Driver pathways and key genes in OSCC

Slides:



Advertisements
Similar presentations
The cBio Cancer Genomics Portal.
Advertisements

Volume 152, Issue 5, Pages (April 2017)
Fig. 8. Recurrent copy number amplification of BRD4 gene was observed across common cancers. Recurrent copy number amplification of BRD4 gene was observed.
Nat. Rev. Clin. Oncol. doi: /nrclinonc
Regional lymph nodes and distal extracranial metastases are not a reliable surrogate for actionable mutation in brain metastases. Regional lymph nodes.
Fig. 3. Copy number loss as a potential resistance mechanism in an independent cohort. Copy number loss as a potential resistance mechanism in an independent.
Epigenetic heterogeneity is associated with genetic heterogeneity in CLL samples. Epigenetic heterogeneity is associated with genetic heterogeneity in.
Clonal evolution in Ewing sarcoma.
Whole-exome sequencing reveals differences between nail apparatus melanoma and acral melanoma  Minho Lee, PhD, Jonghwan Yoon, BS, Yeun-Jun Chung, MD,
Altered interferon signaling with JAK1 loss-of-function mutation in M431 and interferon gamma-inducible PD-L1 expression by 48 melanoma cell lines. Altered.
Genomic alterations in breast cancer cell line MDA-MB-231.
Mutational burden of somatic, protein-altering mutations per subject from WES for patients with advanced colon cancer who participated in PD-1 blockade.
A Tumor Sorting Protocol that Enables Enrichment of Pancreatic Adenocarcinoma Cells and Facilitation of Genetic Analyses  Zachary S. Boyd, Rajiv Raja,
Copy-number alterations in an archival breast cancer sample.
Identification of a MEK2 mutation in a melanoma sample resistant to dabrafenib/trametinib. Identification of a MEK2 mutation in a melanoma sample resistant.
AKT dependence of ovarian cancer cell lines.
A, relationship between weighted mean chromosome copy number and weighted Genome Instability Index (wGII). A, relationship between weighted mean chromosome.
 Design and use of a high-throughput screen to identify tumor cell-induced gene activation events in Salmonella.  Design and use of a high-throughput screen.
Volume 69, Issue 5, Pages (May 2016)
IL32 prompts cell activation and cancer-related pathways.
The BRD4 bromodomain is critical for expression of SASP genes.
K-Means clustering of protein and mRNA expression patterns after PPAR agonists treatments. k-Means clustering of protein and mRNA expression patterns after.
Boosting Signal-to-Noise in Complex Biology: Prior Knowledge Is Power
Hyperplasia is due to Notch pathway activation upon cell fate challenge. Hyperplasia is due to Notch pathway activation upon cell fate challenge. (A) Brightfield.
Landscape of genomic alterations in 444 tumors from 429 patients with mCRPC. Landscape of genomic alterations in 444 tumors from 429 patients with mCRPC.
High-level clonal amplification of FGFR2 predicts for sensitivity to FGFR inhibitor. High-level clonal amplification of FGFR2 predicts for sensitivity.
Gene set enrichment analysis reveals MafA regulation of many key β-cell activities. Gene set enrichment analysis reveals MafA regulation of many key β-cell.
Genetics of hepatocellular carcinoma: The next generation
Qian Cong, Dominika Borek, Zbyszek Otwinowski, Nick V. Grishin 
Enrichment of KEGG pathways in microbial genes in different samples.
A, Top inhibitors of Ba/F3 transformed with CD74–ROS1, color coded by clinical development status: FDA-approved (green), phase III (yellow), phase II (blue),
HER2 mutations identified by colorectal cancer genome sequencing studies increase cell signaling and anchorage-independent growth in a colonic epithelial.
Association between RB pathway alterations and poor prognosis in early-stage lung adenocarcinoma patients. Association between RB pathway alterations and.
Integrated mRNA and microRNA expression and DNA methylation clusters.
KIT mutations in GISTs. A, amino acid sequence of KIT exon 11 mutations in clinical GIST biopsies. –, amino acids that are deleted; italicized amino acids,
M-Wnt and E-Wnt cells cluster tightly with claudin-low and basal-like breast tumors, respectively, by microarray analysis. M-Wnt and E-Wnt cells cluster.
Pancreatic cancer cell lines are sensitive to knockdown of outlier kinases. Pancreatic cancer cell lines are sensitive to knockdown of outlier kinases.
Overview of TIMER modules on the website.
The truncating mutation c
HPV–human protein network map.
Two-way, unsupervised hierarchical clustering representing the 60 tumor cell lines (vertical axis) and the analyzed total, phospho- and cleaved proteins.
Clustering analysis of DTC-associated genes.
High-risk neuroblastoma molecular subtypes classification and inference of master regulators. High-risk neuroblastoma molecular subtypes classification.
The long tail of mutational hotspots in cancer.
Location of the ER mutations and frequencies per cohort.
A and B, two blocks from the original specimen used for TMA demonstrated areas with varying patterns of ALK rearrangement and KRAS mutation status. A and.
BCL-2 and BCL-XL expression alters with maturation stage of the T cell
Global mutational landscape of the 170 lung adenocarcinoma patients (discovery cohort). Global mutational landscape of the 170 lung adenocarcinoma patients.
Molecular definitions of lung adenocarcinoma subtypes.
Mutational Analysis of Ionizing Radiation Induced Neoplasms
Concordance between the genomic landscape identified by whole-exome sequencing of plasma cfDNA and tumor; DNA and recurrence of KDR/VEGFR2 oncogenic mutations.
Single nucleotide polymorphism array analysis can distinguish different genetic mechanisms that lead to loss of heterozygosity (LOH). Single nucleotide.
Identification of RASA1- and NF1-mutated lung cancer cell lines in the CCLE dataset (accessed via the cBioPortal for Cancer Genomics at
Landscape of genomic alterations identified by WES in biopsies of patients with advanced PDAC. Co-mutation plot displaying integrated genomic data for.
A, heatmap of copy number alterations determined by array CGH for a panel of 79 frozen NSCLC samples. A, heatmap of copy number alterations determined.
Distinct subtypes of CAFs are detected in human PDAC
EZH2-driven lung cancer as a molecularly distinct entity.
Gene expression heatmap of non–T-cell-inflamed, intermediate, and T-cell–inflamed testicular germ cell tumors from TCGA. Genes are on the row, and samples.
The ovarian cancer cell lines modestly recapitulate the spectrum of mutations found in primary ovarian tumors. The ovarian cancer cell lines modestly recapitulate.
High genomic fidelity of SCLC PDX models derived from both CTCs and biopsies. High genomic fidelity of SCLC PDX models derived from both CTCs and biopsies.
A, study design for measuring the feasibility, concordance, and accuracy of a plasma-based cfDNA sequencing test compared with biopsy-based sequencing.
CASP8 mutations are associated with fewer CNAs and RAS family mutations. CASP8 mutations are associated with fewer CNAs and RAS family mutations. A, number.
Integrated analysis of gene expression and copy number alterations.
Identification and characterization of activated integrin pathway module by signal transduction representation (A) and unsupervised hierarchical clustering.
Genomic and proteomic profiling of ovarian cancer cell lines.
Molecular characterization of esophagogastric tumors.
Transcriptome traits and clinical characteristics of TME phenotypes in the ACRG cohort. Transcriptome traits and clinical characteristics of TME phenotypes.
TME characteristics of TCGA-STAD subtype and cancer somatic genome.
Transcriptome profiling of PD-L1 antibody–treated macrophages showed inflammatory phenotype, increased survival and proliferation, and decreased apoptosis.
Cxxc1-deficient TH17 cells exhibit a Treg cell–like expression profile
Presentation transcript:

Driver pathways and key genes in OSCC Driver pathways and key genes in OSCC. A, pathway alteration in each sample is indicated by a black box. Driver pathways and key genes in OSCC. A, pathway alteration in each sample is indicated by a black box. Sample identifier sequences are shown at the top and pathway names at the left. Selected clinical variables and clusters from Fig. 3 are indicated with colored boxes. B, Notch pathway. C, mitogenic signaling pathway. D, cell-cycle pathway. E, TP53 pathway. Pathway diagrams indicate the genes included in each pathway. Copy gains are indicated with red, copy losses with blue, mutations with black, and methylation with purple. Percentages shown indicate the frequency of that event. Curtis R. Pickering et al. Cancer Discovery 2013;3:770-781 ©2013 by American Association for Cancer Research