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New therapeutic perspectives in CCDC6 deficient lung cancer cells
Non‐small cell lung cancer (NSCLC) is the main cause of cancer‐related death worldwide and new therapeutic strategies are urgently needed. In this study, we have characterized a panel of NSC lung cancer cell lines for the expression of coiled‐coil‐domain containing 6 (CCDC6), a tumor suppressor gene...
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| Published in: | International journal of cancer 2015-05, Vol.136 (9), p.2146-2157 |
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| container_title | International journal of cancer |
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| creator | Morra, Francesco Luise, Chiara Visconti, Roberta Staibano, Stefania Merolla, Francesco Ilardi, Gennaro Guggino, Gianluca Paladino, Simona Sarnataro, Daniela Franco, Renato Monaco, Roberto Zitomarino, Federica Pacelli, Roberto Monaco, Guglielmo Rocco, Gaetano Cerrato, Aniello Linardopoulos, Spiros Muller, Mark T. Celetti, Angela |
| description | Non‐small cell lung cancer (NSCLC) is the main cause of cancer‐related death worldwide and new therapeutic strategies are urgently needed. In this study, we have characterized a panel of NSC lung cancer cell lines for the expression of coiled‐coil‐domain containing 6 (CCDC6), a tumor suppressor gene involved in apoptosis and DNA damage response. We show that low CCDC6 protein levels are associated with a weak response to DNA damage and a low number of Rad51 positive foci. Moreover, CCDC6 deficient lung cancer cells show defects in DNA repair via homologous recombination. In accordance with its role in the DNA damage response, CCDC6 attenuation confers resistance to cisplatinum, the current treatment of choice for NSCLC, but sensitizes the cells to olaparib, a small molecule inhibitor of the repair enzymes PARP1/2. Remarkably, the combination of the two drugs is more effective than each agent individually, as demonstrated by a combination index |
| doi_str_mv | 10.1002/ijc.29263 |
| format | article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_proquest_journals_1655222126</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3591961171</sourcerecordid><originalsourceid>FETCH-LOGICAL-p2793-ef92280858d2c5aba6ff28f00ab3ebc466e89db0c89bffd4d8a203954104be913</originalsourceid><addsrcrecordid>eNo9kMtOwzAQRS0EoiWw4AeQJdZpx3ac2ssqvIoq2MDacpwxuErTkAdV_57QFlYz0j26ozmEXDOYMAA-DSs34Zqn4oSMGehZDJzJUzIeMohnTKQjctG2KwDGJCTnZMSlAK6EGJP5C25p94mNrbHvgqM1Nm2Nrgvf2NJQ0Sy7y1JaoA8uYNXRsq8-qLOVw4Y6LMv2kpx5W7Z4dZwReX-4f8ue4uXr4yKbL-Oaz7SI0WvOFSipCu6kzW3qPVcewOYCc5ekKSpd5OCUzr0vkkJZDkLLhEGSo2YiIreH3rrZfPXYdma16ZtqOGlYKiXnnA0GInJzpPp8jYWpm7C2zc78fTwA0wOwDSXu_nMG5lelGVSavUqzeM72i_gBbAhkWw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1655222126</pqid></control><display><type>article</type><title>New therapeutic perspectives in CCDC6 deficient lung cancer cells</title><source>Wiley</source><creator>Morra, Francesco ; Luise, Chiara ; Visconti, Roberta ; Staibano, Stefania ; Merolla, Francesco ; Ilardi, Gennaro ; Guggino, Gianluca ; Paladino, Simona ; Sarnataro, Daniela ; Franco, Renato ; Monaco, Roberto ; Zitomarino, Federica ; Pacelli, Roberto ; Monaco, Guglielmo ; Rocco, Gaetano ; Cerrato, Aniello ; Linardopoulos, Spiros ; Muller, Mark T. ; Celetti, Angela</creator><creatorcontrib>Morra, Francesco ; Luise, Chiara ; Visconti, Roberta ; Staibano, Stefania ; Merolla, Francesco ; Ilardi, Gennaro ; Guggino, Gianluca ; Paladino, Simona ; Sarnataro, Daniela ; Franco, Renato ; Monaco, Roberto ; Zitomarino, Federica ; Pacelli, Roberto ; Monaco, Guglielmo ; Rocco, Gaetano ; Cerrato, Aniello ; Linardopoulos, Spiros ; Muller, Mark T. ; Celetti, Angela</creatorcontrib><description>Non‐small cell lung cancer (NSCLC) is the main cause of cancer‐related death worldwide and new therapeutic strategies are urgently needed. In this study, we have characterized a panel of NSC lung cancer cell lines for the expression of coiled‐coil‐domain containing 6 (CCDC6), a tumor suppressor gene involved in apoptosis and DNA damage response. We show that low CCDC6 protein levels are associated with a weak response to DNA damage and a low number of Rad51 positive foci. Moreover, CCDC6 deficient lung cancer cells show defects in DNA repair via homologous recombination. In accordance with its role in the DNA damage response, CCDC6 attenuation confers resistance to cisplatinum, the current treatment of choice for NSCLC, but sensitizes the cells to olaparib, a small molecule inhibitor of the repair enzymes PARP1/2. Remarkably, the combination of the two drugs is more effective than each agent individually, as demonstrated by a combination index <1. Finally, CCDC6 is expressed at low levels in about 30% of the NSCL tumors we analyzed by TMA immunostaining. The weak CCDC6 protein staining is significatively correlated with the presence of lymph node metastasis (p ≤ 0.02) and negatively correlated to the disease free survival (p ≤ 0.01) and the overall survival (p ≤ 0.05). Collectively, the data indicate that CCDC6 levels provide valuable insight for OS. CCDC6 could represent a predictive biomarker of resistance to conventional single mode therapy and yield insight on tumor sensitivity to PARP inhibitors in NSCLC.
What's new?
Non‐small cell lung cancer (NSCLC) is a deadly disease, with fewer than 15% of patients still alive five years post‐diagnosis. But as this study suggests, predictive biomarkers could inform the development of much‐needed novel therapeutic strategies. Defective expression of the tumor suppressor coiled‐coil‐domain containing 6 (CCDC6) was correlated with patient survival and, in NSCLC cells, was associated with deficient homology‐directed repair (HDR), rendering the cells resistant to cisplatinum but sensitive to the PARP inhibitor olaparib. When given in combination, however, the two agents were synergistic. Thus, CCDC6 levels may offer valuable insight for therapeutic decisions in NSCLC.</description><identifier>ISSN: 0020-7136</identifier><identifier>EISSN: 1097-0215</identifier><identifier>DOI: 10.1002/ijc.29263</identifier><identifier>PMID: 25302833</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Aged ; Aged, 80 and over ; Antineoplastic Agents - pharmacology ; Apoptosis - drug effects ; Apoptosis - genetics ; Cancer ; Cancer therapies ; candidate biomarker ; Carcinoma, Non-Small-Cell Lung - drug therapy ; Carcinoma, Non-Small-Cell Lung - genetics ; CCDC6 ; Cell Line, Tumor ; Cisplatin - pharmacology ; Cytoskeletal Proteins - deficiency ; Cytoskeletal Proteins - genetics ; Deoxyribonucleic acid ; Disease-Free Survival ; DNA ; DNA damage ; DNA Damage - drug effects ; DNA Damage - genetics ; DNA damage and homologous‐directed repair ; DNA repair ; DNA Repair - drug effects ; DNA Repair - genetics ; Female ; Humans ; Lung cancer ; Lung Neoplasms - drug therapy ; Lung Neoplasms - genetics ; Lymphatic Metastasis - genetics ; Male ; Medical research ; Middle Aged ; NSCLC ; Phthalazines ; Piperazines ; Rad51 Recombinase - genetics ; resistance to platinum salts and PARP‐1 inhibitor sensitivity</subject><ispartof>International journal of cancer, 2015-05, Vol.136 (9), p.2146-2157</ispartof><rights>2014 UICC</rights><rights>2014 UICC.</rights><rights>2015 UICC</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25302833$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Morra, Francesco</creatorcontrib><creatorcontrib>Luise, Chiara</creatorcontrib><creatorcontrib>Visconti, Roberta</creatorcontrib><creatorcontrib>Staibano, Stefania</creatorcontrib><creatorcontrib>Merolla, Francesco</creatorcontrib><creatorcontrib>Ilardi, Gennaro</creatorcontrib><creatorcontrib>Guggino, Gianluca</creatorcontrib><creatorcontrib>Paladino, Simona</creatorcontrib><creatorcontrib>Sarnataro, Daniela</creatorcontrib><creatorcontrib>Franco, Renato</creatorcontrib><creatorcontrib>Monaco, Roberto</creatorcontrib><creatorcontrib>Zitomarino, Federica</creatorcontrib><creatorcontrib>Pacelli, Roberto</creatorcontrib><creatorcontrib>Monaco, Guglielmo</creatorcontrib><creatorcontrib>Rocco, Gaetano</creatorcontrib><creatorcontrib>Cerrato, Aniello</creatorcontrib><creatorcontrib>Linardopoulos, Spiros</creatorcontrib><creatorcontrib>Muller, Mark T.</creatorcontrib><creatorcontrib>Celetti, Angela</creatorcontrib><title>New therapeutic perspectives in CCDC6 deficient lung cancer cells</title><title>International journal of cancer</title><addtitle>Int J Cancer</addtitle><description>Non‐small cell lung cancer (NSCLC) is the main cause of cancer‐related death worldwide and new therapeutic strategies are urgently needed. In this study, we have characterized a panel of NSC lung cancer cell lines for the expression of coiled‐coil‐domain containing 6 (CCDC6), a tumor suppressor gene involved in apoptosis and DNA damage response. We show that low CCDC6 protein levels are associated with a weak response to DNA damage and a low number of Rad51 positive foci. Moreover, CCDC6 deficient lung cancer cells show defects in DNA repair via homologous recombination. In accordance with its role in the DNA damage response, CCDC6 attenuation confers resistance to cisplatinum, the current treatment of choice for NSCLC, but sensitizes the cells to olaparib, a small molecule inhibitor of the repair enzymes PARP1/2. Remarkably, the combination of the two drugs is more effective than each agent individually, as demonstrated by a combination index <1. Finally, CCDC6 is expressed at low levels in about 30% of the NSCL tumors we analyzed by TMA immunostaining. The weak CCDC6 protein staining is significatively correlated with the presence of lymph node metastasis (p ≤ 0.02) and negatively correlated to the disease free survival (p ≤ 0.01) and the overall survival (p ≤ 0.05). Collectively, the data indicate that CCDC6 levels provide valuable insight for OS. CCDC6 could represent a predictive biomarker of resistance to conventional single mode therapy and yield insight on tumor sensitivity to PARP inhibitors in NSCLC.
What's new?
Non‐small cell lung cancer (NSCLC) is a deadly disease, with fewer than 15% of patients still alive five years post‐diagnosis. But as this study suggests, predictive biomarkers could inform the development of much‐needed novel therapeutic strategies. Defective expression of the tumor suppressor coiled‐coil‐domain containing 6 (CCDC6) was correlated with patient survival and, in NSCLC cells, was associated with deficient homology‐directed repair (HDR), rendering the cells resistant to cisplatinum but sensitive to the PARP inhibitor olaparib. When given in combination, however, the two agents were synergistic. Thus, CCDC6 levels may offer valuable insight for therapeutic decisions in NSCLC.</description><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - genetics</subject><subject>Cancer</subject><subject>Cancer therapies</subject><subject>candidate biomarker</subject><subject>Carcinoma, Non-Small-Cell Lung - drug therapy</subject><subject>Carcinoma, Non-Small-Cell Lung - genetics</subject><subject>CCDC6</subject><subject>Cell Line, Tumor</subject><subject>Cisplatin - pharmacology</subject><subject>Cytoskeletal Proteins - deficiency</subject><subject>Cytoskeletal Proteins - genetics</subject><subject>Deoxyribonucleic acid</subject><subject>Disease-Free Survival</subject><subject>DNA</subject><subject>DNA damage</subject><subject>DNA Damage - drug effects</subject><subject>DNA Damage - genetics</subject><subject>DNA damage and homologous‐directed repair</subject><subject>DNA repair</subject><subject>DNA Repair - drug effects</subject><subject>DNA Repair - genetics</subject><subject>Female</subject><subject>Humans</subject><subject>Lung cancer</subject><subject>Lung Neoplasms - drug therapy</subject><subject>Lung Neoplasms - genetics</subject><subject>Lymphatic Metastasis - genetics</subject><subject>Male</subject><subject>Medical research</subject><subject>Middle Aged</subject><subject>NSCLC</subject><subject>Phthalazines</subject><subject>Piperazines</subject><subject>Rad51 Recombinase - genetics</subject><subject>resistance to platinum salts and PARP‐1 inhibitor sensitivity</subject><issn>0020-7136</issn><issn>1097-0215</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><recordid>eNo9kMtOwzAQRS0EoiWw4AeQJdZpx3ac2ssqvIoq2MDacpwxuErTkAdV_57QFlYz0j26ozmEXDOYMAA-DSs34Zqn4oSMGehZDJzJUzIeMohnTKQjctG2KwDGJCTnZMSlAK6EGJP5C25p94mNrbHvgqM1Nm2Nrgvf2NJQ0Sy7y1JaoA8uYNXRsq8-qLOVw4Y6LMv2kpx5W7Z4dZwReX-4f8ue4uXr4yKbL-Oaz7SI0WvOFSipCu6kzW3qPVcewOYCc5ekKSpd5OCUzr0vkkJZDkLLhEGSo2YiIreH3rrZfPXYdma16ZtqOGlYKiXnnA0GInJzpPp8jYWpm7C2zc78fTwA0wOwDSXu_nMG5lelGVSavUqzeM72i_gBbAhkWw</recordid><startdate>20150501</startdate><enddate>20150501</enddate><creator>Morra, Francesco</creator><creator>Luise, Chiara</creator><creator>Visconti, Roberta</creator><creator>Staibano, Stefania</creator><creator>Merolla, Francesco</creator><creator>Ilardi, Gennaro</creator><creator>Guggino, Gianluca</creator><creator>Paladino, Simona</creator><creator>Sarnataro, Daniela</creator><creator>Franco, Renato</creator><creator>Monaco, Roberto</creator><creator>Zitomarino, Federica</creator><creator>Pacelli, Roberto</creator><creator>Monaco, Guglielmo</creator><creator>Rocco, Gaetano</creator><creator>Cerrato, Aniello</creator><creator>Linardopoulos, Spiros</creator><creator>Muller, Mark T.</creator><creator>Celetti, Angela</creator><general>Wiley Subscription Services, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7T5</scope><scope>7TO</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope></search><sort><creationdate>20150501</creationdate><title>New therapeutic perspectives in CCDC6 deficient lung cancer cells</title><author>Morra, Francesco ; Luise, Chiara ; Visconti, Roberta ; Staibano, Stefania ; Merolla, Francesco ; Ilardi, Gennaro ; Guggino, Gianluca ; Paladino, Simona ; Sarnataro, Daniela ; Franco, Renato ; Monaco, Roberto ; Zitomarino, Federica ; Pacelli, Roberto ; Monaco, Guglielmo ; Rocco, Gaetano ; Cerrato, Aniello ; Linardopoulos, Spiros ; Muller, Mark T. ; Celetti, Angela</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p2793-ef92280858d2c5aba6ff28f00ab3ebc466e89db0c89bffd4d8a203954104be913</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - genetics</topic><topic>Cancer</topic><topic>Cancer therapies</topic><topic>candidate biomarker</topic><topic>Carcinoma, Non-Small-Cell Lung - drug therapy</topic><topic>Carcinoma, Non-Small-Cell Lung - genetics</topic><topic>CCDC6</topic><topic>Cell Line, Tumor</topic><topic>Cisplatin - pharmacology</topic><topic>Cytoskeletal Proteins - deficiency</topic><topic>Cytoskeletal Proteins - genetics</topic><topic>Deoxyribonucleic acid</topic><topic>Disease-Free Survival</topic><topic>DNA</topic><topic>DNA damage</topic><topic>DNA Damage - drug effects</topic><topic>DNA Damage - genetics</topic><topic>DNA damage and homologous‐directed repair</topic><topic>DNA repair</topic><topic>DNA Repair - drug effects</topic><topic>DNA Repair - genetics</topic><topic>Female</topic><topic>Humans</topic><topic>Lung cancer</topic><topic>Lung Neoplasms - drug therapy</topic><topic>Lung Neoplasms - genetics</topic><topic>Lymphatic Metastasis - genetics</topic><topic>Male</topic><topic>Medical research</topic><topic>Middle Aged</topic><topic>NSCLC</topic><topic>Phthalazines</topic><topic>Piperazines</topic><topic>Rad51 Recombinase - genetics</topic><topic>resistance to platinum salts and PARP‐1 inhibitor sensitivity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Morra, Francesco</creatorcontrib><creatorcontrib>Luise, Chiara</creatorcontrib><creatorcontrib>Visconti, Roberta</creatorcontrib><creatorcontrib>Staibano, Stefania</creatorcontrib><creatorcontrib>Merolla, Francesco</creatorcontrib><creatorcontrib>Ilardi, Gennaro</creatorcontrib><creatorcontrib>Guggino, Gianluca</creatorcontrib><creatorcontrib>Paladino, Simona</creatorcontrib><creatorcontrib>Sarnataro, Daniela</creatorcontrib><creatorcontrib>Franco, Renato</creatorcontrib><creatorcontrib>Monaco, Roberto</creatorcontrib><creatorcontrib>Zitomarino, Federica</creatorcontrib><creatorcontrib>Pacelli, Roberto</creatorcontrib><creatorcontrib>Monaco, Guglielmo</creatorcontrib><creatorcontrib>Rocco, Gaetano</creatorcontrib><creatorcontrib>Cerrato, Aniello</creatorcontrib><creatorcontrib>Linardopoulos, Spiros</creatorcontrib><creatorcontrib>Muller, Mark T.</creatorcontrib><creatorcontrib>Celetti, Angela</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><jtitle>International journal of cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Morra, Francesco</au><au>Luise, Chiara</au><au>Visconti, Roberta</au><au>Staibano, Stefania</au><au>Merolla, Francesco</au><au>Ilardi, Gennaro</au><au>Guggino, Gianluca</au><au>Paladino, Simona</au><au>Sarnataro, Daniela</au><au>Franco, Renato</au><au>Monaco, Roberto</au><au>Zitomarino, Federica</au><au>Pacelli, Roberto</au><au>Monaco, Guglielmo</au><au>Rocco, Gaetano</au><au>Cerrato, Aniello</au><au>Linardopoulos, Spiros</au><au>Muller, Mark T.</au><au>Celetti, Angela</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>New therapeutic perspectives in CCDC6 deficient lung cancer cells</atitle><jtitle>International journal of cancer</jtitle><addtitle>Int J Cancer</addtitle><date>2015-05-01</date><risdate>2015</risdate><volume>136</volume><issue>9</issue><spage>2146</spage><epage>2157</epage><pages>2146-2157</pages><issn>0020-7136</issn><eissn>1097-0215</eissn><abstract>Non‐small cell lung cancer (NSCLC) is the main cause of cancer‐related death worldwide and new therapeutic strategies are urgently needed. In this study, we have characterized a panel of NSC lung cancer cell lines for the expression of coiled‐coil‐domain containing 6 (CCDC6), a tumor suppressor gene involved in apoptosis and DNA damage response. We show that low CCDC6 protein levels are associated with a weak response to DNA damage and a low number of Rad51 positive foci. Moreover, CCDC6 deficient lung cancer cells show defects in DNA repair via homologous recombination. In accordance with its role in the DNA damage response, CCDC6 attenuation confers resistance to cisplatinum, the current treatment of choice for NSCLC, but sensitizes the cells to olaparib, a small molecule inhibitor of the repair enzymes PARP1/2. Remarkably, the combination of the two drugs is more effective than each agent individually, as demonstrated by a combination index <1. Finally, CCDC6 is expressed at low levels in about 30% of the NSCL tumors we analyzed by TMA immunostaining. The weak CCDC6 protein staining is significatively correlated with the presence of lymph node metastasis (p ≤ 0.02) and negatively correlated to the disease free survival (p ≤ 0.01) and the overall survival (p ≤ 0.05). Collectively, the data indicate that CCDC6 levels provide valuable insight for OS. CCDC6 could represent a predictive biomarker of resistance to conventional single mode therapy and yield insight on tumor sensitivity to PARP inhibitors in NSCLC.
What's new?
Non‐small cell lung cancer (NSCLC) is a deadly disease, with fewer than 15% of patients still alive five years post‐diagnosis. But as this study suggests, predictive biomarkers could inform the development of much‐needed novel therapeutic strategies. Defective expression of the tumor suppressor coiled‐coil‐domain containing 6 (CCDC6) was correlated with patient survival and, in NSCLC cells, was associated with deficient homology‐directed repair (HDR), rendering the cells resistant to cisplatinum but sensitive to the PARP inhibitor olaparib. When given in combination, however, the two agents were synergistic. Thus, CCDC6 levels may offer valuable insight for therapeutic decisions in NSCLC.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>25302833</pmid><doi>10.1002/ijc.29263</doi><tpages>12</tpages></addata></record> |
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| subjects | Aged Aged, 80 and over Antineoplastic Agents - pharmacology Apoptosis - drug effects Apoptosis - genetics Cancer Cancer therapies candidate biomarker Carcinoma, Non-Small-Cell Lung - drug therapy Carcinoma, Non-Small-Cell Lung - genetics CCDC6 Cell Line, Tumor Cisplatin - pharmacology Cytoskeletal Proteins - deficiency Cytoskeletal Proteins - genetics Deoxyribonucleic acid Disease-Free Survival DNA DNA damage DNA Damage - drug effects DNA Damage - genetics DNA damage and homologous‐directed repair DNA repair DNA Repair - drug effects DNA Repair - genetics Female Humans Lung cancer Lung Neoplasms - drug therapy Lung Neoplasms - genetics Lymphatic Metastasis - genetics Male Medical research Middle Aged NSCLC Phthalazines Piperazines Rad51 Recombinase - genetics resistance to platinum salts and PARP‐1 inhibitor sensitivity |
| title | New therapeutic perspectives in CCDC6 deficient lung cancer cells |
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