bluuebunny/crossref_metadata_2025 huggingface dataset:
Data from A First-in-Class Inhibitor of ER Coregulator PELP1 Targets ER+ Breast Cancer
Authors: Altwegg Kristin A. , Viswanadhapalli Suryavathi , Mann Monica , Chakravarty Dimple , Krishnan Samaya , Liu Zexuan , Liu Junhao , Pratap Uday P. , Ebrahimi Behnam , Sanchez John R. , Li Xiaonan , Ma Shihong , Park Ben H. , Santhamma Bindu , Chen Yidong , Lai Zhao , Raj Ganesh V. , Yuan Yaxia , Zhou Daohong , Sareddy Gangadhara R. , Tekmal Rajeshwar R. , McHardy Stan , Huang Tim H.-M. , Rao Manjeet K. , Vankayalapati Hariprasad , Vadlamudi Ratna K.
Published: March 2023

Abstract
Most patients with estrogen receptor alpha–positive (ER+) breast cancers initially respond to treatment but eventually develop therapy resistance with disease progression. Overexpression of oncogenic ER coregulators, including proline, glutamic acid, and leucine-rich protein 1 (PELP1), are implicated in breast cancer progression. The lack of small molecules that inhibits PELP1 represents a major knowledge gap. Here, using a yeast-two-hybrid screen, we identified novel peptide inhibitors of PELP1 (PIP). Biochemical assays demonstrated that one of these peptides, PIP1, directly interacted with PELP1 to block PELP1 oncogenic functions. Computational modeling of PIP1 revealed key residues contributing to its activity and facilitated the development of a small-molecule inhibitor of PELP1, SMIP34, and further analyses confirmed that SMIP34 directly bound to PELP1. In breast cancer cells, SMIP34 reduced cell growth in a dose-dependent manner. SMIP34 inhibited proliferation of not only wild-type (WT) but also mutant (MT) ER+ and therapy-resistant breast cancer cells, in part by inducing PELP1 degradation via the proteasome pathway. RNA sequencing analyses showed that SMIP34 treatment altered the expression of genes associated with estrogen response, cell cycle, and apoptosis pathways. In cell line–derived and patient-derived xenografts of both WT and MT ER+ breast cancer models, SMIP34 reduced proliferation and significantly suppressed tumor progression. Collectively, these results demonstrate SMIP34 as a first-in-class inhibitor of oncogenic PELP1 signaling in advanced breast cancer.
Significance:
Development of a novel inhibitor of oncogenic PELP1 provides potential therapeutic avenues for treating therapy-resistant, advanced ER+ breast cancer.
Data from Cell–Cell Interactions Drive Metastasis of Circulating Tumor Microemboli
Authors: Tao Jianxin , Zhu Lei , Yakoub Mina , Reißfelder Christoph , Loges Sonja , Schölch Sebastian
Published: March 2023

Abstract
Circulating tumor cells are the cellular mediators of distant metastasis in solid malignancies. Their metastatic potential can be augmented by clustering with other tumor cells or nonmalignant cells, forming circulating tumor microemboli (CTM). Cell–cell interactions are key regulators within CTM that convey enhanced metastatic properties, including improved cell survival, immune evasion, and effective extravasation into distant organs. However, the cellular and molecular mechanism of CTM formation, as well as the biology of interactions between tumor cells and immune cells, platelets, and stromal cells in the circulation, remains to be determined. Here, we review the current literature on cell–cell interactions in homotypic and heterotypic CTM and provide perspectives on therapeutic strategies to attenuate CTM-mediated metastasis by targeting cell–cell interactions.
Data from Imaging Glioblastoma Response to Radiotherapy Using 2H Magnetic Resonance Spectroscopy Measurements of Fumarate Metabolism
Authors: Hesse Friederike , Wright Alan J. , Somai Vencel , Bulat Flaviu , Kreis Felix , Brindle Kevin M.
Published: March 2023

Abstract
Early detection of tumor cell death in glioblastoma following treatment with chemoradiation has the potential to distinguish between true disease progression and pseudoprogression. Tumor cell death can be detected noninvasively in vivo by imaging the production of [2,3-2H2]malate from [2,3-2H2]fumarate using 2H magnetic resonance (MR) spectroscopic imaging. We show here that 2H MR spectroscopy and spectroscopic imaging measurements of [2,3-2H2]fumarate metabolism can detect tumor cell death in orthotopically implanted glioblastoma models within 48 hours following the completion of chemoradiation. Following the injection of [2,3-2H2]fumarate into tumor-bearing mice, production of [2,3-2H2]malate was measured in a human cell line–derived model and in radiosensitive and radioresistant patient-derived models of glioblastoma that were treated with temozolomide followed by targeted fractionated irradiation. The increase in the [2,3-2H2]malate/[2,3-2H2]fumarate signal ratio posttreatment, which correlated with histologic assessment of cell death, was a more sensitive indicator of treatment response than diffusion-weighted and contrast agent–enhanced 1H MRI measurements, which have been used clinically to detect responses of glioblastoma to chemoradiation. Overall, early detection of glioblastoma cell death using 2H MRI of malate production from fumarate could help improve the clinical evaluation of response to chemoradiation.
Significance:
2H magnetic resonance imaging of labeled fumarate metabolism can detect early evidence of tumor cell death following chemoradiation, meeting a clinical need to reliably detect treatment response in glioblastoma.
Data from MAB21L4 Deficiency Drives Squamous Cell Carcinoma via Activation of RET
Authors: Srivastava Ankit , Tommasi Cristina , Sessions Dane , Mah Angela , Bencomo Tomas , Garcia Jasmine M. , Jiang Tiffany , Lee Michael , Shen Joseph Y. , Seow Lek Wei , Nguyen Audrey , Rajapakshe Kimal , Coarfa Cristian , Tsai Kenneth Y. , Lopez-Pajares Vanessa , Lee Carolyn S.
Published: March 2023

Abstract
Epithelial squamous cell carcinomas (SCC) most commonly originate in the skin, where they display disruptions in the normally tightly regulated homeostatic balance between keratinocyte proliferation and terminal differentiation. We performed a transcriptome-wide screen for genes of unknown function that possess inverse expression patterns in differentiating keratinocytes compared with cutaneous SCC (cSCC), leading to the identification of MAB21L4 (C2ORF54) as an enforcer of terminal differentiation that suppresses carcinogenesis. Loss of MAB21L4 in human cSCC organoids increased expression of RET to enable malignant progression. In addition to transcriptional upregulation of RET, deletion of MAB21L4 preempted recruitment of the CacyBP-Siah1 E3 ligase complex to RET and reduced its ubiquitylation. In SCC organoids and in vivo tumor models, genetic disruption of RET or selective inhibition of RET with BLU-667 (pralsetinib) suppressed SCC growth while inducing concomitant differentiation. Overall, loss of MAB21L4 early during SCC development blocks differentiation by increasing RET expression. These results suggest that targeting RET activation is a potential therapeutic strategy for treating SCC.
Significance:
Downregulation of RET mediated by MAB21L4–CacyBP interaction is required to induce epidermal differentiation and suppress carcinogenesis, suggesting RET inhibition as a potential therapeutic approach in squamous cell carcinoma.
Data from The Prostate Cancer Androgen Receptor Cistrome in African American Men Associates with Upregulation of Lipid Metabolism and Immune Response
Authors: Berchuck Jacob E. , Adib Elio , Abou Alaiwi Sarah , Dash Amit K. , Shin Jin Na , Lowder Dallin , McColl Collin , Castro Patricia , Carelli Ryan , Benedetti Elisa , Deng Jenny , Robertson Matthew , Baca Sylvan C. , Bell Connor , McClure Heather M. , El Zarif Talal , Davidsohn Matthew P. , Lakshminarayanan Gitanjali , Rizwan Kinza , Skapura Darlene G. , Grimm Sandra L. , Davis Christel M. , Ehli Erik A. , Kelleher Kaitlin M. , Seo Ji-Heui , Mitsiades Nicholas , Coarfa Cristian , Pomerantz Mark M. , Loda Massimo , Ittmann Michael , Freedman Matthew L. , Kaochar Salma
Published: March 2023

Abstract
African-American (AA) men are more likely to be diagnosed with and die from prostate cancer than European American (EA) men. Despite the central role of the androgen receptor (AR) transcription factor in prostate cancer, little is known about the contribution of epigenetics to observed racial disparities. We performed AR chromatin immunoprecipitation sequencing on primary prostate tumors from AA and EA men, finding that sites with greater AR binding intensity in AA relative to EA prostate cancer are enriched for lipid metabolism and immune response genes. Integration with transcriptomic and metabolomic data demonstrated coinciding upregulation of lipid metabolism gene expression and increased lipid levels in AA prostate cancer. In a metastatic prostate cancer cohort, upregulated lipid metabolism associated with poor prognosis. These findings offer the first insights into ancestry-specific differences in the prostate cancer AR cistrome. The data suggest a model whereby increased androgen signaling may contribute to higher levels of lipid metabolism, immune response, and cytokine signaling in AA prostate tumors. Given the association of upregulated lipogenesis with prostate cancer progression, our study provides a plausible biological explanation for the higher incidence and aggressiveness of prostate cancer observed in AA men.
Significance:
With immunotherapies and inhibitors of metabolic enzymes in clinical development, the altered lipid metabolism and immune response in African-American men provides potential therapeutic opportunities to attenuate racial disparities in prostate cancer.
Data from Meta-Analysis of Human Cancer Single-Cell RNA-Seq Datasets Using the IMMUcan Database
Authors: Camps Jordi , Noël Floriane , Liechti Robin , Massenet-Regad Lucile , Rigade Sidwell , Götz Lou , Hoffmann Caroline , Amblard Elise , Saichi Melissa , Ibrahim Mahmoud M. , Pollard Jack , Medvedovic Jasna , Roider Helge G. , Soumelis Vassili
Published: March 2023

Abstract
The development of single-cell RNA sequencing (scRNA-seq) technologies has greatly contributed to deciphering the tumor microenvironment (TME). An enormous amount of independent scRNA-seq studies have been published representing a valuable resource that provides opportunities for meta-analysis studies. However, the massive amount of biological information, the marked heterogeneity and variability between studies, and the technical challenges in processing heterogeneous datasets create major bottlenecks for the full exploitation of scRNA-seq data. We have developed IMMUcan scDB (https://immucanscdb.vital-it.ch), a fully integrated scRNA-seq database exclusively dedicated to human cancer and accessible to nonspecialists. IMMUcan scDB encompasses 144 datasets on 56 different cancer types, annotated in 50 fields containing precise clinical, technological, and biological information. A data processing pipeline was developed and organized in four steps: (i) data collection; (ii) data processing (quality control and sample integration); (iii) supervised cell annotation with a cell ontology classifier of the TME; and (iv) interface to analyze TME in a cancer type–specific or global manner. This framework was used to explore datasets across tumor locations in a gene-centric (CXCL13) and cell-centric (B cells) manner as well as to conduct meta-analysis studies such as ranking immune cell types and genes correlated to malignant transformation. This integrated, freely accessible, and user-friendly resource represents an unprecedented level of detailed annotation, offering vast possibilities for downstream exploitation of human cancer scRNA-seq data for discovery and validation studies.
Significance:
The IMMUcan scDB database is an accessible supportive tool to analyze and decipher tumor-associated single-cell RNA sequencing data, allowing researchers to maximally use this data to provide new insights into cancer biology.
Data from Targeting RNA Exonuclease XRN1 Potentiates Efficacy of Cancer Immunotherapy
Authors: Ran Xue-Bin , Ding Ling-Wen , Sun Qiao-Yang , Yang Henry , Said Jonathan W. , Zhentang Lao , Madan Vikas , Dakle Pushkar , Xiao Jin-Fen , Loh Xinyi , Li Ying , Xu Liang , Xiang Xiao-Qiang , Wang Ling-Zhi , Goh Boon Cher , Lin De-Chen , Chng Wee Joo , Tan Soo-Yong , Jha Sudhakar , Koeffler H. Phillip
Published: March 2023

Abstract
Despite the remarkable clinical responses achieved with immune checkpoint blockade therapy, the response rate is relatively low and only a subset of patients can benefit from the treatment. Aberrant RNA accumulation can mediate IFN signaling and stimulate an immune response, suggesting that targeting RNA decay machinery might sensitize tumor cells to immunotherapy. With this in mind, we identified an RNA exoribonuclease, XRN1, as a potential therapeutic target to suppress RNA decay and stimulate antitumor immunity. Silencing of XRN1 suppressed tumor growth in syngeneic immunocompetent mice and potentiated immunotherapy efficacy, while silencing of XRN1 alone did not affect tumor growth in immunodeficient mice. Mechanistically, XRN1 depletion activated IFN signaling and the viral defense pathway; both pathways play determinant roles in regulating immune evasion. Aberrant RNA-sensing signaling proteins (RIG-I/MAVS) mediated the expression of IFN genes, as depletion of each of them blunted the elevation of antiviral/IFN signaling in XRN1-silenced cells. Analysis of pan-cancer CRISPR-screening data indicated that IFN signaling triggered by XRN1 silencing is a common phenomenon, suggesting that the effect of XRN1 silencing may be extended to multiple types of cancers. Overall, XRN1 depletion triggers aberrant RNA-mediated IFN signaling, highlighting the importance of the aberrant RNA-sensing pathway in regulating immune responses. These findings provide the molecular rationale for developing XRN1 inhibitors and exploring their potential clinical application in combination with cancer immunotherapy.
Significance:
Targeting XRN1 activates an intracellular innate immune response mediated by RNA-sensing signaling and potentiates cancer immunotherapy efficacy, suggesting inhibition of RNA decay machinery as a novel strategy for cancer treatment.
Data from An Alternatively Spliced p62 Isoform Confers Resistance to Chemotherapy in Breast Cancer
Authors: Guo Qianying , Wang Hao , Duan Jiahao , Luo Wenwu , Zhao Rongrong , Shen Yuting , Wang Bijun , Tao Siqi , Sun Yi , Ye Qian , Bi Xiaomin , Yuan Hui , Wu Qiang , Lobie Peter E. , Zhu Tao , Tan Sheng , Huang Xing , Wu Zhengsheng
Published: March 2023

Abstract
Resistance to chemotherapy remains a major obstacle to the successful treatment of breast cancer. More than 80% of patients who receive neoadjuvant chemotherapy (NAC) do not achieve a pathologic complete response. In this study, we report a novel p62 mRNA isoform with a short 3′-UTR (untranslated region; p62-SU, 662-nt) that is associated with chemoresistance in breast cancer cells and tissue specimens. The p62 mRNA isoform was identified by RNA sequencing with qRT-PCR, 3′-RACE, and Northern blot analysis. In vitro and in vivo, ectopic expression of p62-SU promoted breast cancer cell proliferation, migration, invasion, and chemoresistance compared with the p62 mRNA isoform with a full-length 3′-UTR (p62-LU, 1,485-nt). Mechanistically, cleavage and polyadenylation specific factor 1 (CPSF1) modulated the 3′-UTR of p62 through alternative polyadenylation. In addition, p62-SU escaped miR-124-3p–mediated repression and upregulated p62-SU protein expression, thereby inducing p62-dependent chemoresistance. These data suggest that a CPSF1-p62-miR-124-3p signaling axis is responsible for reduced sensitivity of breast cancer to chemotherapy.
Significance:
Resistance to NAC in breast cancer is driven by a novel p62 mRNA isoform that escapes miRNA-mediated repression and leads to increased p62 protein expression.
Data from A Genomically and Clinically Annotated Patient-Derived Xenograft Resource for Preclinical Research in Non–Small Cell Lung Cancer
Authors: Woo Xing Yi , Srivastava Anuj , Mack Philip C. , Graber Joel H. , Sanderson Brian J. , Lloyd Michael W. , Chen Mandy , Domanskyi Sergii , Gandour-Edwards Regina , Tsai Rebekah A. , Keck James , Cheng Mingshan , Bundy Margaret , Jocoy Emily L. , Riess Jonathan W. , Holland William , Grubb Stephen C. , Peterson James G. , Stafford Grace A. , Paisie Carolyn , Neuhauser Steven B. , Karuturi R. Krishna Murthy , George Joshy , Simons Allen K. , Chavaree Margaret , Tepper Clifford G. , Goodwin Neal , Airhart Susan D. , Lara Primo N. , Openshaw Thomas H. , Liu Edison T. , Gandara David R. , Bult Carol J.
Published: March 2023

Abstract
Patient-derived xenograft (PDX) models are an effective preclinical in vivo platform for testing the efficacy of novel drugs and drug combinations for cancer therapeutics. Here we describe a repository of 79 genomically and clinically annotated lung cancer PDXs available from The Jackson Laboratory that have been extensively characterized for histopathologic features, mutational profiles, gene expression, and copy-number aberrations. Most of the PDXs are models of non–small cell lung cancer (NSCLC), including 37 lung adenocarcinoma (LUAD) and 33 lung squamous cell carcinoma (LUSC) models. Other lung cancer models in the repository include four small cell carcinomas, two large cell neuroendocrine carcinomas, two adenosquamous carcinomas, and one pleomorphic carcinoma. Models with both de novo and acquired resistance to targeted therapies with tyrosine kinase inhibitors are available in the collection. The genomic profiles of the LUAD and LUSC PDX models are consistent with those observed in patient tumors from The Cancer Genome Atlas and previously characterized gene expression-based molecular subtypes. Clinically relevant mutations identified in the original patient tumors were confirmed in engrafted PDX tumors. Treatment studies performed in a subset of the models recapitulated the responses expected on the basis of the observed genomic profiles. These models therefore serve as a valuable preclinical platform for translational cancer research.
Significance:
Patient-derived xenografts of lung cancer retain key features observed in the originating patient tumors and show expected responses to treatment with standard-of-care agents, providing experimentally tractable and reproducible models for preclinical investigations.
Data from Lipid-Associated Macrophages Are Induced by Cancer-Associated Fibroblasts and Mediate Immune Suppression in Breast Cancer
Authors: Timperi Eleonora , Gueguen Paul , Molgora Martina , Magagna Ilaria , Kieffer Yann , Lopez-Lastra Silvia , Sirven Philemon , Baudrin Laura G. , Baulande Sylvain , Nicolas André , Champenois Gabriel , Meseure Didier , Vincent-Salomon Anne , Tardivon Anne , Laas Enora , Soumelis Vassili , Colonna Marco , Mechta-Grigoriou Fatima , Amigorena Sebastian , Romano Emanuela
Published: March 2023

Abstract
Tumor-associated macrophages (TAM) play a detrimental role in triple-negative breast cancer (TNBC). In-depth analysis of TAM characteristics and interactions with stromal cells, such as cancer-associated fibroblast (CAF), could provide important biological and therapeutic insights. Here we identify at the single-cell level a monocyte-derived STAB1+TREM2high lipid-associated macrophage (LAM) subpopulation with immune suppressive capacities that is expanded in patients resistant to immune checkpoint blockade (ICB). Genetic depletion of this LAM subset in mice suppressed TNBC tumor growth. Flow cytometry and bulk RNA sequencing data demonstrated that coculture with TNBC-derived CAFs led to reprogramming of blood monocytes towards immune suppressive STAB1+TREM2high LAMs, which inhibit T-cell activation and proliferation. Cell-to-cell interaction modeling and assays in vitro demonstrated the role of the inflammatory CXCL12–CXCR4 axis in CAF–myeloid cell cross-talk and recruitment of monocytes in tumor sites. Altogether, these data suggest an inflammation model whereby monocytes recruited to the tumor via the CAF-driven CXCL12–CXCR4 axis acquire protumorigenic LAM capacities to support an immunosuppressive microenvironment.
Significance:
This work identifies a novel lipid–associated macrophage subpopulation with immune suppressive functions, offering new leads for therapeutic interventions in triple-negative breast cancer.
Data from Combination Therapies with CDK4/6 Inhibitors to Treat KRAS-Mutant Pancreatic Cancer
Authors: Goodwin Craig M. , Waters Andrew M. , Klomp Jennifer E. , Javaid Sehrish , Bryant Kirsten L. , Stalnecker Clint A. , Drizyte-Miller Kristina , Papke Bjoern , Yang Runying , Amparo Amber M. , Ozkan-Dagliyan Irem , Baldelli Elisa , Calvert Valerie , Pierobon Mariaelena , Sorrentino Jessica A. , Beelen Andrew P. , Bublitz Natalie , Lüthen Mareen , Wood Kris C. , Petricoin Emanuel F. , Sers Christine , McRee Autumn J. , Cox Adrienne D. , Der Channing J.
Published: March 2023

Abstract
Mutational loss of CDKN2A (encoding p16INK4A) tumor-suppressor function is a key genetic step that complements activation of KRAS in promoting the development and malignant growth of pancreatic ductal adenocarcinoma (PDAC). However, pharmacologic restoration of p16INK4A function with inhibitors of CDK4 and CDK6 (CDK4/6) has shown limited clinical efficacy in PDAC. Here, we found that concurrent treatment with both a CDK4/6 inhibitor (CDK4/6i) and an ERK–MAPK inhibitor (ERKi) synergistically suppresses the growth of PDAC cell lines and organoids by cooperatively blocking CDK4/6i-induced compensatory upregulation of ERK, PI3K, antiapoptotic signaling, and MYC expression. On the basis of these findings, a Phase I clinical trial was initiated to evaluate the ERKi ulixertinib in combination with the CDK4/6i palbociclib in patients with advanced PDAC (NCT03454035). As inhibition of other proteins might also counter CDK4/6i-mediated signaling changes to increase cellular CDK4/6i sensitivity, a CRISPR-Cas9 loss-of-function screen was conducted that revealed a spectrum of functionally diverse genes whose loss enhanced CDK4/6i growth inhibitory activity. These genes were enriched around diverse signaling nodes, including cell-cycle regulatory proteins centered on CDK2 activation, PI3K–AKT–mTOR signaling, SRC family kinases, HDAC proteins, autophagy-activating pathways, chromosome regulation and maintenance, and DNA damage and repair pathways. Novel therapeutic combinations were validated using siRNA and small-molecule inhibitor–based approaches. In addition, genes whose loss imparts a survival advantage were identified (e.g., RB1, PTEN, FBXW7), suggesting possible resistance mechanisms to CDK4/6 inhibition. In summary, this study has identified novel combinations with CDK4/6i that may have clinical benefit to patients with PDAC.
Significance:
CRISPR-Cas9 screening and protein activity mapping reveal combinations that increase potency of CDK4/6 inhibitors and overcome drug-induced compensations in pancreatic cancer.
Data from Targeting DNA Repair with Combined Inhibition of NHEJ and MMEJ Induces Synthetic Lethality in TP53-Mutant Cancers
Authors: Patterson-Fortin Jeffrey , Bose Arindam , Tsai Wei-Chih , Grochala Carter , Nguyen Huy , Zhou Jia , Parmar Kalindi , Lazaro Jean-Bernard , Liu Joyce , McQueen Kelsey , Shapiro Geoffrey I. , Kozono David , D'Andrea Alan D.
Published: March 2023

Abstract
DNA repair pathway inhibitors are a new class of anticancer drugs that are advancing in clinical trials. Peposertib is an inhibitor of DNA-dependent protein kinase (DNA-PK), which is a key driver of nonhomologous end-joining (NHEJ). To identify regulators of response to peposertib, we performed a genome-wide CRISPR knockout screen and found that loss of POLQ (polymerase theta, POLθ) and other genes in the microhomology-mediated end-joining (MMEJ) pathway are key predictors of sensitivity to DNA-PK inhibition. Simultaneous disruption of two DNA repair pathways via combined treatment with peposertib plus a POLθ inhibitor novobiocin exhibited synergistic synthetic lethality resulting from accumulation of toxic levels of DNA double-strand break end resection. TP53-mutant tumor cells were resistant to peposertib but maintained elevated expression of POLQ and increased sensitivity to novobiocin. Consequently, the combination of peposertib plus novobiocin resulted in synthetic lethality in TP53-deficient tumor cell lines, organoid cultures, and patient-derived xenograft models. Thus, the combination of a targeted DNA-PK/NHEJ inhibitor with a targeted POLθ/MMEJ inhibitor may provide a rational treatment strategy for TP53-mutant solid tumors.
Significance:
Combined inhibition of NHEJ and MMEJ using two nontoxic, targeted DNA repair inhibitors can effectively induce toxic DNA damage to treat TP53-deficient cancers.
Data from Targeting STAT5 Signaling Overcomes Resistance to IDH Inhibitors in Acute Myeloid Leukemia through Suppression of Stemness
Authors: Liu Alex C.H. , Cathelin Severine , Yang Yitong , Dai David L. , Ayyathan Dhanoop Manikoth , Hosseini Mohsen , Minden Mark D. , Tierens Anne , Chan Steven M.
Published: March 2023

Abstract
Mutant isocitrate dehydrogenase 1 (IDH1) and IDH2 block the differentiation of acute myeloid leukemia (AML) cells through production of R-2-hydroxyglutarate (R-2-HG). IDH inhibitors can induce differentiation of AML cells by lowering R-2-HG but have limited clinical efficacy as single agents. Here, we performed a genome-wide CRISPR knockout screen in an Idh1-mutated hematopoietic progenitor cell line to identify genes that increased the differentiation response to ivosidenib, an IDH1 inhibitor. The screen identified C-type lectin member 5a (Clec5a), which encodes a spleen tyrosine kinase (SYK)-coupled surface receptor, as one of the top hits. Knockout of Clec5a and Syk rendered cells more sensitive to ivosidenib-induced differentiation through a reduction in STAT5-dependent expression of stemness-related genes, including genes in the homeobox (HOX) family. Importantly, direct inhibition of STAT5 activity was sufficient to increase the differentiation response to IDH inhibitors in primary human IDH1- and IDH2-mutated AML cells, including those harboring mutations in receptor tyrosine kinase (RTK) and MAPK genes that have been linked to drug resistance. In patient-derived xenograft models of IDH1-mutated AML, combination treatment with ivosidenib and the STAT5 inhibitor pimozide was superior to each agent alone in inducing differentiation in leukemic cells without compromising normal hematopoiesis. These findings demonstrate that STAT5 is a critical mediator of resistance to IDH inhibitors and provide the rationale for combining STAT5 and IDH inhibitors in the treatment of IDH-mutated AML.
Significance:
A CRISPR knockout screen identifies a mechanism of resistance to IDH inhibitors in AML involving activated STAT5 signaling, suggesting a potential strategy to improve the clinical efficacy of IDH inhibitors.
Data from Extracellular Vesicle-Mediated Transfer of LncRNA IGFL2-AS1 Confers Sunitinib Resistance in Renal Cell Carcinoma
Authors: Pan Yihui , Lu Xuanxuan , Shu Guannan , Cen Junjie , Lu Jun , Zhou Mi , Huang Kangbo , Dong Jiaqi , Li Jiaying , Lin Haishan , Song Hongde , Xu Quanhui , Han Hui , Chen Zhenhua , Chen Wei , Luo Junhang , Wei Jinhuan , Zhang Jiaxing
Published: March 2023

Abstract
Sunitinib resistance remains a serious challenge to the treatment of advanced and metastatic renal cell carcinoma (RCC), yet the mechanisms underlying this resistance are not fully understood. Here, we report that the long noncoding RNA IGFL2-AS1 is a driver of therapy resistance in RCC. IGFL2-AS1 was highly upregulated in sunitinib-resistant RCC cells and was associated with poor prognosis in patients with clear cell RCC (ccRCC) who received sunitinib therapy. IGFL2-AS1 enhanced TP53INP2 expression by competitively binding to hnRNPC, a multifunctional RNA-binding protein that posttranscriptionally suppresses TP53INP2 expression through alternative splicing. Upregulated TP53INP2 enhanced autophagy and ultimately led to sunitinib resistance. Meanwhile, IGFL2-AS1 was packaged into extracellular vesicles through hnRNPC, thus transmitting sunitinib resistance to other cells. N6-methyladenosine modification of IGFL2-AS1 was critical for its interaction with hnRNPC. In a patient-derived xenograft model of sunitinib-resistant ccRCC, injection of chitosan-solid lipid nanoparticles containing antisense oligonucleotide-IGFL2-AS1 successfully reversed sunitinib resistance. These findings indicate a novel molecular mechanism of sunitinib resistance in RCC and suggest that IGFL2-AS1 may serve as a prognostic indicator and potential therapeutic target to overcome resistance.
Significance:
Extracellular vesicle-packaged IGFL2-AS1 promotes sunitinib resistance by regulating TP53INP2-triggered autophagy, implicating this lncRNA as a potential therapeutic target in renal cell carcinoma.
Data from Common Germline Risk Variants Impact Somatic Alterations and Clinical Features across Cancers
Authors: Namba Shinichi , Saito Yuki , Kogure Yasunori , Masuda Tatsuo , Bondy Melissa L. , Gharahkhani Puya , Gockel Ines , Heider Dominik , Hillmer Axel , Jankowski Janusz , MacGregor Stuart , Maj Carlo , Melin Beatrice , Ostrom Quinn T. , Palles Claire , Schumacher Johannes , Tomlinson Ian , Whiteman David C. , Okada Yukinori , Kataoka Keisuke
Published: March 2023

Abstract
Aggregation of genome-wide common risk variants, such as polygenic risk score (PRS), can measure genetic susceptibility to cancer. A better understanding of how common germline variants associate with somatic alterations and clinical features could facilitate personalized cancer prevention and early detection. We constructed PRSs from 14 genome-wide association studies (median n = 64,905) for 12 cancer types by multiple methods and calibrated them using the UK Biobank resources (n = 335,048). Meta-analyses across cancer types in The Cancer Genome Atlas (n = 7,965) revealed that higher PRS values were associated with earlier cancer onset and lower burden of somatic alterations, including total mutations, chromosome/arm somatic copy-number alterations (SCNA), and focal SCNAs. This contrasts with rare germline pathogenic variants (e.g., BRCA1/2 variants), showing heterogeneous associations with somatic alterations. Our results suggest that common germline cancer risk variants allow early tumor development before the accumulation of many somatic alterations characteristic of later stages of carcinogenesis.
Significance:
Meta-analyses across cancers show that common germline risk variants affect not only cancer predisposition but the age of cancer onset and burden of somatic alterations, including total mutations and copy-number alterations.
Data from KDM6A Loss Triggers an Epigenetic Switch That Disrupts Urothelial Differentiation and Drives Cell Proliferation in Bladder Cancer
Authors: Qiu Hong , Makarov Vladimir , Bolzenius Jennifer K. , Halstead Angela , Parker Yvonne , Wang Allen , Iyer Gopakumar V. , Wise Hannah , Kim Daniel , Thayaparan Varna , Lindner Daniel J. , Haber Georges-Pascal , Ting Angela H. , Ren Bing , Chan Timothy A. , Arora Vivek , Solit David B. , Lee Byron H.
Published: March 2023

Abstract
Disruption of KDM6A, a histone lysine demethylase, is one of the most common somatic alternations in bladder cancer. Insights into how KDM6A mutations affect the epigenetic landscape to promote carcinogenesis could help reveal potential new treatment approaches. Here, we demonstrated that KDM6A loss triggers an epigenetic switch that disrupts urothelial differentiation and induces a neoplastic state characterized by increased cell proliferation. In bladder cancer cells with intact KDM6A, FOXA1 interacted with KDM6A to activate genes instructing urothelial differentiation. KDM6A-deficient cells displayed simultaneous loss of FOXA1 target binding and genome-wide redistribution of the bZIP transcription factor ATF3, which in turn repressed FOXA1-target genes and activated cell-cycle progression genes. Importantly, ATF3 depletion reversed the cell proliferation phenotype induced by KDM6A deficiency. These data establish that KDM6A loss engenders an epigenetic state that drives tumor growth in an ATF3-dependent manner, creating a potentially targetable molecular vulnerability.
Significance:
A gain-of-function epigenetic switch that disrupts differentiation is triggered by inactivating KDM6A mutations in bladder cancer and can serve as a potential target for novel therapies.
Supplementary Table 2 from Identifying Genes for Establishing a Multigenic Test for Hepatocellular Carcinoma Surveillance in Hepatitis C Virus-Positive Cirrhotic Patients
Authors: Archer Kellie J. , Mas Valeria R. , David Krystle , Maluf Daniel G. , Bornstein Karen , Fisher Robert A.
Published: March 2023

Supplementary Table 2 from Identifying Genes for Establishing a Multigenic Test for Hepatocellular Carcinoma Surveillance in Hepatitis C Virus-Positive Cirrhotic Patients
Supplementary Tables 1 - 3 from Imaging Features of HER2 Overexpression in Breast Cancer: A Systematic Review and Meta-analysis
Authors: Elias Sjoerd G. , Adams Arthur , Wisner Dorota J. , Esserman Laura J. , van't Veer Laura J. , Mali Willem P.Th.M. , Gilhuijs Kenneth G.A. , Hylton Nola M.
Published: March 2023

PDF file - 101KB, Supplementary Table S1 - Matching between BI-RADS and non BI-RADS mammography descriptors. Supplementary Table S2 - Matching between BI-RADS and non BI-RADS ultrasound descriptors. Supplementary Table S3 - Matching between BI-RADS and non BI-RADS MRI descriptors.
Data Supplement from Low Folate Levels Are Associated with Reduced Risk of Colorectal Cancer in a Population with Low Folate Status
Authors: Gylling Björn , Van Guelpen Bethany , Schneede Jörn , Hultdin Johan , Ueland Per Magne , Hallmans Göran , Johansson Ingegerd , Palmqvist Richard
Published: March 2023

Supplementary Table 2: Multivariate odds ratios for colorectal cancer risk according to plasma vitamin B12 after stratification by baseline and tumor characteristics.
Supplementary Table 1 from The 6q22.33 Locus and Breast Cancer Susceptibility
Authors: Kirchhoff Tomas , Chen Zhang-qun , Gold Bert , Pal Prodipto , Gaudet Mia M. , Kosarin Kristi , Levine Douglas A. , Gregersen Peter , Spencer Sara , Harlan Megan , Robson Mark , Klein Robert J. , Hudis Clifford A. , Norton Larry , Dean Michael , Offit Kenneth
Published: March 2023

Supplementary Table 1 from The 6q22.33 Locus and Breast Cancer Susceptibility
Supplementary Table 2 from Assessing Tumor Mutations to Gain Insight into Base Excision Repair Sequence Polymorphisms and Smoking in Colon Cancer
Authors: Curtin Karen , Samowitz Wade S. , Wolff Roger K. , Ulrich Cornelia M. , Caan Bette J. , Potter John D. , Slattery Martha L.
Published: March 2023

Supplementary Table 2 from Assessing Tumor Mutations to Gain Insight into Base Excision Repair Sequence Polymorphisms and Smoking in Colon Cancer
Supplementary Tables 1 and 2 from Salivary Auto-Antibodies as Noninvasive Diagnostic Markers of Oral Cavity Squamous Cell Carcinoma
Authors: Wu Chih-Ching , Chang Ya-Ting , Chang Kai-Ping , Liu Yu-Ling , Liu Hao-Ping , Lee I-Ling , Yu Jau-Song , Chiang Wei-Fan
Published: March 2023

PDf - 62K, Supplementary Table S1, levels of autoantibody (auto-Ab) and IgA in saliva samples. Supplementary Table S2, estimated odds ratio (OR) with and without adjusting for co-variables.
Supplementary Table 1 from Assessing Tumor Mutations to Gain Insight into Base Excision Repair Sequence Polymorphisms and Smoking in Colon Cancer
Authors: Curtin Karen , Samowitz Wade S. , Wolff Roger K. , Ulrich Cornelia M. , Caan Bette J. , Potter John D. , Slattery Martha L.
Published: March 2023

Supplementary Table 1 from Assessing Tumor Mutations to Gain Insight into Base Excision Repair Sequence Polymorphisms and Smoking in Colon Cancer
Supplementary Figure 1 from High-Throughput Simultaneous Analysis of Five Urinary Metabolites of Areca Nut and Tobacco Alkaloids by Isotope-Dilution Liquid Chromatography-Tandem Mass Spectrometry with On-Line Solid-Phase Extraction
Authors: Hu Chiung-Wen , Chang Yan-Zin , Wang Hsiao-Wen , Chao Mu-Rong
Published: March 2023

Supplementary Figure 1 from High-Throughput Simultaneous Analysis of Five Urinary Metabolites of Areca Nut and Tobacco Alkaloids by Isotope-Dilution Liquid Chromatography-Tandem Mass Spectrometry with On-Line Solid-Phase Extraction
Data Supplement from Biomarkers for Early Detection of Colorectal Cancer and Polyps: Systematic Review
Authors: Shah Reena , Jones Emma , Vidart Victoire , Kuppen Peter J.K. , Conti John A. , Francis Nader K.
Published: March 2023

Supplementary Table 2. Calculations of Positive and Negative Predictive Values of iFOBT within the Context of CRC Disease Prevalence
Supplementary Figure Legends from Use of Multiple Imputation to Correct for Bias in Lung Cancer Incidence Trends by Histologic Subtype
Authors: Yu Mandi , Feuer Eric J. , Cronin Kathleen A. , Caporaso Neil E.
Published: March 2023

PDF - 80K, Legend for Supplementary Figure 1.
Supplementary Table 1 from Genetic Variants in the LEPR, CRY1, RNASEL, IL4, and ARVCF Genes Are Prognostic Markers of Prostate Cancer-Specific Mortality
Authors: Lin Daniel W. , FitzGerald Liesel M. , Fu Rong , Kwon Erika M. , Zheng Siqun Lilly , Kolb Suzanne , Wiklund Fredrik , Stattin Pär , Isaacs William B. , Xu Jianfeng , Ostrander Elaine A. , Feng Ziding , Grönberg Henrik , Stanford Janet L.
Published: March 2023

XLS file - 88K
Supplementary Tables 1 - 2 from Comparison of Mammographic Density Assessed as Volumes and Areas among Women Undergoing Diagnostic Image-Guided Breast Biopsy
Authors: Gierach Gretchen L. , Geller Berta M. , Shepherd John A. , Patel Deesha A. , Vacek Pamela M. , Weaver Donald L. , Chicoine Rachael E. , Pfeiffer Ruth M. , Fan Bo , Mahmoudzadeh Amir Pasha , Wang Jeff , Johnson Jason M. , Herschorn Sally D. , Brinton Louise A. , Sherman Mark E.
Published: March 2023

Supplementary Table 1. Age- and BMI-adjusted linear regression results for the association between participant characteristics and standardized volume and area mammographic density measures. Supplementary Table 2. Spearman's rank correlation coefficients for volume and area density measures, unadjusted and adjusted for age and body mass index.
Supplementary Tables 1-5, Figure 1 from A Novel Approach to Predict the Likelihood of Specific Ovarian Tumor Pathology Based on Serum CA-125: A Multicenter Observational Study
Authors: Van Calster Ben , Valentin Lil , Van Holsbeke Caroline , Zhang Jing , Jurkovic Davor , Lissoni Andrea Alberto , Testa Antonia Carla , Czekierdowski Artur , Fischerová Daniela , Domali Ekaterini , Van de Putte Gregg , Vergote Ignace , Van Huffel Sabine , Bourne Tom , Timmerman Dirk
Published: March 2023

Supplementary Tables 1-5, Figure 1 from A Novel Approach to Predict the Likelihood of Specific Ovarian Tumor Pathology Based on Serum CA-125: A Multicenter Observational Study
Supplementary Figures 1-2, Tables 1-4 from Performance of the Genomic Evaluators of Metastatic Prostate Cancer (GEMCaP) Tumor Biomarker for Identifying Recurrent Disease in African American Patients
Authors: Levin Albert M. , Lindquist Karla J. , Avila Andrew , Witte John S. , Paris Pamela L. , Rybicki Benjamin A.
Published: March 2023

PDF - 159K, Supplementary Figure 1 - Distribution of GEMCaP scores in African American and European American prostate cancer cases. Supplementary Figure 2 - Bland-Altman plot assessing the agreement between copy number estimates for the GEMCaP loci for four African American tumor samples profiled using both sequencing and SNP array technologies. Supplementary Table 1 - Demographic and clinicopathologic characteristics of the study participants (n=62) by self-identified race-ethnicity. Supplementary Table 2 - GEMCaP loci human genome build 19 base-pair locations. Supplementary Table 3 - Comparison of copy number estimates from next generation sequencing and SNP array technologies for the GEMCaP loci from four African American prostate tumors. Supplementary Table 4 - Evidence for CNAs in other studies of African American prostate tumors for the GEMCaP loci.
Supplementary Figure 1 from Genetic Polymorphisms in Adaptive Immunity Genes and Childhood Acute Lymphoblastic Leukemia
Authors: Chang Jeffrey S. , Wiemels Joseph L. , Chokkalingam Anand P. , Metayer Catherine , Barcellos Lisa F. , Hansen Helen M. , Aldrich Melinda C. , Guha Neela , Urayama Kevin Y. , Scélo Ghislaine , Green Janet , May Suzanne L. , Kiley Vincent A. , Wiencke John K. , Buffler Patricia A.
Published: March 2023

Supplementary Figure 1 from Genetic Polymorphisms in Adaptive Immunity Genes and Childhood Acute Lymphoblastic Leukemia
Supplementary Table 3 from A Prospective Cohort Study on Overweight, Smoking, Alcohol Consumption, and Risk of Barrett's Esophagus
Authors: Steevens Jessie , Schouten Leo J. , Driessen Ann L.C. , Huysentruyt Clément J.R. , Keulemans Yolande C.A. , Goldbohm R. Alexandra , van den Brandt Piet A.
Published: March 2023

Supplementary Table 3 from A Prospective Cohort Study on Overweight, Smoking, Alcohol Consumption, and Risk of Barrett's Esophagus
Supplementary Table 1 from Cancer Survivorship Research: A Review of the Literature and Summary of Current NCI-Designated Cancer Center Projects
Authors: Harrop J. Phil , Dean Julie A. , Paskett Electra D.
Published: March 2023

XLS file - 136K
Supplementary Figure 4 from Collagen XXIII: A Potential Biomarker for the Detection of Primary and Recurrent Non–Small Cell Lung Cancer
Authors: Spivey Kristin A. , Banyard Jacqueline , Solis Luisa M. , Wistuba Ignacio I. , Barletta Justine A. , Gandhi Leena , Feldman Henry A. , Rodig Scott J. , Chirieac Lucian R. , Zetter Bruce R.
Published: March 2023

Supplementary Figure 4 from Collagen XXIII: A Potential Biomarker for the Detection of Primary and Recurrent Non–Small Cell Lung Cancer
Supplementary Figure 7 from Global Patterns of Cancer Incidence and Mortality Rates and Trends
Authors: Jemal Ahmedin , Center Melissa M. , DeSantis Carol , Ward Elizabeth M.
Published: March 2023

Supplementary Figure 7 from Global Patterns of Cancer Incidence and Mortality Rates and Trends
Supplementary Figure 3 from Global Patterns of Cancer Incidence and Mortality Rates and Trends
Authors: Jemal Ahmedin , Center Melissa M. , DeSantis Carol , Ward Elizabeth M.
Published: March 2023

Supplementary Figure 3 from Global Patterns of Cancer Incidence and Mortality Rates and Trends
Supplementary Table 2 from Confirmation of 5p12 As a Susceptibility Locus for Progesterone-Receptor–Positive, Lower Grade Breast Cancer
Authors: Milne Roger L. , Goode Ellen L. , García-Closas Montserrat , Couch Fergus J. , Severi Gianluca , Hein Rebecca , Fredericksen Zachary , Malats Núria , Zamora M. Pilar , Pérez Jose Ignacio Arias , Benítez Javier , Dörk Thilo , Schürmann Peter , Karstens Johann H. , Hillemanns Peter , Cox Angela , Brock Ian W. , Elliot Graeme , Cross Simon S. , Seal Sheila , Turnbull Clare , Renwick Anthony , Rahman Nazneen , Shen Chen-Yang , Yu Jyh-Cherng , Huang Chiun-Sheng , Hou Ming-Feng , Nordestgaard Børge G. , Bojesen Stig E. , Lanng Charlotte , Alnæs Grethe Grenaker , Kristensen Vessela , Børrensen-Dale Anne-Lise , Hopper John L. , Dite Gillian S. , Apicella Carmel , Southey Melissa C. , Lambrechts Diether , Yesilyurt Betül T. , Floris Giuseppe , Leunen Karin , Sangrajrang Suleeporn , Gaborieau Valerie , Brennan Paul , McKay James , Chang-Claude Jenny , Wang-Gohrke Shan , Radice Paolo , Peterlongo Paolo , Manoukian Siranoush , Barile Monica , Giles Graham G. , Baglietto Laura , John Esther M. , Miron Alexander , Chanock Stephen J. , Lissowska Jolanta , Sherman Mark E. , Figueroa Jonine D. , Bogdanova Natalia V. , Antonenkova Natalia N. , Zalutsky Iosif V. , Rogov Yuri I. , Fasching Peter A. , Bayer Christian M. , Ekici Arif B. , Beckmann Matthias W. , Brenner Hermann , Müller Heiko , Arndt Volker , Stegmaier Christa , Andrulis Irene L. , Knight Julia A. , Glendon Gord , Mulligan Anna Marie , Mannermaa Arto , Kataja Vesa , Kosma Veli-Matti , Hartikainen Jaana M. , Meindl Alfons , Heil Joerg , Bartram Claus R. , Schmutzler Rita K. , Thomas Gilles D. , Hoover Robert N. , Fletcher Olivia , Gibson Lorna J. , dos Santos Silva Isabel , Peto Julian , Nickels Stefan , Flesch-Janys Dieter , Anton-Culver Hoda , Ziogas Argyrios , Sawyer Elinor , Tomlinson Ian , Kerin Michael , Miller Nicola , Schmidt Marjanka K. , Broeks Annegien , Van ‘t Veer Laura J. , Tollenaar Rob A.E.M. , Pharoah Paul D.P. , Dunning Alison M. , Pooley Karen A. , Marme Frederik , Schneeweiss Andreas , Sohn Christof , Burwinkel Barbara , Jakubowska Anna , Lubinski Jan , Jaworska Katarzyna , Durda Katarzyna , Kang Daehee , Yoo Keun-Young , Noh Dong-Young , Ahn Sei-Hyun , Hunter David J. , Hankinson Susan E. , Kraft Peter , Lindstrom Sara , Chen Xiaoqing , Beesley Jonathan , Hamann Ute , Harth Volker , Justenhoven Christina , Winqvist Robert , Pylkäs Katri , Jukkola-Vuorinen Arja , Grip Mervi , Hooning Maartje , Hollestelle Antoinette , Oldenburg Rogier A. , Tilanus-Linthorst Madeleine , Khusnutdinova Elza , Bermisheva Marina , Prokofieva Darya , Farahtdinova Albina , Olson Janet E. , Wang Xianshu , Humphreys Manjeet K. , Wang Qin , Chenevix-Trench Georgia , Easton Douglas F.
Published: March 2023

PDF file - 94K
Supplementary Figure Legends 1-2 from Generalizability and Epidemiologic Characterization of Eleven Colorectal Cancer GWAS Hits in Multiple Populations
Authors: He Jing , Wilkens Lynne R. , Stram Daniel O. , Kolonel Laurence N. , Henderson Brian E. , Wu Anna H. , Le Marchand Loic , Haiman Christopher A.
Published: March 2023

Supplementary Figure Legends 1-2 from Generalizability and Epidemiologic Characterization of Eleven Colorectal Cancer GWAS Hits in Multiple Populations
Supplementary Figure Legend from Analytic Variability in Immunohistochemistry Biomarker Studies
Authors: Anagnostou Valsamo K. , Welsh Allison W. , Giltnane Jennifer M. , Siddiqui Summar , Liceaga Camil , Gustavson Mark , Syrigos Konstantinos N. , Reiter Jill L. , Rimm David L.
Published: March 2023

Supplementary Figure Legend from Analytic Variability in Immunohistochemistry Biomarker Studies
Supplementary Document A from A Candidate Molecular Biomarker Panel for the Detection of Bladder Cancer
Authors: Urquidi Virginia , Goodison Steve , Cai Yunpeng , Sun Yijun , Rosser Charles J.
Published: March 2023

PDF file - 84K, Molecular Biomarker Signature for the Non-Invasive Detection of Bladder Cancer
Supplementary Figure 1 from ST14 Gene Variant and Decreased Matriptase Protein Expression Predict Poor Breast Cancer Survival
Authors: Kauppinen Jaana M. , Kosma Veli-Matti , Soini Ylermi , Sironen Reijo , Nissinen Minna , Nykopp Timo K. , Kärjä Vesa , Eskelinen Matti , Kataja Vesa , Mannermaa Arto
Published: March 2023

Supplementary Figure 1 from ST14 Gene Variant and Decreased Matriptase Protein Expression Predict Poor Breast Cancer Survival
Supplementary Tables 1-3 from Polymorphisms in Telomere Maintenance Genes and Risk of Lung Cancer
Authors: Choi Jin Eun , Kang Hyo-Gyoung , Jang Jin Sung , Choi Yi Young , Kim Min Jung , Kim Jong Sik , Jeon Hyo-Sung , Lee Won Kee , Cha Sung Ick , Kim Chang Ho , Kam Sin , Jung Tae Hoon , Park Jae Yong
Published: March 2023

Supplementary Tables 1-3 from Polymorphisms in Telomere Maintenance Genes and Risk of Lung Cancer
Data Supplement from Breast Cancer Susceptibility Variants and Mammographic Density Phenotypes in Norwegian Postmenopausal Women
Authors: Ellingjord-Dale Merete , Grotmol Tom , Lee Eunjung , Van Den Berg David J. , Hofvind Solveig , Couto Elisabeth , Sovio Ulla , dos-Santos-Silva Isabel , Ursin Giske
Published: March 2023

Supplementary Table 1. Per minor allele associations between breast cancer SNPs and mammographic density by breast cancer risk factors and confidence intervals, identified by lower (lowerCL) and upper (upperCL) confidence limits
Data Supplement from Breast Cancer Susceptibility Variants and Mammographic Density Phenotypes in Norwegian Postmenopausal Women
Authors: Ellingjord-Dale Merete , Grotmol Tom , Lee Eunjung , Van Den Berg David J. , Hofvind Solveig , Couto Elisabeth , Sovio Ulla , dos-Santos-Silva Isabel , Ursin Giske
Published: March 2023

Supplementary Table 2. Per minor allele associations between breast cancer SNPs and mammographic density by breast cancer risk factors and confidence intervals, identified by lower (lowerCL) and upper (upperCL) confidence limits
Data Supplement from Follow-up to Abnormal Cancer Screening Tests: Considering the Multilevel Context of Care
Authors: Zapka Jane M. , Edwards Heather M. , Chollette Veronica , Taplin Stephen H.
Published: March 2023

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