cellular and transcriptomic changes observed during in vivo metastasis formation. First, formation of mature CSCs occurred at a multicellular stage and promoted growth. Conversely, failure of immature CSCs to generate more differentiated cells arrested growth, implying that cellular heterogeneity is required for continuous growth. Second, early-stage YAP activity was required for the survival of organoid-forming cells. However, subsequent attenuation of early-stage YAP activity was essential to allow for the formation of cell type heterogeneity, while persistent YAP signaling locked micro-organoids in a cellularly homogenous and growth-stalled state. Analysis of metastasis formation in mouse livers using single-cell RNA sequencing confirmed the transient presence of early-stage YAP activity, followed by emergence of CSC and non-CSC phenotypes, irrespective of the initial phenotype of the metastatic cell of origin. Thus, establishment of cellular heterogeneity after an initial YAP-controlled outgrowth phase marks the transition to continuously growing macrometastases.
Significance:
Characterization of the cell type dynamics, composition, and transcriptome of early colorectal cancer liver metastases reveals that failure to establish cellular heterogeneity through YAP-controlled epithelial self-organization prohibits the outgrowth of micrometastases.

See related commentary by LeBleu, p. 1870
Data from TET2 Suppresses VHL Deficiency-Driven Clear Cell Renal Cell Carcinoma by Inhibiting HIF Signaling
Authors: Zhang Xinchao , Li Shuyan , He Jing , Jin Yunjie , Zhang Ruonan , Dong Wenjing , Lin Mingen , Yang Yajing , Tian Tongguan , Zhou Yuefan , Xu Yixin , Lei Qun-Ying , Zhang Jing , Zhang Qing , Xu Yanping , Lv Lei
Published: March 2023

Abstract
Inactivating mutations of von Hippel–Lindau (VHL) are highly prevalent in clear cell renal cell carcinoma (ccRCC). Improved understanding of the vulnerabilities of VHL-deficient ccRCC could lead to improved treatment strategies. The activity of DNA dioxygenase ten-eleven translocation (TET)2 is significantly reduced in multiple cancers by different mechanisms, but its role in ccRCC progression remains unclear. Here, we report that increased expression of TET2, but not TET1 and TET3, is negatively associated with tumor metastasis and advanced tumor stage and is positively associated with good prognosis uniquely in ccRCC among all 33 types of cancer in The Cancer Genome Atlas datasets. TET2 restrained glycolysis and pentose phosphate pathway metabolism in a VHL deficiency–dependent manner, thereby suppressing ccRCC progression. Notably, TET2 and VHL mutations tended to cooccur in ccRCC, providing genetic evidence that they cooperate to inhibit the progression of ccRCC. Mechanistically, TET2 was recruited by transcription factor HNF4α to activate FBP1 expression, which antagonized the function of hypoxia-inducible factor-1/2α (HIF1/2α) in metabolic reprogramming to impede ccRCC growth. Stimulating the TET2-FBP1 axis with vitamin C repressed the growth of VHL-deficient ccRCC with wild-type TET2 and increased the sensitivity to glycolysis inhibitors. Moreover, combined expression levels of the HNF4α–TET2-FBP1 axis served as a biomarker of prognosis in patients with ccRCC. This study reveals a unique function of TET2 in the suppression of tumor metabolism and HIF signaling, and it also provides therapeutic targets, potential drugs, and prognostic markers for the management of ccRCC.
Significance:
The identification of TET2-mediated inhibition of HIF signaling and tumor metabolic reprogramming provides insights for new therapeutic strategies for VHL-deficient ccRCC.
Data from Chemotherapy-Induced Collagen IV Drives Cancer Cell Motility through Activation of Src and Focal Adhesion Kinase
Authors: Fatherree Jackson P. , Guarin Justinne R. , McGinn Rachel A. , Naber Stephen P. , Oudin Madeleine J.
Published: March 2023

Abstract
Triple-negative breast cancer (TNBC) is the most aggressive and deadly subtype of breast cancer, accounting for 30,000 cases annually in the United States. While there are several clinical trials ongoing to identify new agents to treat TNBC, the majority of patients with TNBC are treated with anthracycline- or taxane-based chemotherapies in the neoadjuvant setting, followed by surgical resection and adjuvant chemotherapy. While many patients respond well to this approach, as many as 25% will suffer local or metastatic recurrence within 5 years. Understanding the mechanisms that drive recurrence after chemotherapy treatment is critical to improving survival for patients with TNBC. It is well established that the extracellular matrix (ECM), which provides structure and support to tissues, is a major driver of tumor growth, local invasion, and dissemination of cancer cells to distant metastatic sites. In the present study, we show that decellularized ECM (dECM) obtained from chemotherapy-treated mice increases motility of treatment-naïve breast cancer cells compared with vehicle-treated dECM. Tandem-mass–tag proteomics revealed that anthracycline- and taxane-based chemotherapies induce drug-specific changes in tumor ECM composition. The basement membrane protein collagen IV was significantly upregulated in the ECM of chemotherapy-treated mice and patients treated with neoadjuvant chemotherapy. Collagen IV drove invasion via activation of Src and focal adhesion kinase signaling downstream of integrin α1 and α2, and inhibition of collagen IV–driven signaling decreased motility in chemotherapy-treated dECM. These studies provide a novel mechanism by which chemotherapy may induce metastasis via its effects on ECM composition.
Significance:
Cytotoxic chemotherapy induces significant changes in the composition of tumor ECM, inducing a more invasive and aggressive phenotype in residual tumor cells following chemotherapy.
Data from RNA Helicase DDX24 Stabilizes LAMB1 to Promote Hepatocellular Carcinoma Progression
Authors: Liu Tianze , Gan Hairun , He Simeng , Deng Jia , Hu Xinyan , Li Luting , Cai Li , He Jianzhong , Long Haoyu , Cai Jianxun , Li Hanjie , Zhang Qianqian , Wang Lijie , Chen Fangbin , Chen Yuming , Zhang Haopei , Li Jian , Yang Lukun , Liu Ye , Yang Jian-Hua , Kuang Dong-Ming , Pang Pengfei , He Huanhuan , Shan Hong
Published: March 2023

Abstract
Hepatocellular carcinoma (HCC) is one of the most aggressive malignancies. Elucidating the underlying mechanisms of this disease could provide new therapeutic strategies for treating HCC. Here, we identified a novel role of DEAD-box helicase 24 (DDX24), a member of the DEAD-box protein family, in promoting HCC progression. DDX24 levels were significantly elevated in HCC tissues and were associated with poor prognosis of HCC. Overexpression of DDX24 promoted HCC migration and proliferation in vitro and in vivo, whereas suppression of DDX24 inhibited both functions. Mechanistically, DDX24 bound the mRNA618–624nt of laminin subunit beta 1 (LAMB1) and increased its stability in a manner dependent upon the interaction between nucleolin and the C-terminal region of DDX24. Moreover, regulatory factor X8 (RFX8) was identified as a DDX24 promoter-binding protein that transcriptionally upregulated DDX24 expression. Collectively, these findings demonstrate that the RFX8/DDX24/LAMB1 axis promotes HCC progression, providing potential therapeutic targets for HCC.
Significance:
The identification of a tumor-promoting role of DDX24 and the elucidation of the underlying regulatory mechanism provide potential prognostic indicators and therapeutic approaches to help improve the outcome of patients with hepatocellular carcinoma.
Data from HOXA5-Mediated Stabilization of IκBα Inhibits the NF-κB Pathway and Suppresses Malignant Transformation of Breast Epithelial Cells
Authors: Pai Priya , Wang Guannan , Teo Wei Wen , Raez-Rodriguez Diana , Gabrielson Kathleen L. , Győrffy Balázs , Downs Bradley M. , Aggarwal Akanksha , Sukumar Saraswati
Published: March 2023

Abstract
HOXA5 is a transcription factor and tumor suppressor that promotes differentiation of breast epithelial cells and is frequently lost during malignant transformation. HOXA5 loss alone, however, does not confer tumorigenicity. To determine which molecular alterations combined with loss of HOXA5 expression can transform cells, we examined isogenic derivatives of a nonmalignant breast epithelial cell line containing knock-in or knockout mutations in key breast cancer genes. Knockdown (KD) of HOXA5 in cells harboring double knock-in (DKI) of mutated PIK3CA (E545K) and HER2 (V777L) induced epithelial–mesenchymal transition and migration and promoted invasive tumor outgrowth within mouse mammary ducts. The NF-κB pathway was significantly upregulated in DKI cells following HOXA5 KD. HOXA5 KD upregulated multiple NF-κB target genes, including IL6. IκBα protein, but not RNA, expression was reduced in HOXA5-KD cells. HOXA5 bound and stabilized IκBα, forming a nuclear HOXA5-IκBα complex. Chromatin immunoprecipitation sequencing database queries revealed that HOXA5 and IκBα are co-enriched at 528 genomic loci. In patients with breast cancer, high coexpression of HOXA5 and IκBα conferred a significantly better overall and progression-free survival. Collectively, these data suggest that HOXA5 suppresses malignancy in breast epithelial cells by blunting NF-κB action via stabilization of its inhibitor IκBα.
Significance:
Loss of HOXA5 reduces IκBα stability and increases NF-κB signaling to exacerbate breast cancer aggressiveness, providing new insights into the tumor suppressor functions of HOXA5.
Data from Immunogenetic Determinants of Susceptibility to Head and Neck Cancer in the Million Veteran Program Cohort
Authors: Liu Yanhong , Kramer Jennifer R. , Sandulache Vlad C. , Yu Robert , Li Guojun , Chen Liang , Yusuf Zenab I. , Shi Yunling , Pyarajan Saiju , Tsavachidis Spyros , Jiao Li , Mierzwa Michelle L. , Chiao Elizabeth , Mowery Yvonne M. , Shuman Andrew , Shete Sanjay , Sikora Andrew G. , White Donna L.
Published: March 2023

Abstract
Increasing rates of human papillomavirus (HPV)–driven oropharyngeal cancer (OPC) have largely offset declines in tobacco-associated head and neck squamous cell carcinoma (HNSCC) at non-OPC sites. Host immunity is an important modulator of HPV infection, persistence, and clearance, and also of immune evasion in both virally- and nonvirally-driven cancers. However, the association between collective known cancer-related immune gene variants and HNSCC susceptibility has not been fully characterized. Here, we conducted a genetic association study in the multiethnic Veterans Affairs Million Veteran Program cohort, evaluating 16,050 variants in 1,576 immune genes in 4,012 HNSCC cases (OPC = 1,823; non-OPC = 2,189) and 16,048 matched controls. Significant polymorphisms were further examined in a non-Hispanic white (NHW) validation cohort (OPC = 1,206; non-OPC = 955; controls = 4,507). For overall HNSCC susceptibility in NHWs, we discovered and validated a novel 9q31.1 SMC2 association and replicated the known 6p21.32 HLA-DQ-DR association. Six loci/genes for overall HNSCC susceptibility were selectively enriched in African-Americans (6p21.32 HLA-G, 9q21.33 GAS1, 11q12.2 CD6, 11q23.2 NCAM1/CD56, 17p13.1 CD68, 18q22.2 SOCS6); all 6 genes function in antigen-presenting regulation and T-cell activation. Two additional loci (10q26 DMBT1, 15q22.2 TPM1) were uncovered for non-OPC susceptibility, and three loci (11q24 CRTAM, 16q21 CDH5, 18q12.1 CDH2) were identified for HPV-positive OPC susceptibility. This study underscores the role of immune gene variants in modulating susceptibility for both HPV-driven and non-HPV-driven HNSCC. Additional large studies, particularly in racially diverse populations, are needed to further validate the associations and to help elucidate other potential immune factors and mechanisms that may underlie HNSCC risk.
Significance:
Several inherited variations in immune system genes are significantly associated with susceptibility to head and neck cancer, which could help improve personalized cancer risk estimates.
Data from YAP-Activated SATB2 Is a Coactivator of NRF2 That Amplifies Antioxidative Capacity and Promotes Tumor Progression in Renal Cell Carcinoma
Authors: Jin Juan , Chen Fen , He Wenfang , Zhao Li , Lin Bo , Zheng Danna , Chen Li , He Hongchao , He Qiang
Published: March 2023

Abstract
Aberrant epigenetic reprogramming contributes to the progression of renal cell carcinoma (RCC). Elucidation of key regulators of epigenetic reprogramming in RCC could help identify therapeutic vulnerabilities to improve treatment. Here, we report upregulation of the nuclear matrix-associated protein, special AT-rich binding protein-2 (SATB2), in RCC samples, which correlated with poor prognosis. SATB2 inhibition suppressed RCC growth and self-renewal capacities. YAP/TEAD4 activated SATB2 expression and depended on SATB2 to enhance cell proliferation. Transcriptome analysis implicated that SATB2 regulates NRF2 downstream targets to suppress oxidative stress without altering NRF2 levels. Integrated chromatin immunoprecipitation sequencing and assay for transposase-accessible chromatin using sequencing analyses demonstrated that SATB2 coordinated with NRF2 to drive enhancer–promoter interactions, amplifying transcriptional activity. SATB2 recruited SWI/SNF complex subunits, including BRD7 or BRG1, to sustain DNA accessibility. Increased SATB2 triggered chromatin remodeling into configurations that rendered RCC more sensitive to SATB2 deficiency. Moreover, SATB2 ablation promoted the sensitivity of RCC to chemotherapy-induced apoptosis. Finally, targeting SATB2 or BRD7 effectively restricted the proliferation of YAP-high tumors in patient-derived xenografts and patient-derived organoids. Together, SATB2 is an oncogenic chromatin organizer in RCC, and targeting SATB2 is an effective strategy to suppress the YAP-high RCC.
Significance:
A YAP-SATB2-NRF2 regulatory axis amplifies antioxidative stress signaling and provides potential therapeutic targets to enhance response to chemotherapy in renal cell carcinoma.
Data from PARP Inhibition Induces Synthetic Lethality and Adaptive Immunity in LKB1-Mutant Lung Cancer
Authors: Long Li-Li , Ma Si-Cong , Guo Ze-Qin , Zhang Yan-Pei , Fan Zhenzhen , Liu Li-Juan , Liu Li , Han Duan-Duan , Leng Meng-Xin , Wang Jian , Guo Xue-Jun , Tan Jia-Le , Cai Xiao-Ting , Lin Yan , Pan Xinghua , Wu De-Hua , Bai Xue , Dong Zhong-Yi
Published: March 2023

Abstract
Contradictory characteristics of elevated mutational burden and a “cold” tumor microenvironment (TME) coexist in liver kinase B1 (LKB1)–mutant non–small cell lung cancers (NSCLC). The molecular basis underlying this paradox and strategies tailored to these historically difficult to treat cancers are lacking. Here, by mapping the single-cell transcriptomic landscape of genetically engineered mouse models with Kras versus Kras/Lkb1-driven lung tumors, we detected impaired tumor-intrinsic IFNγ signaling in Kras/Lkb1-driven tumors that explains the inert immune context. Mechanistic analysis showed that mutant LKB1 led to deficiency in the DNA damage repair process and abnormally activated PARP1. Hyperactivated PARP1 attenuated the IFNγ pathway by physically interacting with and enhancing the poly(ADP-ribosyl)ation of STAT1, compromising its phosphorylation and activation. Abrogation of the PARP1-driven program triggered synthetic lethality in NSCLC on the basis of the LKB1 mutation–mediated DNA repair defect, while also restoring phosphorylated STAT1 to favor an immunologically “hot” TME. Accordingly, PARP1 inhibition restored the disrupted IFNγ signaling and thus mounted an adaptive immune response to synergize with PD-1 blockade in multiple LKB1-deficient murine tumor models. Overall, this study reveals an unexplored interplay between the DNA repair process and adaptive immune response, providing a molecular basis for dual PARP1 and PD-1 inhibition in treating LKB1-mutant NSCLC.
Significance:
Targeting PARP exerts dual effects to overcome LKB1 loss–driven immunotherapy resistance through triggering DNA damage and adaptive immunity, providing a rationale for dual PARP and PD-1 inhibition in treating LKB1-mutant lung cancers.
Data from Estimation of Neutral Mutation Rates and Quantification of Somatic Variant Selection Using cancereffectsizeR
Authors: Mandell Jeffrey D. , Cannataro Vincent L. , Townsend Jeffrey P.
Published: March 2023

Abstract
Somatic nucleotide mutations can contribute to cancer cell survival, proliferation, and pathogenesis. Although research has focused on identifying which mutations are “drivers” versus “passengers," quantifying the proliferative effects of specific variants within clinically relevant contexts could reveal novel aspects of cancer biology. To enable researchers to estimate these cancer effects, we developed cancereffectsizeR, an R package that organizes somatic variant data, facilitates mutational signature analysis, calculates site-specific mutation rates, and tests models of selection. Built-in models support effect estimation from single nucleotides to genes. Users can also estimate epistatic effects between paired sets of variants, or design and test custom models. The utility of cancer effect was validated by showing in a pan-cancer dataset that somatic variants classified as likely pathogenic or pathogenic in ClinVar exhibit substantially higher effects than most other variants. Indeed, cancer effect was a better predictor of pathogenic status than variant prevalence or functional impact scores. In addition, the application of this approach toward pairwise epistasis in lung adenocarcinoma showed that driver mutations in BRAF, EGFR, or KRAS typically reduce selection for alterations in the other two genes. Companion reference data packages support analyses using the hg19 or hg38 human genome builds, and a reference data builder enables use with any species or custom genome build with available genomic and transcriptomic data. A reference manual, tutorial, and public source code repository are available at https://townsend-lab-yale.github.io/cancereffectsizeR. Comprehensive estimation of cancer effects of somatic mutations can provide insights into oncogenic trajectories, with implications for cancer prognosis and treatment.
Significance:
An R package provides streamlined, customizable estimation of underlying nucleotide mutation rates and of the oncogenic and epistatic effects of mutations in cancer cohorts.
Data from PINK1-Mediated Mitophagy Promotes Oxidative Phosphorylation and Redox Homeostasis to Induce Drug-Tolerant Persister Cancer Cells
Authors: Li Yun , Chen Hengxing , Xie Xuan , Yang Bing , Wang Xiaojuan , Zhang Jingyuan , Qiao Tian , Guan Jiao , Qiu Yuntan , Huang Yong-Xin , Tian Duanqing , Yao Xinyi , Lu Daning , Koeffler H. Phillip , Zhang Yin , Yin Dong
Published: March 2023

Abstract
The drug-tolerant persister (DTP) state enables cancer cells to evade cytotoxic stress from anticancer therapy. However, the mechanisms governing DTP generation remain poorly understood. Here, we observed that lung adenocarcinoma (LUAD) cells and organoids entered a quiescent DTP state to survive MAPK inhibitor treatment. DTP cells following MAPK inhibition underwent a metabolic switch from glycolysis to oxidative phosphorylation (OXPHOS). PTEN-induced kinase 1 (PINK1), a serine/threonine kinase that initiates mitophagy, was upregulated to maintain mitochondrial homeostasis during DTP generation. PINK1-mediated mitophagy supported DTP cell survival and contributed to poor prognosis. Mechanistically, MAPK pathway inhibition resulted in MYC-dependent transcriptional upregulation of PINK1, leading to mitophagy activation. Mitophagy inhibition using either clinically applicable chloroquine or depletion of PINK1 eradicated drug tolerance and allowed complete response to MAPK inhibitors. This study uncovers PINK1-mediated mitophagy as a novel tumor protective mechanism for DTP generation, providing a therapeutic opportunity to eradicate DTP and achieve complete responses.
Significance:
DTP cancer cells that cause relapse after anticancer therapy critically depend on PINK1-mediated mitophagy and metabolic reprogramming, providing a therapeutic opportunity to eradicate persister cells to prolong treatment efficacy.
Supplementary Tables 1-2 from Reduced Plasma Level of CXC Chemokine Ligand 7 in Patients with Pancreatic Cancer
Authors: Matsubara Junichi , Honda Kazufumi , Ono Masaya , Tanaka Yoshinori , Kobayashi Michimoto , Jung Giman , Yanagisawa Koji , Sakuma Tomohiro , Nakamori Shoji , Sata Naohiro , Nagai Hideo , Ioka Tatsuya , Okusaka Takuji , Kosuge Tomoo , Tsuchida Akihiko , Shimahara Masashi , Yasunami Yohichi , Chiba Tsutomu , Hirohashi Setsuo , Yamada Tesshi
Published: March 2023

Supplementary Tables 1-2 from Reduced Plasma Level of CXC Chemokine Ligand 7 in Patients with Pancreatic Cancer
Supplementary Figures 1-3 from Reduced Plasma Level of CXC Chemokine Ligand 7 in Patients with Pancreatic Cancer
Authors: Matsubara Junichi , Honda Kazufumi , Ono Masaya , Tanaka Yoshinori , Kobayashi Michimoto , Jung Giman , Yanagisawa Koji , Sakuma Tomohiro , Nakamori Shoji , Sata Naohiro , Nagai Hideo , Ioka Tatsuya , Okusaka Takuji , Kosuge Tomoo , Tsuchida Akihiko , Shimahara Masashi , Yasunami Yohichi , Chiba Tsutomu , Hirohashi Setsuo , Yamada Tesshi
Published: March 2023

Supplementary Figures 1-3 from Reduced Plasma Level of CXC Chemokine Ligand 7 in Patients with Pancreatic Cancer
Supplementary Table 1 from Polymorphisms in the TOX3/LOC643714 Locus and Risk of Breast Cancer in African-American Women
Authors: Ruiz-Narváez Edward A. , Rosenberg Lynn , Cozier Yvette C. , Cupples L. Adrienne , Adams-Campbell Lucile L. , Palmer Julie R.
Published: March 2023

Supplementary Table 1 from Polymorphisms in the TOX3/LOC643714 Locus and Risk of Breast Cancer in African-American Women
Supplementary Figure 2 from Polymorphisms in the TOX3/LOC643714 Locus and Risk of Breast Cancer in African-American Women
Authors: Ruiz-Narváez Edward A. , Rosenberg Lynn , Cozier Yvette C. , Cupples L. Adrienne , Adams-Campbell Lucile L. , Palmer Julie R.
Published: March 2023

Supplementary Figure 2 from Polymorphisms in the TOX3/LOC643714 Locus and Risk of Breast Cancer in African-American Women
Supplementary Table 1 from Obesity and Thyroid Cancer Risk among U.S. Men and Women: A Pooled Analysis of Five Prospective Studies
Authors: Kitahara Cari M. , Platz Elizabeth A. , Freeman Laura E. Beane , Hsing Ann W. , Linet Martha S. , Park Yikyung , Schairer Catherine , Schatzkin Arthur , Shikany James M. , Berrington de González Amy
Published: March 2023

Supplementary Table 1 from Obesity and Thyroid Cancer Risk among U.S. Men and Women: A Pooled Analysis of Five Prospective Studies
Editorial for this Article from Prediagnostic Total and High-Density Lipoprotein Cholesterol and Risk of Cancer
Authors: Ahn Jiyoung , Lim Unhee , Weinstein Stephanie J. , Schatzkin Arthur , Hayes Richard B. , Virtamo Jarmo , Albanes Demetrius
Published: March 2023

Editorial for this Article from Prediagnostic Total and High-Density Lipoprotein Cholesterol and Risk of Cancer
Supplementary Table 2 from Evaluation of Multiplexed Cytokine and Inflammation Marker Measurements: a Methodologic Study
Authors: Chaturvedi Anil K. , Kemp Troy J. , Pfeiffer Ruth M. , Biancotto Angelique , Williams Marcus , Munuo Stella , Purdue Mark P. , Hsing Ann W. , Pinto Ligia , McCoy J. Philip , Hildesheim Allan
Published: March 2023

Supplementary Table 2 from Evaluation of Multiplexed Cytokine and Inflammation Marker Measurements: a Methodologic Study
Supplementary Tables 1 through 3 from National Trends and Disparities in Cervical Cancer Screening among Commercially Insured Women, 2001–2010
Authors: Wharam J. Frank , Zhang Fang , Xu Xin , Landon Bruce E. , Ross-Degnan Dennis
Published: March 2023

Supplementary Table 1: Claims-based codes used to define numerator events and exclude women from the denominator. Supplementary Table 2: Adjusted 3-year cervical cancer screening rates and disparities among women age 21-29 from 2001 to 2010. Supplementary Table 3: Adjusted 3-year cervical cancer screening rates and disparities among women age 30-64 from 2001 to 2010.
Supplementary Table 1B from State Disparities in Colorectal Cancer Mortality Patterns in the United States
Authors: Naishadham Deepa , Lansdorp-Vogelaar Iris , Siegel Rebecca , Cokkinides Vilma , Jemal Ahmedin
Published: March 2023

PDF file - 83K, Mortality rates and trends in Colorectal Cancer, by State, US, 1990-2007, Non-Hispanic Blacks
Supplementary Methods from CYP19A1 Genetic Variation in Relation to Prostate Cancer Risk and Circulating Sex Hormone Concentrations in Men from the Breast and Prostate Cancer Cohort Consortium
Authors: Travis Ruth C. , Schumacher Fredrick , Hirschhorn Joel N. , Kraft Peter , Allen Naomi E. , Albanes Demetrius , Berglund Goran , Berndt Sonja I. , Boeing Heiner , Bueno-de-Mesquita H. Bas , Calle Eugenia E. , Chanock Stephen , Dunning Alison M. , Hayes Richard , Feigelson Heather Spencer , Gaziano J. Michael , Giovannucci Edward , Haiman Christopher A. , Henderson Brian E. , Kaaks Rudolf , Kolonel Laurence N. , Ma Jing , Rodriguez Laudina , Riboli Elio , Stampfer Meir , Stram Daniel O. , Thun Michael J. , Tjønneland Anne , Trichopoulos Dimitrios , Vineis Paolo , Virtamo Jarmo , Le Marchand Loïc , Hunter David J.
Published: March 2023

Supplementary Methods from CYP19A1 Genetic Variation in Relation to Prostate Cancer Risk and Circulating Sex Hormone Concentrations in Men from the Breast and Prostate Cancer Cohort Consortium
Data Supplement from Are HIV-Infected Men Vulnerable to Prostate Cancer Treatment Disparities?
Authors: Murphy Adam B. , Bhatia Ramona , Martin Iman K. , Klein David A. , Hollowell Courtney M.P. , Nyame Yaw , Dielubanza Elodi , Achenbach Chad , Kittles Rick A.
Published: March 2023

Supplemental Table 3:chi-square analysis of RP treatment vs HIV infection stratified by NCCN risk group.
Supplementary Table 1 from Improved Stool DNA Integrity Method for Early Colorectal Cancer Diagnosis
Authors: Rengucci Claudia , De Maio Giulia , Menghi Maura , Scarpi Emanuela , Guglielmo Simona , Fusaroli Pietro , Caletti Giancarlo , Saragoni Luca , Gardini Andrea Casadei , Zoli Wainer , Falcini Fabio , Amadori Dino , Calistri Daniele
Published: March 2023

Supplementary Table 1. CRC and CRC+HRA prevalence as a function of different FL-DNA cut offs in negative-positive iFOBTs separated by the median value of all positive iFOBTs
Data Supplement from Allergic Diseases and Risk of Hematopoietic Malignancies in a Cohort of Postmenopausal Women: A Report from the Iowa Women's Health Study
Authors: Linabery Amy M. , Prizment Anna E. , Anderson Kristin E. , Cerhan James R. , Poynter Jenny N. , Ross Julie A.
Published: March 2023

Supplementary Table 1. Classification of myeloid and lymphoid malignancies using International Classification of Diseases for Oncology, Third Edition (ICD-O-3) morphology codes.
Supplementary Table 3 from Adherence to Dietary and Lifestyle Recommendations and Prostate Cancer Risk in the Prostate Testing for Cancer and Treatment (ProtecT) Trial
Authors: Er Vanessa , Lane J. Athene , Martin Richard M. , Emmett Pauline , Gilbert Rebecca , Avery Kerry N.L. , Walsh Eleanor , Donovan Jenny L. , Neal David E. , Hamdy Freddie C. , Jeffreys Mona
Published: March 2023

Supplementary Table 3. Associations of the components of prostate cancer dietary index and prostate cancer risk (adherence vs. non-adherence to each dietary component)
Supplementary Table 2 from Nicotine Withdrawal Sensitivity, Linkage to chr6q26, and Association of OPRM1 SNPs in the SMOking in FAMilies (SMOFAM) Sample
Authors: Hardin Jill , He Yungang , Javitz Harold S. , Wessel Jennifer , Krasnow Ruth E. , Tildesley Elizabeth , Hops Hyman , Swan Gary E. , Bergen Andrew W.
Published: March 2023

Supplementary Table 2 from Nicotine Withdrawal Sensitivity, Linkage to chr6q26, and Association of OPRM1 SNPs in the SMOking in FAMilies (SMOFAM) Sample
Supplementary Table 2 from Adherence to Dietary and Lifestyle Recommendations and Prostate Cancer Risk in the Prostate Testing for Cancer and Treatment (ProtecT) Trial
Authors: Er Vanessa , Lane J. Athene , Martin Richard M. , Emmett Pauline , Gilbert Rebecca , Avery Kerry N.L. , Walsh Eleanor , Donovan Jenny L. , Neal David E. , Hamdy Freddie C. , Jeffreys Mona
Published: March 2023

Supplementary Table 2. Associations of the components of WCRF/AICR index and prostate cancer risk by cancer grade
Supplementary Table 1 from Adherence to Dietary and Lifestyle Recommendations and Prostate Cancer Risk in the Prostate Testing for Cancer and Treatment (ProtecT) Trial
Authors: Er Vanessa , Lane J. Athene , Martin Richard M. , Emmett Pauline , Gilbert Rebecca , Avery Kerry N.L. , Walsh Eleanor , Donovan Jenny L. , Neal David E. , Hamdy Freddie C. , Jeffreys Mona
Published: March 2023

Supplementary Table 1. Baseline characteristics of controls by WCRF/AICR index score
Supplementary Figure 1 from Adherence to Dietary and Lifestyle Recommendations and Prostate Cancer Risk in the Prostate Testing for Cancer and Treatment (ProtecT) Trial
Authors: Er Vanessa , Lane J. Athene , Martin Richard M. , Emmett Pauline , Gilbert Rebecca , Avery Kerry N.L. , Walsh Eleanor , Donovan Jenny L. , Neal David E. , Hamdy Freddie C. , Jeffreys Mona
Published: March 2023

Supplementary Figure 1. Flow chart showing reasons for exclusion and numbers of men that were excluded
Supplementary Figure 4 from Epigenetic Deregulation Across Chromosome 2q14.2 Differentiates Normal from Prostate Cancer and Provides a Regional Panel of Novel DNA Methylation Cancer Biomarkers
Authors: Devaney James , Stirzaker Clare , Qu Wenjia , Song Jenny Z. , Statham Aaron L. , Patterson Kate I. , Horvath Lisa G. , Tabor Bruce , Coolen Marcel W. , Hulf Toby , Kench James G. , Henshall Susan M. , Pe Benito Ruth , Haynes Anne-Maree , Mayor Regina , Peinado Miguel A. , Sutherland Robert L. , Clark Susan J.
Published: March 2023

Supplementary Figure 4 from Epigenetic Deregulation Across Chromosome 2q14.2 Differentiates Normal from Prostate Cancer and Provides a Regional Panel of Novel DNA Methylation Cancer Biomarkers
Supplementary Table 1 from Polymorphisms in MicroRNAs Are Associated with Survival in Non–Small Cell Lung Cancer
Authors: Zhao Yang , Wei Qingyi , Hu Lingming , Chen Feng , Hu Zhibin , Heist Rebecca S. , Su Li , Amos Christopher I. , Shen Hongbing , Christiani David C.
Published: March 2023

Supplementary Table 1: all the results from the Harvard cohort.
Supplementary Figure 3 from Polymorphisms in MicroRNAs Are Associated with Survival in Non–Small Cell Lung Cancer
Authors: Zhao Yang , Wei Qingyi , Hu Lingming , Chen Feng , Hu Zhibin , Heist Rebecca S. , Su Li , Amos Christopher I. , Shen Hongbing , Christiani David C.
Published: March 2023

Supplementary Figure 3: The cumulative AUC estimates of the combined model (rs7522956+clinical score) at different time points were greater than those when the model included clinical risk score only.
Data Supplement from Downregulation of microRNAs 145-3p and 145-5p Is a Long-term Predictor of Postmenopausal Breast Cancer Risk: The ORDET Prospective Study
Authors: Muti Paola , Sacconi Andrea , Hossain Ahmed , Donzelli Sara , Ben Moshe Noa Bossel , Ganci Federica , Sieri Sabina , Krogh Vittorio , Berrino Franco , Biagioni Francesca , Strano Sabrina , Beyene Joseph , Yarden Yosef , Blandino Giovanni
Published: March 2023

Supplementary Table 1 - miR-125a-5p expression across different databases; Supplementary Table 2 - miR-99b expression across different databases; Supplementary Table 3 - miR-199a-5p expression across different databases; Supplementary Table 4 - miR-199b-5p expression across different databases; Supplementary Table 5 - miR-892b expression across different databases; Supplementary Table 6 - miR-141 expression across different databases; Supplementary Table 7 - miR-582-5p expression across different databases; Supplementary Table 8 - miR-138 expression across different databases; Supplementary Table 9 - miR-181c* expression across different databases; Supplementary Table 10 - miR-28-3p expression across different databases; Supplementary Table 11 - miR-1288 expression across different databases; Supplementary Table 12 - miR-224 expression across different databases; Supplementary Table 13 - miR-520a-3p expression across different databases; Supplementary Table 14 - miR-223 expression across different databases; Supplementary Table 15 - miR-539 expression across different databases; Supplementary Table 16 - miR-542-5p expression across different databases; Supplementary Table 17 - miR-122* expression across different databases; Supplementary Table 18 - miR-920 expression across different databases.
Supplementary Figure 2 from Polymorphisms in MicroRNAs Are Associated with Survival in Non–Small Cell Lung Cancer
Authors: Zhao Yang , Wei Qingyi , Hu Lingming , Chen Feng , Hu Zhibin , Heist Rebecca S. , Su Li , Amos Christopher I. , Shen Hongbing , Christiani David C.
Published: March 2023

Supplementary Figure 2: The 4 plots provided the Kaplan-Meier curves of rs17111728, rs2042253, rs550894 and rs7227168 for late-stage NSCLC patients.
Supplementary Figure 1 from Polymorphisms in MicroRNAs Are Associated with Survival in Non–Small Cell Lung Cancer
Authors: Zhao Yang , Wei Qingyi , Hu Lingming , Chen Feng , Hu Zhibin , Heist Rebecca S. , Su Li , Amos Christopher I. , Shen Hongbing , Christiani David C.
Published: March 2023

Supplementary Figure 1: The 3 plots provided the Kaplan-Meier curves of chr7:129197463, rs11048315 and rs7522956 for early-stage NSCLC patients.
Supplementary Tables 1-3 from Determinants of Hair Nicotine Concentrations in Nonsmoking Women and Children: A Multicountry Study of Secondhand Smoke Exposure in Homes
Authors: Kim Sungroul , Wipfli Heather , Navas-Acien Ana , Dominici Francesca , Avila-Tang Erika , Onicescu Georgiana , Breysse Patrick , Samet Jonathan M.
Published: March 2023

Supplementary Tables 1-3 from Determinants of Hair Nicotine Concentrations in Nonsmoking Women and Children: A Multicountry Study of Secondhand Smoke Exposure in Homes
Supplementary Table 1 from Comparative Biomarker Expression and RNA Integrity in Biospecimens Derived from Radical Retropubic and Robot-Assisted Laparoscopic Prostatectomies
Authors: Ricciardelli Carmela , Bianco-Miotto Tina , Jindal Shalini , Dodd Thomas J. , Cohen Penelope A. , Marshall Villis R. , Sutherland Peter D. , Samaratunga Hemamali , Kench James G. , Dong Ying , Wang Hong , Clements Judith A. , Risbridger Gail P. , Sutherland Robert L. , Tilley Wayne D. , Horsfall David J.
Published: March 2023

Supplementary Table 1 from Comparative Biomarker Expression and RNA Integrity in Biospecimens Derived from Radical Retropubic and Robot-Assisted Laparoscopic Prostatectomies
Supplementary Figure 1 from Prognostic Significance of Cytoplasmic p27 Expression in Human Melanoma
Authors: Chen Guangdi , Cheng Yabin , Zhang Zhizhong , Martinka Magdalena , Li Gang
Published: March 2023

PDF file -72K
Supplementary Tables 1-2 from Genetic Polymorphisms in 15q25 and 19q13 Loci, Cotinine Levels, and Risk of Lung Cancer in EPIC
Authors: Timofeeva Maria N. , McKay James D. , Davey Smith George , Johansson Mattias , Byrnes Graham B. , Chabrier Amélie , Relton Caroline , Ueland Per Magne , Vollset Stein Emil , Midttun Øivind , Nygård Ottar , Slimani Nadia , Romieu Isabelle , Clavel-Chapelon Françoise , Boutron-Ruault Marie-Christine , Fagherazzi Guy , Kaaks Rudolf , Teucher Birgit , Boeing Heiner , Weikert Cornelia , Bueno-de-Mesquita H. Bas , van Gils Carla , Peeters Petra H.M. , Agudo Antonio , Barricarte Aurelio , Huerta Jose-Maria , Rodríguez Laudina , Sánchez Maria-José , Larrañaga Nerea , Khaw Kay-Tee , Wareham Nick , Allen Naomi E. , Travis Ruth C. , Gallo Valentina , Norat Teresa , Krogh Vittorio , Masala Giovanna , Panico Salvatore , Sacerdote Carlotta , Tumino Rosario , Trichopoulou Antonia , Lagiou Pagona , Trichopoulos Dimitrios , Rasmuson Torgny , Hallmans Göran , Riboli Elio , Vineis Paolo , Brennan Paul
Published: March 2023

PDF file - 57K
Data Supplement from Gene–Environment Interaction Involving Recently Identified Colorectal Cancer Susceptibility Loci
Authors: Kantor Elizabeth D. , Hutter Carolyn M. , Minnier Jessica , Berndt Sonja I. , Brenner Hermann , Caan Bette J. , Campbell Peter T. , Carlson Christopher S. , Casey Graham , Chan Andrew T. , Chang-Claude Jenny , Chanock Stephen J. , Cotterchio Michelle , Du Mengmeng , Duggan David , Fuchs Charles S. , Giovannucci Edward L. , Gong Jian , Harrison Tabitha A. , Hayes Richard B. , Henderson Brian E. , Hoffmeister Michael , Hopper John L. , Jenkins Mark A. , Jiao Shuo , Kolonel Laurence N. , Le Marchand Loic , Lemire Mathieu , Ma Jing , Newcomb Polly A. , Ochs-Balcom Heather M. , Pflugeisen Bethann M. , Potter John D. , Rudolph Anja , Schoen Robert E. , Seminara Daniela , Slattery Martha L. , Stelling Deanna L. , Thomas Fridtjof , Thornquist Mark , Ulrich Cornelia M. , Warnick Greg S. , Zanke Brent W. , Peters Ulrike , Hsu Li , White Emily
Published: March 2023

Supplemental Table 1. SNP details, by study
Supplementary Figure Legends 1-4 from Relationship of Extreme Chromosomal Instability with Long-term Survival in a Retrospective Analysis of Primary Breast Cancer
Authors: Roylance Rebecca , Endesfelder David , Gorman Patricia , Burrell Rebecca A. , Sander Jil , Tomlinson Ian , Hanby Andrew M. , Speirs Valerie , Richardson Andrea L. , Birkbak Nicolai J. , Eklund Aron C. , Downward Julian , Kschischo Maik , Szallasi Zoltan , Swanton Charles
Published: March 2023

PDF file - 65K
Supplementary Figure 1 from p53 Autoantibodies as Potential Detection and Prognostic Biomarkers in Serous Ovarian Cancer
Authors: Anderson Karen S. , Wong Jessica , Vitonis Allison , Crum Christopher P. , Sluss Patrick M. , LaBaer Joshua , Cramer Daniel
Published: March 2023

Supplementary Figure 1 from p53 Autoantibodies as Potential Detection and Prognostic Biomarkers in Serous Ovarian Cancer
Supplementary Table 1 from Metabolic Health Reduces Risk of Obesity-Related Cancer in Framingham Study Adults
Authors: Moore Lynn L. , Chadid Susan , Singer Martha R. , Kreger Bernard E. , Denis Gerald V.
Published: March 2023

Prevalence of site-specific obesity-related cancers according to exposure group.
Supplementary Materials from Body Mass Index, Hormone Replacement Therapy, and Endometrial Cancer Risk: A Meta-Analysis
Authors: Crosbie Emma J. , Zwahlen Marcel , Kitchener Henry C. , Egger Matthias , Renehan Andrew G.
Published: March 2023

Supplementary Materials from Body Mass Index, Hormone Replacement Therapy, and Endometrial Cancer Risk: A Meta-Analysis
Supplementary Table 5 from Childhood Exposure to Secondhand Smoke and Functional Mannose Binding Lectin Polymorphisms Are Associated with Increased Lung Cancer Risk
Authors: Olivo-Marston Susan E. , Yang Ping , Mechanic Leah E. , Bowman Elise D. , Pine Sharon R. , Loffredo Christopher A. , Alberg Anthony J. , Caporaso Neil , Shields Peter G. , Chanock Stephen , Wu Yanhong , Jiang Ruoxiang , Cunningham Julie , Jen Jin , Harris Curtis C.
Published: March 2023

Supplementary Table 5 from Childhood Exposure to Secondhand Smoke and Functional Mannose Binding Lectin Polymorphisms Are Associated with Increased Lung Cancer Risk