Temporal and spatial dissection of mutation spectra in esophageal adenocarcinoma samples. Temporal and spatial dissection of mutation spectra in esophageal.

Slides:

Advertisements

Similar presentations

DNA Bases. Adenine: Adenine: (A) pairs with Thymine (T) only.

Advertisements

Copyright © 2007 American Medical Association. All rights reserved.

WEE1 inhibition forces S-phase–arrested cancer cells into mitosis.

Nick Macklon, M.D., Ph.D. Fertility and Sterility

Nicholas McGranahan, Charles Swanton Cell

Empirical mutation-selection phase diagram of tumor evolution.

Ewing sarcoma tumors acquire somatic aberrancies with treatment.

Empirical mutation-selection phase diagram of tumor evolution.

18F-FDG uptake is a noninvasive biomarker of combined MEK–mTORC1 inhibition. 18F-FDG uptake is a noninvasive biomarker of combined MEK–mTORC1 inhibition.

Fig. 1 Number of somatic mutations in representative human cancers, detected by genome-wide sequencing studies. Number of somatic mutations in representative.

Geographic distribution in situ of MSI and MSS colorectal cancer–infiltrating lymphocytes. Geographic distribution in situ of MSI and MSS colorectal cancer–infiltrating.

Identification of a MEK2 mutation in a melanoma sample resistant to dabrafenib/trametinib. Identification of a MEK2 mutation in a melanoma sample resistant.

Volume 7, Issue 5, Pages (June 2014)

Whole-exome sequencing identifies NF1 mutations in tumors of melanoma patients exhibiting resistance to vemurafenib. Whole-exome sequencing identifies.

Volume 24, Issue 4, Pages (July 2018)

Categorization of the top 200 N

Functional enrichment of differentially expressed genes.

Number of 0.5-Mb windows with chromosome lesions that reached statistical significance across patients in early (BE early and BE instability) and late.

Core promoter methylation in mediators of adipogenesis.

RNA-seq results at the SAM

Differential binding of H3K36me3 in G34-mutant KNS42 cells drives pediatric GBM expression signatures. Differential binding of H3K36me3 in G34-mutant KNS42.

Comparison of N. gonorrhoeae gene expression in infected men in vivo and isolates grown in vitro. Comparison of N. gonorrhoeae gene expression in infected.

Temporal order of mutational processes during cancer evolution.

Cancer mutations in enriched RBP motifs.

EEG-based classification accuracy for across- and within-expression discrimination of facial identity with temporally cumulative data (50–650 ms after.

Derivation of ImSig. Derivation of ImSig. A, An example of a correlation network generated from a tissue data set where nodes represent unique genes and.

The expression of SPINDLIN1 in cancer tissues.

EZH2 overexpression establishes a unique and conserved super-enhancer–associated transcriptional landscape. EZH2 overexpression establishes a unique and.

Temporal analysis of clonal evolution in typical FL and matched TFL samples. Temporal analysis of clonal evolution in typical FL and matched TFL samples.

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.

Immune signatures of patients with short-, medium-, and long-term survival. Immune signatures of patients with short-, medium-, and long-term survival.

Inhibitory effect of different doses of IP6 on prostate tumor progression in TRAMP mice. Inhibitory effect of different doses of IP6 on prostate tumor.

Pancreatic cancer cell lines are sensitive to knockdown of outlier kinases. Pancreatic cancer cell lines are sensitive to knockdown of outlier kinases.

Fig. 3 Avoidable fraction of heat-related deaths if the current trajectory warming of 3°C is brought down to the 1.5° or 2°C Paris Agreement thresholds.

Plasma and tissue EGFR allele analyses.

Duration of treatment and intervals of radiographic and ctDNA response

Ki-67 expression in M31- and H3-treated tumors (A) and respective Ki-67 labeling indices in the two groups of tumors (B). Ki-67 expression in M31- and.

CREBBP loss-of-function results in gene expression repression signature. CREBBP loss-of-function results in gene expression repression signature. A–D,

Serial chest CT scans of 33-year-old male with lung adenocarcinoma harboring EGFR-KDD documenting response to afatinib and subsequent acquired resistance.

Antitumor activity. Antitumor activity. A, maximum change in target lesion size from baseline assessed according to RECIST 1.0 (n = 26). Six patients had.

Clustering analysis of DTC-associated genes.

Intratumoral changes in critical lymphocyte populations and numbers after NKTR-214 treatment. Intratumoral changes in critical lymphocyte populations and.

Pancreatic adenocarcinoma, chronic pancreatitis, and normal pancreas samples can be distinguished on the basis of gene expression profiling. Pancreatic.

Location of the ER mutations and frequencies per cohort.

Change in FES uptake in the tumor during fulvestrant treatment.

Fig. 1 Number of somatic mutations in representative human cancers, detected by genome-wide sequencing studies. Number of somatic mutations in representative.

Representative patient responses to ulixertinib.

Ten most frequent TCRs in the bulk 12TILs comprise >99% of the TIL population, and the neoantigens are shown to be the most dominant clones. Ten most frequent.

Frequently mutated genes in colorectal cancer.

Molecular definitions of lung adenocarcinoma subtypes.

Genomic determinants of response to cytotoxic chemotherapy.

Cell lines from hematologic cancers, including multiple myeloma (MM), AML, and DLBCL, exhibit a strong dependency on MCL1 for survival. Cell lines from.

Survival, subsequent therapies, and response.

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.

Detection of BRCA reversion mutations in pretreatment cfDNA and tumor biopsy. Detection of BRCA reversion mutations in pretreatment cfDNA and tumor biopsy.

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.

SCLC PDX model responses to first-line chemotherapy reflect patient treatment histories. SCLC PDX model responses to first-line chemotherapy reflect patient.

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.

NUAK1 overexpression correlates with tumor progression, lymph node infiltrates, and reduced overall survival (OS) in human colorectal cancer. NUAK1 overexpression.

In vivo shRNA screening strategy.

Driver pathways and key genes in OSCC

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.

Characteristic gene expression patterns distinguish LCH cells from other immune cells present in LCH lesions. Characteristic gene expression patterns distinguish.

Comparison of shRNA scoring approaches.

Presentation transcript:

Temporal and spatial dissection of mutation spectra in esophageal adenocarcinoma samples. Temporal and spatial dissection of mutation spectra in esophageal adenocarcinoma samples. A, stacked bar plot showing the fraction of early mutations (trunk) and late mutations (branch) accounted for by each of the six mutation types in all M-seq samples and per case. The number of mutations analyzed is displayed on top of each bar. The difference between the spectra for trunk and branch mutations across all cases was assessed using a χ2 test. For specific mutation types, a Fisher exact test was used, and significant P values are shown. B, stacked bar plot showing the fraction of pre-chemotherapy mutations and post-chemotherapy mutations accounted for by each of the six mutation types in all M-seq samples and per case. The number of mutations analyzed is displayed on top of each bar. The difference between the spectra for trunk and branch mutations across all cases was assessed using a χ2 test. For specific mutation types, a Fisher exact test was used, and significant P values are shown. C>G, cytosine to guanine. C, bar plot showing platinum signature enrichment OR for pre-chemotherapy (red bars) and post-chemotherapy (green bars) mutations for M-seq samples. The platinum signature encompasses cytosine to adenine (C>A) in CpC context (25). Values for 95% confidence intervals for the Fisher exact test are indicated. D, a model of tumor progression in esophageal adenocarcinoma. Inferring the evolutionary trajectories of esophageal adenocarcinoma tumors through NAC by M-seq, early and late mutational processes and the selective pressure of platinum treatment are identified. Nirupa Murugaesu et al. Cancer Discovery 2015;5:821-831 ©2015 by American Association for Cancer Research