6048 results for "canc*"

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• Transcriptional Signatures Indicating RB Function Correlate with Response to CDK4/6 Inhibition in Endometrial Cancer

  Here we provide exome-capture RNA sequencing data from 39 endometrial cancer samples from women who participated in two separate abemaciclib combination clinical trials. In addition, whole exome sequencing data are provided for a subset of the tumors for which enough material remained. In the original publication, specific RNA sequencing results were matched to objective response status of the patients in the trials, and it was shown that specific transcriptional signatures could predict function of the RB tumor suppressor and response to abemaciclib in the trials. This study is published. Please cite the original source publication Yang, et al., 2026, PMID: 42531366, for which the data were generated and analyzed.

  Study phs004904

• HINTS Geo-Coded Data 2012 (HINTS 4 Cycle 2)

  The Health Information National Trends Survey (HINTS) is a nationally representative survey which has been administered every few years by the National Cancer Institute since 2003. HINTS 4 includes four mail-mode data collection cycles over the course of three years. The second of these cycles (Cycle 2) was conducted from October 2012 through January 2013, including a total of 3,630 respondents.

  Study phs004207

• Identifying and Reducing Disparities in Patient-Reported Outcomes Among African American Prostate Cancer Survivors

  This research study aimed to identify disparities in prostate cancer symptom burden and their contributors among African American, Hispanic, and non-Hispanic White prostate cancer survivors. We collected patient-reported outcomes data, focusing on various aspects of the survivors' health and well-being, clinical data, demographics data, and germline genomic data.

  Study phs003745

• Translational Genomics in Cervical Cancer

  This study characterizes the mutational trajectories of locally-advanced cervical cancer (LACC) cases during the course of standard of care chemoradiation therapy (CRT) treatment at Washington University School of Medicine. Tissue biopsied from primary LACC tumors prior to the start of therapy and at mid-treatment and normal blood were collected for sequencing. Whole exome sequencing (WES) was performed on the Illumina NovaSeq 6000 and whole genome sequencing (WGS) was performed on the Illumina NovaSeq X. The most frequently mutated genes and tumor mutational burden were consistent with previously published cervical cancer studies. Raw sequencing reads for all samples are made available here.

  Study phs004441

• NCTN: ASSURE: Adjuvant Sorafenib or Sunitinib for Unfavorable Renal Carcinoma (E2805)

  Study ID: E2805 NCT Number: NCT00326898 ECOG-ACRIN Cancer Research Group Submitted in collaboration with the NCTN/NCORP Data Archive Trial Title: NCTN: ASSURE: Adjuvant Sorafenib or Sunitinib for Unfavorable Renal Carcinoma (E2805) Trial Description: This randomized phase III trial studies sunitinib malate to see how well it works compared to sorafenib tosylate or placebo in treating patients with kidney cancer that has been removed by surgery. Sunitinib malate and sorafenib tosylate may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth and by blocking blood flow to the tumor. Giving sunitinib malate or sorafenib tosylate after surgery may kill any tumor cells that remain after surgery. It is not yet known whether sunitinib malate is more effective than sorafenib tosylate or placebo in treating kidney cancer. Clinical data presented in the following publication(s): • PMID 26969090 • PMID 30130544 • PMID 31471309 • Additional unpublished data from E2805 Disease type(s): Kidney Neoplasm - Renal Cell Carcinoma Clinical Dataset(s) included: • NCT00326898-D1 (PMID 26969090): There are two datasets for E2805's primary publication 26969090 (-D1 and -D2). This dataset, NCT00326898-D1, contains baseline characteristics, stratification factors, treatment dose, number of cycles received, surgery type (radical or partial nephrectomy), and outcome data. Patient ID 1410 corresponds to a duplicate registration for which no data was collected and therefore excluded. NCT00326898-D2 contains toxicity data. Patients in the NCT00326898-D1 through -D7 datasets have the same deidentified patient IDs. • NCT00326898-D2 (PMID 26969090): There are two datasets for E2805's primary publication 26969090 (-D1 and -D2). This dataset, NCT00326898-D2, contains toxicity data. NCT00326898-D1 contains baseline characteristics, stratification factors, treatment dose, number of cycles received, surgery type (radical or partial nephrectomy), and outcome data. Patients in the NCT00326898-D1 through -D7 datasets have the same deidentified patient IDs. • NCT00326898-D3 (Unpublished data): This dataset, NCT00326898-D3, contains data collected on ECOG-ACRIN trial E2805, which are not published in the primary, nonclear cell renal cell carcinoma cohort, or cytokine analysis publication for the trial. NCT00326898-D3 includes information on arm A (Sunitinib) and arm B (Sorafenib) patients that started treatment for E2805 study. The dataset contains information on the time interval from randomization to treatment start date, treatment dose, and reasons for dose modification by cycle. Treatment arm information can be found in D1. Patients in the NCT00326898-D1 through -D7 datasets have the same deidentified patient IDs. • NCT00326898-D4 (Unpublished data): This dataset, NCT00326898-D4, contains data collected on ECOG-ACRIN trial E2805, which are not published in the primary, nonclear cell renal cell carcinoma cohort, or cytokine analysis publication for the trial. NCT00326898-D4 contains toxicity data (by cycle) on hypertension, diarrhea, hand-foot reaction, and/or rash/desquamation while on treatment for E2805 study, including treatment attribution and time interval from randomization to toxicity start date. Patients in the NCT00326898-D1 through -D7 datasets have the same deidentified patient IDs. Treatment arm information can be found in D1. • NCT00326898-D5 (PMID 30130544): There is one dataset for PMID 30130544 (-D5). This dataset, NCT00326898-D5, contains the analysis data published in PMID 30130544, a publication focusing on the nonccRCC subgroup of ECOG-ACRIN trial E2805. This dataset contains recurrence site data, competing risk indicators, and updated survival times. Variables reported in this publication such as age, sex, treatment arm, and histology are identical to those presented in NCT00326898-D1 (for the trial's primary publication, PMID 26969090) and are thus not duplicated in this dataset. NCT00326898-D5 can be used together with the NCT00326898-D6 dataset to obtain updated, complete information on sites of recurrence. Patients in the NCT00326898-D1 through -D7 datasets have the same deidentified patient IDs.• NCT00326898-D6 (Unpublished data): This dataset, NCT00326898-D6, contains data collected on ECOG-ACRIN trial E2805, which are not published in the primary, nonclear cell renal cell carcinoma cohort, or cytokine analysis publication for the trial. NCT00326898-D6 contains information (the time interval from nephrectomy to randomisation, cause of death, histology components, and clarification about what sites the "other" and "other organs" (-D5) include for sites of recurrence) collected on the trial but not published. Both NCT00326898-D5 and NCT00326898-D6 datasets together provide updated, complete information on sites of recurrence. Patients in the NCT00326898-D1 through -D7 datasets have the same deidentified patient IDs. COD data is consistent with survival information presented in D5. • NCT00326898-D7 (PMID 31471309): There is one dataset for PMID 31471309 (-D7). This dataset contains the cytokine analysis data published in PMID 31471309 based on trial NCT00326898. Variables reported in this publication such as treatment arm, T-stage, Fuhrman grade, ECOG PS, DFS, and DFS event are identical to those presented in NCT00326898-D1 (for the trial's primary publication, PMID 26969090) and are thus not duplicated in this dataset. You are encouraged to view the PDF data dictionaries found in the "Documents" tab of the dbGaP study page, which may contain additional information regarding the data or the associated publication(s).

  Study phs004235

• Aberrant Activation of Wound Healing Programs within the Metastatic Niche Facilitates Lung Colonization by Osteosarcoma Cells

  Lung metastasis is responsible for nearly all deaths caused by osteosarcoma, the most common pediatric bone tumor. How malignant bone cells coerce the lung microenvironment to support metastatic growth is unclear. This study delineates how osteosarcoma cells educate the lung microenvironment during metastatic progression.Using single-cell transcriptomics (scRNA-seq), we characterized genome– and tissue-wide molecular changes induced within lung tissues by disseminated osteosarcoma cells in both immunocompetent murine models of metastasis and patient samples. We confirmed transcriptomic findings at the protein level and determined spatial relationships with multi-parameter immunofluorescence. We evaluated the ability of nintedanib to impair metastatic colonization and prevent osteosarcoma-induced education of the lung microenvironment in both immunocompetent murine osteosarcoma and immunodeficient human xenograft models.Osteosarcoma cells induced acute alveolar epithelial injury upon lung dissemination. scRNA-seq demonstrated that the surrounding lung stroma adopts a chronic, non-resolving wound-healing phenotype similar to that seen in other models of lung injury. Accordingly, metastasis-associated lung demonstrated marked fibrosis, likely due to the accumulation of pathogenic, pro-fibrotic, partially-differentiated epithelial intermediates. Inhibition of fibrotic pathways with nintedanib prevented metastatic progression in multiple murine and human xenograft models. Our work demonstrates that osteosarcoma cells co-opt fibrosis to promote metastatic outgrowth. When harmonized with data from adult epithelial cancers, our results support a generalized model wherein aberrant mesenchymal-epithelial interactions are critical for promoting lung metastasis. Adult epithelial carcinomas induce fibrotic pathways in normal lung fibroblasts, whereas osteosarcoma, a pediatric mesenchymal tumor, exhibits fibrotic reprogramming in response to the aberrant wound-healing behaviors of an otherwise normal lung epithelium, which are induced by tumor cell interactions.

  Study phs003569

• Precision Interception of Gastric Cancer Precursors Through Molecular and Cellular Risk Stratification

  The GAstric Precancerous conditions Study (GAPS, NCT04191551) is a cross-sectional study of patients undergoing endoscopy who are at increased risk of gastric cancer. Enrolled patients are administered a standardized questionnaire, undergo clinical biopsy collection using the Sydney system, and consent for the collection of saliva, blood, and additional gastric tissue. All patients are scored for intestinal metaplasia using the operative link on gastric intestinal metaplasia (OLGIM) scoring system.

  Study phs003648

• NCTN: A Randomized Phase III Trial of Three Different Regimens of CPT-11 Plus 5-Fluorouracil and Leucovorin Compared to 5-Fluorouracil and Leucovorin in Patients with Advanced Adenocarcinoma of the Colon and Rectum (N9741)

  Study ID: N9741 NCT Number: NCT00003594 Alliance for Clinical Trials in Oncology Submitted in collaboration with the NCTN/NCORP Data Archive Trial Title: NCTN: A Randomized Phase III Trial of Three Different Regimens of CPT-11 plus 5-Fluorouracil and Leucovorin compared to 5-Fluorouracil and Leucovorin in Patients with Advanced Adenocarcinoma of the Colon and Rectum (N9741) Trial Description: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. Combining more than one drug may kill more tumor cells. It is not yet known which regimen of combination chemotherapy is most effective in treating advanced colorectal cancer. PURPOSE: Randomized phase III trial to compare the effectiveness of various combination chemotherapy regimens in treating patients who have advanced, recurrent, or metastatic colorectal cancer that cannot be treated with surgery or radiation therapy. Clinical data presented in the following publication(s): PMID 14665611 Disease type(s): Gastrointestinal Neoplasm - Colorectal Cancer Clinical dataset(s) included: NCT00003594-D1 (PMID 14665611): The NCT00003594-D1 dataset is one of 4 datasets associated with PubMed ID 14665611. This dataset contains information regarding patient-level information including eligibility, treatment arm, baseline characteristics, grade 4 and 5 toxicity data, and best response. It also includes information to analyze overall survival and time to progression. NCT00003594-D2 (PMID 14665611): The NCT00003594-D2 dataset is one of 4 datasets associated with PubMed ID 14665611. This dataset contains information per patient, per cycle regarding dosing, reasons for treatment delays, and overall response assessment status. NCT00003594-D3 (PMID 14665611): The NCT00003594-D3 dataset is one of 4 datasets associated with PubMed ID 14665611. This dataset contains information per patient, per cycle, per adverse event during treatment. NCT00003594-D4 (PMID 14665611): The NCT00003594-D4 dataset is one of 4 datasets associated with PubMed ID 14665611. This dataset contains information per patient regarding end of treatment timing and reason. Additional genomic data are available for this trial under phs001290. You are encouraged to view the PDF data dictionaries found in the “Documents” tab of the dbGaP study page, which may contain additional information regarding the data or the associated publication(s).

  Study phs004259

• A genotype-phenotype study of tumors from patients with inherited mutations in DNA repair genes

  This study investigated the genomic landscape of tumors from patients with inherited mutations in DNA repair genes. The aim of this study was to determine the relationship between locus-specific loss of heterozygosity (LOH) and genomic signatures of homologous recombination-based DNA repair (HR) deficiency in tumors associated with pathogenic germline variants in DNA repair genes. Cohorts of pathogenic germline variant (PGV) carriers with different cancer types were identified via a cancer genetics registry and clinical practice at Penn Medicine and through our collaborator network. Tumors were analyzed with next generation sequencing (whole exome and/or targeted panel sequencing) with or without transcriptomic analyses. Sub-study #1 "Non-breast/ovarian tumors in germline BRCA1/2 carriers". This study investigated primary non-breast/ovarian tumors that arise in individuals with BRCA1/BRCA2 pathogenic germline variants (PGVs). Whole exome sequencing (WES) using Agilent All-Exon Kit v7 hybrid capture probes was performed on matched tumor and blood germline normal DNA on an Illumina HiSeq. Individual WES data from DNA samples from tumor and normal are available. Sub-study #2: "Breast tumors in germline CHEK2 carriers". This study investigated primary breast tumors that arise in individuals with CHEK2 pathogenic germline variants (PGVs). Whole exome sequencing (WES) using Agilent All-Exon Kit v7 hybrid capture probes was performed on matched tumor and blood germline normal DNA on an Illumina HiSeq. Whole transcriptome RNAseq was performed on tumors. Individual WES data from DNA samples from tumor and normal and RNAseq data from tumor are available. Sub-study #3: "Breast tumors in germline TP53 carriers". This study investigated primary breast tumors that arise in individuals with TP53 pathogenic germline variants (PGVs). Whole genome sequencing (WGS) and/or custom panel targeted sequencing was performed on matched tumor and blood germline normal DNA on an Illumina HiSeq. Whole transcriptome RNAseq was performed on tumors and normal breast tissue. Individual WGS or targeted data from DNA samples from tumor and normal and RNASeq data from tumor and normal are available. Sub-study #4: "Prostate tumors in germline DNA repair carriers". This study investigated prostate tumors that arise in individuals with a variety of pathogenic germline variants (PGVs). Whole genome sequencing (WGS) and/or custom panel targeted sequencing was performed on matched tumor and blood germline normal DNA on an Illumina HiSeq. Whole transcriptome RNAseq was performed on tumors and normal prostate tissue. Individual WGS or targeted data from DNA samples from tumor and normal and RNASeq data from tumor and normal are available.

  Study phs003348

• Cellular and Molecular Profiling of Epithelial Ovarian Cancers and Associated Normal Tissues

  This collection of data includes bulk RNA-seq and whole genome bisulfite sequencing (WGBS) for ovarian cancer samples (microdissected into carcinoma and stroma compartments), as well as single-cell RNA-seq (scRNA-Seq) and bulk WGBS and enzymatic methyl-seq (EM-seq) normal human Fallopian tube samples. The data from the ovarian cancer samples was collected to understand cellular and molecular alterations associated with histological and molecular subtypes of ovarian cancer. Data for these samples are included in Djirackor, Heinze et al. (accepted at Cancer Research). The scRNA-Seq data was generated to identify the developmental trajectory, cell type composition, and point towards the cell-of-origin for high grade serous ovarian carcinoma (HGSOC). Further, this was intended to establish a normal RNA reference for the cancer data. Results from this study are described in Johnson, Majewski et al. (accepted at Nature Communications, preprint PMID: 40475517). The data from bulk DNA methylation on normal Fallopian tubes was used to optimize the bisulfite-conversion process for the cancer samples and to serve as an epigenetic reference in the cancer studies. This data is described in Morrison et al. (PMID: 34147133). Any questions can be directed to Hui Shen (hui.shen@vai.org).

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