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10.1186/s13045-017-0468-1 http://scihub22266oqcxt.onion/10.1186/s13045-017-0468-1 C5418716!5418716 !28472989     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28472989 &cmd=llinks): Failed to open stream: HTTP request failed! 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Circulating mutational portrait of cancer: manifestation of aggressive clonal events in both early and late stages |pdf=|usr=}}{{28472989 }} gab.com Text Circulating mutational portrait of cancer: manifestation of aggressive clonal events in both early and late stages JO: J Hematol Oncol http://www.kidney.de/pget.php?&tw=1&pmid=28472989 #FOAvip BACKGROUND: Solid tumors residing in tissues and organs leave footprints in circulation through circulating tumor cells (CTCs) and circulating tumor DNAs (ctDNA). Characterization of the ctDNA portraits and comparison with tumor DNA mutational portraits may reveal clinically actionable information on solid tumors that is traditionally achieved through more invasive approaches. METHODS: We isolated ctDNAs from plasma of patients of 103 lung cancer and 74 other solid tumors of different tissue origins. Deep sequencing using the Guardant360 test was performed to identify mutations in 73 clinically actionable genes, and the results were associated with clinical characteristics of the patient. The mutation profiles of 37 lung cancer cases with paired ctDNA and tumor genomic DNA sequencing were used to evaluate clonal representation of tumor in circulation. Five lung cancer cases with longitudinal ctDNA sampling were monitored for cancer progression or response to treatments. RESULTS: Mutations in TP53, EGFR, and KRAS genes are most prevalent in our cohort. Mutation rates of ctDNA are similar in early (I and II) and late stage (III and IV) cancers. Mutation in DNA repair genes BRCA1, BRCA2, and ATM are found in 18.1% (32/177) of cases. Patients with higher mutation rates had significantly higher mortality rates. Lung cancer of never smokers exhibited significantly higher ctDNA mutation rates as well as higher EGFR and ERBB2 mutations than ever smokers. Comparative analysis of ctDNA and tumor DNA mutation data from the same patients showed that key driver mutations could be detected in plasma even when they were present at a minor clonal population in the tumor. Mutations of key genes found in the tumor tissue could remain in circulation even after frontline radiotherapy and chemotherapy suggesting these mutations represented resistance mechanisms. Longitudinal sampling of five lung cancer cases showed distinct changes in ctDNA mutation portraits that are consistent with cancer progression or response to EGFR drug treatment. CONCLUSIONS: This study demonstrates that ctDNA mutation rates in the key tumor-associated genes are clinical parameters relevant to smoking status and mortality. Mutations in ctDNA may serve as an early detection tool for cancer. This study quantitatively confirms the hypothesis that ctDNAs in circulation is the result of dissemination of aggressive tumor clones and survival of resistant clones. This study supports the use of ctDNA profiling as a less-invasive approach to monitor cancer progression and selection of appropriate drugs during cancer evolution. Twit Text FOAVip Circulating mutational portrait of cancer: manifestation of aggressive clonal events in both early and late stages ????J Hematol Oncol http://www.kidney.de/pget.php?&tw=1&pmid=28472989 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28472989 #FOAvip English Wikipedia <ref>{{Cite pmid|28472989 }}</ref> Circulating mutational portrait of cancer: manifestation of aggressive clonal events in both early and late stages #MMPMID28472989 Yang M ; Topaloglu U ; Petty WJ ; Pagni M ; Foley KL ; Grant SC ; Robinson M ; Bitting RL ; Thomas A ; Alistar AT ; Desnoyers RJ ; Goodman M ; Albright C ; Porosnicu M ; Vatca M ; Qasem SA ; DeYoung B ; Kytola V ; Nykter M ; Chen K ; Levine EA ; Staren ED ; D'Agostino RB Jr ; Petro RM ; Blackstock W ; Powell BL ; Abraham E ; Pasche B ; Zhang W J Hematol Oncol 2017[May]; 10 (1 ): 100 PMID28472989 show ga BACKGROUND: Solid tumors residing in tissues and organs leave footprints in circulation through circulating tumor cells (CTCs) and circulating tumor DNAs (ctDNA). Characterization of the ctDNA portraits and comparison with tumor DNA mutational portraits may reveal clinically actionable information on solid tumors that is traditionally achieved through more invasive approaches. METHODS: We isolated ctDNAs from plasma of patients of 103 lung cancer and 74 other solid tumors of different tissue origins. Deep sequencing using the Guardant360 test was performed to identify mutations in 73 clinically actionable genes, and the results were associated with clinical characteristics of the patient. The mutation profiles of 37 lung cancer cases with paired ctDNA and tumor genomic DNA sequencing were used to evaluate clonal representation of tumor in circulation. Five lung cancer cases with longitudinal ctDNA sampling were monitored for cancer progression or response to treatments. RESULTS: Mutations in TP53, EGFR, and KRAS genes are most prevalent in our cohort. Mutation rates of ctDNA are similar in early (I and II) and late stage (III and IV) cancers. Mutation in DNA repair genes BRCA1, BRCA2, and ATM are found in 18.1% (32/177) of cases. Patients with higher mutation rates had significantly higher mortality rates. Lung cancer of never smokers exhibited significantly higher ctDNA mutation rates as well as higher EGFR and ERBB2 mutations than ever smokers. Comparative analysis of ctDNA and tumor DNA mutation data from the same patients showed that key driver mutations could be detected in plasma even when they were present at a minor clonal population in the tumor. Mutations of key genes found in the tumor tissue could remain in circulation even after frontline radiotherapy and chemotherapy suggesting these mutations represented resistance mechanisms. Longitudinal sampling of five lung cancer cases showed distinct changes in ctDNA mutation portraits that are consistent with cancer progression or response to EGFR drug treatment. CONCLUSIONS: This study demonstrates that ctDNA mutation rates in the key tumor-associated genes are clinical parameters relevant to smoking status and mortality. Mutations in ctDNA may serve as an early detection tool for cancer. This study quantitatively confirms the hypothesis that ctDNAs in circulation is the result of dissemination of aggressive tumor clones and survival of resistant clones. This study supports the use of ctDNA profiling as a less-invasive approach to monitor cancer progression and selection of appropriate drugs during cancer evolution. |*Mutation [MESH] |*Neoplastic Cells, Circulating [MESH] |Adult [MESH] |Aged [MESH] |Aged, 80 and over [MESH] |Antineoplastic Agents/therapeutic use [MESH] |Chemoradiotherapy [MESH] |Clone Cells [MESH] |DNA, Neoplasm/*genetics [MESH] |Disease Progression [MESH] |ErbB Receptors/antagonists & inhibitors [MESH] |Erlotinib Hydrochloride/therapeutic use [MESH] |Female [MESH] |Gene Expression Profiling [MESH] |Genes, Neoplasm [MESH] |Genes, erbB-1 [MESH] |Genes, p53 [MESH] |Genes, ras [MESH] |Humans [MESH] |Lung Neoplasms/genetics/mortality/therapy [MESH] |Male [MESH] |Middle Aged [MESH] |Neoplasm Invasiveness/*genetics [MESH] |Neoplasm Proteins/genetics [MESH] |Neoplasms/*genetics/mortality/pathology [MESH] |Neoplastic Stem Cells [MESH] |Protein Kinase Inhibitors/therapeutic use [MESH] |Retrospective Studies [MESH] |Sequence Analysis, DNA [MESH]Circulating mutational portrait of cancer: manifestation of aggressive(epmc).pdf DeepDyve Pubget Overpricing