A, Changes in BRAFV600E cfDNA allele fraction from baseline after one dose of treatment for 12 patients with serial samples available, classified according.

Slides:



Advertisements
Similar presentations
Baseline Characteristics of the Patient Population (n=525) Colin Berry, et al. Circulation 2007;115:
Advertisements

Dose-escalation patient response.
In vivo effects of eltrombopag on platelet function in immune thrombocytopenia: no evidence of platelet activation by Bethan Psaila, James B. Bussel, Matthew.
A, baseline and 4-week PET scan from patient 2 (MET c
Mutational burden of somatic, protein-altering mutations per subject from WES for patients with advanced colon cancer who participated in PD-1 blockade.
Emergence of resistance to immune checkpoint blockade is associated with elimination of mutation-associated neoantigens by LOH and a more diverse T-cell.
Figure 4 Treatment plans using stereotactic body radiotherapy (SBRT)
Identification of a MEK2 mutation in a melanoma sample resistant to dabrafenib/trametinib. Identification of a MEK2 mutation in a melanoma sample resistant.
AR signaling in CTCs from CRPC patients treated with abiraterone acetate. AR signaling in CTCs from CRPC patients treated with abiraterone acetate. A,
Kinetic changes of sPD-L1 and cytokines, and kinetic radiographic reduction in tumor size after ipilimumab plus bevacizumab treatment. Kinetic changes.
Issue Highlights Clinical Gastroenterology and Hepatology
Use of Alefacept for Preconditioning in Multiply Transfused Pediatric Patients with Nonmalignant Diseases  Elizabeth O. Stenger, Kuang-Yueh Chiang, Ann.
AG-221 can reduce intracellular 2HG levels and induce differentiation in primary human IDH2R140Q- or IDH2R172K-mutant AML patient samples treated ex vivo.
Figure 3 Responder subset (A) Percentage of “responders” (nonprogressing patients) at week 25 after 6 months of treatment; percentage of “responders” in.
Expression of apocrine markers at various stages of apocrine carcinoma progression. Expression of apocrine markers at various stages of apocrine carcinoma.
Hospital-level procedural sedation rates among pediatric patients in the earliest year, (2009, red circle) and the most recent year (2014, blue bar). Hospital-level.
Distribution of informative SNPs with LOH (black bars) on each chromosome (rows, oriented p-arm at the bottom and q-arm at the top of each chromosome)
Number of 0.5-Mb windows with chromosome lesions that reached statistical significance across patients in early (BE early and BE instability) and late.
Serial computed tomography (CT) imaging for monitoring disease progression in patients with idiopathic pulmonary fibrosis. Serial computed tomography (CT)
BRAF amplification causes clinical acquired resistance to combined RAF/EGFR inhibition. BRAF amplification causes clinical acquired resistance to combined.
(A through C) Mean eGFR during follow-up according to treatment assignment in patients with normoalbuminuria (A), microalbuminuria (B), and macroalbuminuria.
High-level clonal amplification of FGFR2 predicts for sensitivity to FGFR inhibitor. High-level clonal amplification of FGFR2 predicts for sensitivity.
Computed tomographic images from a patient with BRAFL597S-mutant metastatic melanoma responding to therapy with the MEK inhibitor TAK-733. Computed tomographic.
A. A. Percentages of patients with active dactylitis in ≥ 4 digits (fingers or toes) at baseline and Week 12. *p < versus baseline. Data are observed.
Antitumor efficacy of PI3K inhibitor NVP-BKM120 alone and in combination with olaparib. Antitumor efficacy of PI3K inhibitor NVP-BKM120 alone and in combination.
Gene expression changes associated with response to combination CPI-444 and anti–PD-L1 treatment in MC38 tumors. Gene expression changes associated with.
Changes in glycated hemoglobin (HbA1c) levels after 12 weeks’ treatment with lixisenatide (according to dose increase regimen) or placebo. Changes in glycated.
Serum bicarbonate increased by ≥3, ≥4, and ≥5 mEq/L in 52%, 39%, and 22% of patients, respectively, in the combined TRC101 dose group compared with 6%,
Diagnostic performance of dentist clinical impression.
Saturation analysis and the discovery of actionability of mutational hotspots. Saturation analysis and the discovery of actionability of mutational hotspots.
Personalized, 16-plex assays accurately detect ctDNA ahead of clinical relapse. Personalized, 16-plex assays accurately detect ctDNA ahead of clinical.
Distribution of percent consistent facility aspirin use.
The treatment history and genomic landscape of a metastatic carcinoma with an extreme outlier response to combination therapy. The treatment history and.
A, unsupervised clustering of all BRCA1 (red), BRCA2 (blue), and sporadic (green) breast tumors of our collection using the regions reported as discriminative.
Plasma and tissue EGFR allele analyses.
Increase in proliferation and activation of immune cells in peripheral blood after NKTR-214 treatment. Increase in proliferation and activation of immune.
Immunologic and pharmacokinetic studies.
Kaplan-Meier survival analysis of p53 mutation in the overall breast tumor series. Kaplan-Meier survival analysis of p53 mutation in the overall breast.
Serial chest CT scans of 33-year-old male with lung adenocarcinoma harboring EGFR-KDD documenting response to afatinib and subsequent acquired resistance.
WP1066 inhibits the progression of OCIM2 cells through the cell cycle.
Correlations of the breast cancer hypoxia metagene with Ki67 and the proliferation metagene. Correlations of the breast cancer hypoxia metagene with Ki67.
Noninvasive detection of acquired MET amplification as a mechanism of afatinib/trastuzumab resistance using cfDNA. Noninvasive detection of acquired MET.
BH3 profiling reveals BCL-2 dependence in ETP-ALL in a separate cohort of DFCI patient samples. BH3 profiling reveals BCL-2 dependence in ETP-ALL in a.
Intratumoral changes in critical lymphocyte populations and numbers after NKTR-214 treatment. Intratumoral changes in critical lymphocyte populations and.
A 63-year-old female with lung adenocarcinoma treated with nivolumab, who experienced pseudoprogression. A 63-year-old female with lung adenocarcinoma.
Molecular heterogeneity can drive mixed response and treatment failure in EGC. A, PET images from Patient #4 obtained before treatment and upon disease.
Kaplan–Meier curves for RFS and OS by various marker groups.
Efficacy summary for patients with gastric/GEJ adenocarcinoma (part B)
Individual treatment outcomes of 20 patients treated with afatinib and 12 patients treated with afatinib and trastuzumab. Individual treatment outcomes.
Change in FES uptake in the tumor during fulvestrant treatment.
Frequent coamplification of RTKs in MET-amplified EGC
Representative patient responses to ulixertinib.
Mean percentage change from baseline in total IGF-I and the R1507 serum concentration values following a single i.v. administration of R mg/kg (n.
ROC analysis of MIC-1 and CA19-9.
A, Selected 4 quantitative imaging features significantly associated with 3 imaging subtypes, including tumor volume, tumor sphericity, tumor homogeneity.
The best response for target lesions per patient for patients with target lesions assessed at baseline and at least 1 follow-up. The best response for.
Concordance between the genomic landscape identified by whole-exome sequencing of plasma cfDNA and tumor; DNA and recurrence of KDR/VEGFR2 oncogenic mutations.
Tracking resistance to TRKA inhibition in ctDNA of a patient with colorectal cancer. Tracking resistance to TRKA inhibition in ctDNA of a patient with.
Survival, subsequent therapies, and response.
BRAF in-frame deletion confers response to MAPK inhibition.
Germline variants influencing primary tumor type.
SD-101 and low-dose radiation induces responses in patients with indolent lymphoma. SD-101 and low-dose radiation induces responses in patients with indolent.
Detection of BRCA reversion mutations in pretreatment cfDNA and tumor biopsy. Detection of BRCA reversion mutations in pretreatment cfDNA and tumor biopsy.
A–D, FGFR3 gatekeeper mutations detected in 4 patients.
SCLC PDX models recapitulate patient responses to an experimental therapy. SCLC PDX models recapitulate patient responses to an experimental therapy. A,
by Christian Grommes, Sarah S. Tang, Julia Wolfe, Thomas J
A, study design for measuring the feasibility, concordance, and accuracy of a plasma-based cfDNA sequencing test compared with biopsy-based sequencing.
Cross-species computational analyses of adverse treatment response.
Driver pathways and key genes in OSCC
MITF-low/NF-κB–high transcriptional class is present and associated with resistance to MAPK pathway inhibition in human tumors. MITF-low/NF-κB–high transcriptional.
Presentation transcript:

A, Changes in BRAFV600E cfDNA allele fraction from baseline after one dose of treatment for 12 patients with serial samples available, classified according to radiographic responders (blue) or nonresponders (black). A, Changes in BRAFV600E cfDNA allele fraction from baseline after one dose of treatment for 12 patients with serial samples available, classified according to radiographic responders (blue) or nonresponders (black). B, Percentage change in BRAFV600E cfDNA fraction versus percent change in radiographic volume of target lesions at the time of first restaging (after 4 doses of treatment), according to radiographic responders (black) or nonresponders (red). Representative trends in cfDNA fraction (black) and radiographic changes (red) for patients with radiographic response (C) and progression (D). David S. Hong et al. Cancer Discov 2016;6:1352-1365 ©2016 by American Association for Cancer Research