Targetable alterations and pathways in TNBCs after NAC

Slides:



Advertisements
Similar presentations
Supplementary Figure 1. Somatic mutation spectrum # Substitutions # Substitutions per Mb b c a Repeats Pseudogenes Whole genome Splice sites Non-coding.
Advertisements

Michael Birrer Ian McNeish New Developments in Biology and Targets of Epithelial Ovarian Cancer.
Molecular profiling of residual TNBC after neoadjuvant chemotherapy Yonsei Genomics Center Hanna Lee.
Cell lineStatus FGFR1 DMS-114Gene amplification NCI-H520Gene amplification NCI-H1581Gene amplification FGFR2 NCI-H716Gene amplification KATO-IIIGene amplification.
Cancer Genome Landscapes
Cancer genetics - the case of hepatocellular carcinoma
Mouse Double Minute 2 (MDM2)
The cBio Cancer Genomics Portal.
Summary of genetic alterations in resistant biopsies among patients progressing on ceritinib or alectinib. Summary of genetic alterations in resistant.
Fig. 8. Recurrent copy number amplification of BRD4 gene was observed across common cancers. Recurrent copy number amplification of BRD4 gene was observed.
The Genomics of Cancer and Molecular Testing:
Mutual exclusivity analysis identifies oncogenic
Nat. Rev. Clin. Oncol. doi: /nrclinonc
WES detects a limited number of clinically targetable alterations in patients with advanced cancer. WES detects a limited number of clinically targetable.
Volume 72, Issue 4, Pages (October 2017)
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.
Combined inhibition of MAP kinase and KIT signaling destabilizes ETV1 protein and results in enhanced growth suppression of human GIST cells. Combined.
Intrinsic and acquired trastuzumab resistance.
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.
Tumor intrinsic subtype is reflected in cancer-adjacent tissue.
Class Prediction Based on Gene Expression Data Issues in the Design and Analysis of Microarray Experiments Michael D. Radmacher, Ph.D. Biometric Research.
Recurrence-Associated Long Non-coding RNA Signature for Determining the Risk of Recurrence in Patients with Colon Cancer  Meng Zhou, Long Hu, Zicheng.
Patterns of Somatically Acquired Amplifications and Deletions in Apparently Normal Tissues of Ovarian Cancer Patients  Leila Aghili, Jasmine Foo, James.
Properties of proteins and residues with frequent hotspot mutations
Volume 155, Issue 4, Pages (November 2013)
Genetic landscape of salivary duct carcinoma.
Patterns of Somatically Acquired Amplifications and Deletions in Apparently Normal Tissues of Ovarian Cancer Patients  Leila Aghili, Jasmine Foo, James.
Genome-Wide SNP Analysis in Cancer: Leukemia Shows the Way
Fig. 2. Clinically actionable somatic genomic alterations in various tumor types. Clinically actionable somatic genomic alterations in various tumor types.
Distinct molecular and clinical correlates of H3F3A mutation subgroups
Leukemic blasts express a “hypoxia signature
Integrated mRNA and microRNA expression and DNA methylation clusters.
Measurement of Relative Copy Number of CDKN2A/ARF and CDKN2B in Bladder Cancer by Real-Time Quantitative PCR and Multiplex Ligation-Dependent Probe Amplification 
Heat map of genes for which CR significantly altered expression versus AL. Cluster analysis of genes significantly changed by the CR intervention compared.
CHCHD2 and EGFR protein expression in NSCLC
Predictive value of the FGFR3 mutation assay increases with multiple consecutive FGFR3-positive urine samples. Predictive value of the FGFR3 mutation assay.
Overview of TIMER modules on the website.
EN1 expression in breast cancer and clinical outcome.
The treatment history and genomic landscape of a metastatic carcinoma with an extreme outlier response to combination therapy. The treatment history and.
Molecular signatures are independent of tumor stage and grade.
HGSOC mutational processes are established early and are patient-specific. HGSOC mutational processes are established early and are patient-specific. A,
Representative photograph of somatic mutations detected by PCR-SSCP.
Clustering analysis of DTC-associated genes.
High-risk neuroblastoma molecular subtypes classification and inference of master regulators. High-risk neuroblastoma molecular subtypes classification.
Location of the ER mutations and frequencies per cohort.
Reduced number and impaired effector functions of TILs in tumors with PTEN deletion or loss-of-function mutations in PTEN. Cutaneous melanoma patients.
Identification of general and tissue-specific essential genes.
Frequently mutated genes in colorectal cancer.
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.
Western blotting confirming the presence of fusion proteins in tumor lysates and showing increased signaling pathway activation in respective tumors. Western.
Concordance between the genomic landscape identified by whole-exome sequencing of plasma cfDNA and tumor; DNA and recurrence of KDR/VEGFR2 oncogenic mutations.
A and B, linearity of the preamplification step shown by a similar expression pattern of ERα mRNA in four breast tumor samples pre– and post–linear amplification.
Landscape of genomic alterations identified by WES in biopsies of patients with advanced PDAC. Co-mutation plot displaying integrated genomic data for.
Enrichment of two rare SNPs among ABC DLBCL tumors.
Identification of putative TET1 targets in TNBC
KRAS-mutant lung adenocarcinoma subsets exhibit distinct patterns of immune system engagement. KRAS-mutant lung adenocarcinoma subsets exhibit distinct.
Global analysis of the chemical–genetic interaction map.
Mutational signature analysis of WES data from patients with advanced PDAC. A, Projection of signatures representing four main mutational processes identified.
The ovarian cancer cell lines modestly recapitulate the spectrum of mutations found in primary ovarian tumors. The ovarian cancer cell lines modestly recapitulate.
Subtype classification of breast functional screening results.
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.
Driver pathways and key genes in OSCC
Integrated analysis of gene expression and copy number alterations.
Genomic instability is a core feature of ovarian cancer that frequently involves DNA-damage repair genes. Genomic instability is a core feature of ovarian.
Genomic and proteomic profiling of ovarian cancer cell lines.
Molecular characterization of esophagogastric tumors.
Presentation transcript:

Targetable alterations and pathways in TNBCs after NAC Targetable alterations and pathways in TNBCs after NAC. A, most common recurrently altered genes detected by NGS, representing amplifications, deletions, rearrangements, and known somatic mutations. Targetable alterations and pathways in TNBCs after NAC. A, most common recurrently altered genes detected by NGS, representing amplifications, deletions, rearrangements, and known somatic mutations. B, organization and representation of altered genes (n = 81 tumors) into five functional and targetable pathways. A total of 118 genomic alterations were identified across 81 tumors (1.5 alterations/tumor). C, integrated molecular analysis of residual tumors, using unsupervised clustering based on gene expression patterns (NanoString). D, scatterplots depicting the differences among the clusters identified in C for cellularity in the entire FFPE block cross-section; cellularity in the sampled (macrodissected) hotspot; Ki67 score; TGF-β response signature; MEK signature; and DUSP4 gene expression. *, P < 0.05; **, P < 0.01; ***, P < 0.001. Justin M. Balko et al. Cancer Discovery 2014;4:232-245 ©2014 by American Association for Cancer Research