�ݺ�ߣshows by User: DavidSalzman1

�ݺ�ߣshows by User: DavidSalzman1 / http://www.slideshare.net/images/logo.gif �ݺ�ߣshows by User: DavidSalzman1 / Wed, 10 Sep 2014 12:36:15 GMT �ݺ�ߣShare feed for �ݺ�ߣshows by User: DavidSalzman1 Clinical Cancer Research Publication /slideshow/a-let-7-micro-rnabinding-site-polymorphism-in-kras/38934791 alet-7microrna-bindingsitepolymorphisminkras-140910123615-phpapp01
Purpose: An inherited mutation in KRAS (LCS6-variant or rs61764370) results in altered control of the KRAS oncogene. We studied this biomarker’s correlation to anti-EGFR monoclonal antibody (mAb) therapy response in patients with metastatic colorectal cancer. Experimental Design: LCS6-variant and KRAS/BRAF mutational status was determined in 512 patients with metastatic colorectal cancer treated with salvage anti-EGFR mAb therapy, and findings correlated with outcome. Reporters were tested in colon cancer cell lines to evaluate the differential response of the LCS6- variant allele to therapy exposure. Results: In this study, 21.2% (109 of 512) of patients with metastatic colorectal cancer had the LCS6- variant (TG/GG), which was found twice as frequently in the BRAF-mutated versus the wild-type (WT) group (P = 0.03). LCS6-variant patients had significantly longer progression- free survival (PFS) with anti-EGFR mAb monotherapy treatment in the whole cohort (16.85 vs. 7.85 weeks; P = 0.019) and in the double WT (KRAS and BRAF) patient population (18 vs. 10.4 weeks; P = 0.039). Combination therapy (mAbs plus chemotherapy) led to improved PFS and overall survival (OS) for nonvariant patients, and brought their outcome to levels comparable with LCS6-variant patients receiving anti-EGFR mAb monotherapy. Combination therapy did not lead to improved PFS or OS for LCS6-variant patients. Cell line studies confirmed a unique response of the LCS6-variant allele to both anti-EGFR mAb monotherapy and chemotherapy. Conclusions: LCS6-variant patients with metastatic colorectal cancer have an excellent response to anti-EGFR mAb monotherapy, without any benefit from the addition of chemotherapy. These findings further confirm the importance of thismutation as a biomarker of anti-EGFR mAb response in patients with metastatic colorectal cancer, and warrant further prospective confirmation.]]>
Purpose: An inherited mutation in KRAS (LCS6-variant or rs61764370) results in altered control of the KRAS oncogene. We studied this biomarker’s correlation to anti-EGFR monoclonal antibody (mAb) therapy response in patients with metastatic colorectal cancer. Experimental Design: LCS6-variant and KRAS/BRAF mutational status was determined in 512 patients with metastatic colorectal cancer treated with salvage anti-EGFR mAb therapy, and findings correlated with outcome. Reporters were tested in colon cancer cell lines to evaluate the differential response of the LCS6- variant allele to therapy exposure. Results: In this study, 21.2% (109 of 512) of patients with metastatic colorectal cancer had the LCS6- variant (TG/GG), which was found twice as frequently in the BRAF-mutated versus the wild-type (WT) group (P = 0.03). LCS6-variant patients had significantly longer progression- free survival (PFS) with anti-EGFR mAb monotherapy treatment in the whole cohort (16.85 vs. 7.85 weeks; P = 0.019) and in the double WT (KRAS and BRAF) patient population (18 vs. 10.4 weeks; P = 0.039). Combination therapy (mAbs plus chemotherapy) led to improved PFS and overall survival (OS) for nonvariant patients, and brought their outcome to levels comparable with LCS6-variant patients receiving anti-EGFR mAb monotherapy. Combination therapy did not lead to improved PFS or OS for LCS6-variant patients. Cell line studies confirmed a unique response of the LCS6-variant allele to both anti-EGFR mAb monotherapy and chemotherapy. Conclusions: LCS6-variant patients with metastatic colorectal cancer have an excellent response to anti-EGFR mAb monotherapy, without any benefit from the addition of chemotherapy. These findings further confirm the importance of thismutation as a biomarker of anti-EGFR mAb response in patients with metastatic colorectal cancer, and warrant further prospective confirmation.]]> Wed, 10 Sep 2014 12:36:15 GMT /slideshow/a-let-7-micro-rnabinding-site-polymorphism-in-kras/38934791 DavidSalzman1@slideshare.net(DavidSalzman1) Clinical Cancer Research Publication DavidSalzman1 Purpose: An inherited mutation in KRAS (LCS6-variant or rs61764370) results in altered control of the KRAS oncogene. We studied this biomarker’s correlation to anti-EGFR monoclonal antibody (mAb) therapy response in patients with metastatic colorectal cancer. Experimental Design: LCS6-variant and KRAS/BRAF mutational status was determined in 512 patients with metastatic colorectal cancer treated with salvage anti-EGFR mAb therapy, and findings correlated with outcome. Reporters were tested in colon cancer cell lines to evaluate the differential response of the LCS6- variant allele to therapy exposure. Results: In this study, 21.2% (109 of 512) of patients with metastatic colorectal cancer had the LCS6- variant (TG/GG), which was found twice as frequently in the BRAF-mutated versus the wild-type (WT) group (P = 0.03). LCS6-variant patients had significantly longer progression- free survival (PFS) with anti-EGFR mAb monotherapy treatment in the whole cohort (16.85 vs. 7.85 weeks; P = 0.019) and in the double WT (KRAS and BRAF) patient population (18 vs. 10.4 weeks; P = 0.039). Combination therapy (mAbs plus chemotherapy) led to improved PFS and overall survival (OS) for nonvariant patients, and brought their outcome to levels comparable with LCS6-variant patients receiving anti-EGFR mAb monotherapy. Combination therapy did not lead to improved PFS or OS for LCS6-variant patients. Cell line studies confirmed a unique response of the LCS6-variant allele to both anti-EGFR mAb monotherapy and chemotherapy. Conclusions: LCS6-variant patients with metastatic colorectal cancer have an excellent response to anti-EGFR mAb monotherapy, without any benefit from the addition of chemotherapy. These findings further confirm the importance of thismutation as a biomarker of anti-EGFR mAb response in patients with metastatic colorectal cancer, and warrant further prospective confirmation. <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/alet-7microrna-bindingsitepolymorphisminkras-140910123615-phpapp01-thumbnail.jpg?width=120&height=120&fit=bounds" /> Purpose: An inherited mutation in KRAS (LCS6-variant or rs61764370) results in altered control of the KRAS oncogene. We studied this biomarker’s correlation to anti-EGFR monoclonal antibody (mAb) therapy response in patients with metastatic colorectal cancer. Experimental Design: LCS6-variant and KRAS/BRAF mutational status was determined in 512 patients with metastatic colorectal cancer treated with salvage anti-EGFR mAb therapy, and findings correlated with outcome. Reporters were tested in colon cancer cell lines to evaluate the differential response of the LCS6- variant allele to therapy exposure. Results: In this study, 21.2% (109 of 512) of patients with metastatic colorectal cancer had the LCS6- variant (TG/GG), which was found twice as frequently in the BRAF-mutated versus the wild-type (WT) group (P = 0.03). LCS6-variant patients had significantly longer progression- free survival (PFS) with anti-EGFR mAb monotherapy treatment in the whole cohort (16.85 vs. 7.85 weeks; P = 0.019) and in the double WT (KRAS and BRAF) patient population (18 vs. 10.4 weeks; P = 0.039). Combination therapy (mAbs plus chemotherapy) led to improved PFS and overall survival (OS) for nonvariant patients, and brought their outcome to levels comparable with LCS6-variant patients receiving anti-EGFR mAb monotherapy. Combination therapy did not lead to improved PFS or OS for LCS6-variant patients. Cell line studies confirmed a unique response of the LCS6-variant allele to both anti-EGFR mAb monotherapy and chemotherapy. Conclusions: LCS6-variant patients with metastatic colorectal cancer have an excellent response to anti-EGFR mAb monotherapy, without any benefit from the addition of chemotherapy. These findings further confirm the importance of thismutation as a biomarker of anti-EGFR mAb response in patients with metastatic colorectal cancer, and warrant further prospective confirmation.

Clinical Cancer Research Publication from David W. Salzman

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0 A germline mutation in the brca1 3'utr predicts stage iv breast cancer /slideshow/a-germline-mutation-in-the-brca1-3utr-predicts-stage-iv-breast-cancer/36964508 agermlinemutationinthebrca13utrpredictsstageivbreastcancer-140714131847-phpapp02
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]]> Mon, 14 Jul 2014 13:18:47 GMT /slideshow/a-germline-mutation-in-the-brca1-3utr-predicts-stage-iv-breast-cancer/36964508 DavidSalzman1@slideshare.net(DavidSalzman1) A germline mutation in the brca1 3'utr predicts stage iv breast cancer DavidSalzman1 <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/agermlinemutationinthebrca13utrpredictsstageivbreastcancer-140714131847-phpapp02-thumbnail.jpg?width=120&height=120&fit=bounds" />

A germline mutation in the brca1 3'utr predicts stage iv breast cancer from David W. Salzman

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0 P68 RNA helicase unwinds the human let-7 microRNA precursor duplex and is required for let-7-directed silencing of gene expression. /slideshow/p68-rna-helicase-unwinds-the-human-let7-microrna-precursor-duplex-and-is-required-for-let7directed-silencing-of-gene-expression/25465873 32773-130821163354-phpapp02
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]]> Wed, 21 Aug 2013 16:33:54 GMT /slideshow/p68-rna-helicase-unwinds-the-human-let7-microrna-precursor-duplex-and-is-required-for-let7directed-silencing-of-gene-expression/25465873 DavidSalzman1@slideshare.net(DavidSalzman1) P68 RNA helicase unwinds the human let-7 microRNA precursor duplex and is required for let-7-directed silencing of gene expression. DavidSalzman1 <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/32773-130821163354-phpapp02-thumbnail.jpg?width=120&height=120&fit=bounds" />

P68 RNA helicase unwinds the human let-7 microRNA precursor duplex and is required for let-7-directed silencing of gene expression. from David W. Salzman

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0 The 5' terminal uracil of let-7a is critical for the recruitment of mRNA to Argonaute2. /slideshow/the-5-terminal-uracil-of-let7a-is-critical-for-the-recruitment-of-mrna-to-argonaute2/25465657 4220329-130821162433-phpapp02
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]]> Wed, 21 Aug 2013 16:24:33 GMT /slideshow/the-5-terminal-uracil-of-let7a-is-critical-for-the-recruitment-of-mrna-to-argonaute2/25465657 DavidSalzman1@slideshare.net(DavidSalzman1) The 5' terminal uracil of let-7a is critical for the recruitment of mRNA to Argonaute2. DavidSalzman1 <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/4220329-130821162433-phpapp02-thumbnail.jpg?width=120&height=120&fit=bounds" />

The 5' terminal uracil of let-7a is critical for the recruitment of mRNA to Argonaute2. from David W. Salzman

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0 miRNAs in the spotlight: Making 'silent' mutations speak up. /slideshow/nm0811-934/25465323 nm0811-934-130821160814-phpapp01
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]]> Wed, 21 Aug 2013 16:08:14 GMT /slideshow/nm0811-934/25465323 DavidSalzman1@slideshare.net(DavidSalzman1) miRNAs in the spotlight: Making 'silent' mutations speak up. DavidSalzman1 <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/nm0811-934-130821160814-phpapp01-thumbnail.jpg?width=120&height=120&fit=bounds" />

miRNAs in the spotlight: Making 'silent' mutations speak up. from David W. Salzman

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0 ATM /slideshow/atm-24815901/24815901 mn043220-130731153540-phpapp02
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]]> Wed, 31 Jul 2013 15:35:40 GMT /slideshow/atm-24815901/24815901 DavidSalzman1@slideshare.net(DavidSalzman1) ATM DavidSalzman1 <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/mn043220-130731153540-phpapp02-thumbnail.jpg?width=120&height=120&fit=bounds" />

ATM from David W. Salzman

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0 miRNA-Target Site SNPs as Predictors for Cancer Risk and Treatment Response /slideshow/mirnatarget-site-snps-as-predictors-for-cancer-risk-and-treatment-response/24815263 lungspore-130731152048-phpapp02
9th Annual miRNA Meeting: To]]>
9th Annual miRNA Meeting: To]]> Wed, 31 Jul 2013 15:20:48 GMT /slideshow/mirnatarget-site-snps-as-predictors-for-cancer-risk-and-treatment-response/24815263 DavidSalzman1@slideshare.net(DavidSalzman1) miRNA-Target Site SNPs as Predictors for Cancer Risk and Treatment Response DavidSalzman1 9th Annual miRNA Meeting: To <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/lungspore-130731152048-phpapp02-thumbnail.jpg?width=120&height=120&fit=bounds" /> 9th Annual miRNA Meeting: To

miRNA-Target Site SNPs as Predictors for Cancer Risk and Treatment Response from David W. Salzman

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0 https://cdn.slidesharecdn.com/profile-photo-DavidSalzman1-48x48.jpg?cb=1556547457 Proficient and entrepreneurial scientist with 14 years of research and project management experience in academic and industry settings. I have a proven success record in increasing portfolio value through the conceptualization, discovery, development, and implementation of fit-for-purpose, PD/biomarker assays used in tissue or fluid samples for patient enrollment and end-point stratification. As an ASCP-certified Molecular Biologist, I have extensive experience in the technical development and oversight of high complexity assays, with a specialty in deriving biomarkers from NGS DNA and RNA sequencing data and developing (single or multiplex, qualitative or quantitative) qPCR genotyping, ... https://cdn.slidesharecdn.com/ss_thumbnails/alet-7microrna-bindingsitepolymorphisminkras-140910123615-phpapp01-thumbnail.jpg?width=320&height=320&fit=bounds slideshow/a-let-7-micro-rnabinding-site-polymorphism-in-kras/38934791 Clinical Cancer Resear... https://cdn.slidesharecdn.com/ss_thumbnails/agermlinemutationinthebrca13utrpredictsstageivbreastcancer-140714131847-phpapp02-thumbnail.jpg?width=320&height=320&fit=bounds slideshow/a-germline-mutation-in-the-brca1-3utr-predicts-stage-iv-breast-cancer/36964508 A germline mutation in... https://cdn.slidesharecdn.com/ss_thumbnails/32773-130821163354-phpapp02-thumbnail.jpg?width=320&height=320&fit=bounds slideshow/p68-rna-helicase-unwinds-the-human-let7-microrna-precursor-duplex-and-is-required-for-let7directed-silencing-of-gene-expression/25465873 P68 RNA helicase unwin...