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Pregled bibliografske jedinice broj: 829107

Ercc1 Deficiency Promotes Tumorigenesis and Increases Cisplatin Sensitivity in a TP53 Context-specific Manner

Jokić, Mladen; Vlašić, Ignacija; Rinneburger, Miriam; Klümper, Niklas; Spiro, Judith; Vogel, Wenzel; Offermann, Anne; Kümpers, Christiane; Fritz, Christian; Schmitt, Anna et al.
Ercc1 Deficiency Promotes Tumorigenesis and Increases Cisplatin Sensitivity in a TP53 Context-specific Manner // Molecular cancer research, 14 (2016), 11; 1110-1123 doi:10.1158/1541-7786.MCR-16-0094 (međunarodna recenzija, članak, znanstveni)

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Naslov
Ercc1 Deficiency Promotes Tumorigenesis and Increases Cisplatin Sensitivity in a TP53 Context-specific Manner

Autori
Jokić, Mladen ; Vlašić, Ignacija ; Rinneburger, Miriam ; Klümper, Niklas ; Spiro, Judith ; Vogel, Wenzel ; Offermann, Anne ; Kümpers, Christiane ; Fritz, Christian ; Schmitt, Anna ; Riabinska, Arina ; Wittersheim, Maike ; Michels, Sebastian ; Ozretić, Luka ; Florin, Alexandra ; Welcker, Daniela ; Akyuz, Mehmet Deniz ; Nowak, Michael ; Erkel, Martin ; Wolf, Jürgen ; Büttner, Reinhard ; Schumacher, Björn ; Thomale, Jürgen ; Persigehl, Thorsten ; Maintz, David ; Perner, Sven ; Reinhardt, Hans Christian

Izvornik
Molecular cancer research (1541-7786) 14 (2016), 11; 1110-1123

Vrsta, podvrsta i kategorija rada
Radovi u časopisima, članak, znanstveni

Ključne riječi
Ercc1 ; TP53 ; lung adenocarcinoma ; cisplatin

Sažetak
KRAS-mutant lung adenocarcinoma is among the most common cancer entities and, in advanced stages, typically displays poor prognosis due to acquired resistance against chemotherapy, which is still largely based on cisplatin containing combination regimens. Mechanisms of cisplatin resistance have been extensively investigated and ERCC1 has emerged as a key player, due to its central role in the repair of cisplatin-induced DNA lesions. However, clinical data have not unequivocally confirmed ERCC1 status as a predictor of the response to cisplatin treatment. Therefore, we employed an autochthonous mouse model of Kras-driven lung adenocarcinoma resembling human lung adenocarcinoma to investigate the role of Ercc1 in the response to cisplatin treatment. Our data show that Ercc1 deficiency in Tp53-deficient murine lung adenocarcinoma induces a more aggressive tumor phenotype that displays enhanced sensitivity to cisplatin treatment. Furthermore, tumors that relapsed after cisplatin treatment in our model develop a robust etoposide sensitivity that is independent of the Ercc1 status and depends solely on previous cisplatin exposure. Our results provide a solid rationale for the further investigation of the possibility of preselection of lung adenocarcinoma patients according to the functional ERCC1- and mutational TP53 status where functionally ERCC1-incompetent patients might benefit from sequential cisplatin and etoposide chemotherapy.

Izvorni jezik
Engleski

Znanstvena područja
Biologija, Temeljne medicinske znanosti



POVEZANOST RADA

Profili:

Avatar Url Mladen Jokić (autor)

Avatar Url Ignacija Vlašić (autor)

Poveznice na cjeloviti tekst rada:

doi

Citiraj ovu publikaciju:

Jokić, Mladen; Vlašić, Ignacija; Rinneburger, Miriam; Klümper, Niklas; Spiro, Judith; Vogel, Wenzel; Offermann, Anne; Kümpers, Christiane; Fritz, Christian; Schmitt, Anna et al.
Ercc1 Deficiency Promotes Tumorigenesis and Increases Cisplatin Sensitivity in a TP53 Context-specific Manner // Molecular cancer research, 14 (2016), 11; 1110-1123 doi:10.1158/1541-7786.MCR-16-0094 (međunarodna recenzija, članak, znanstveni)
Jokić, M., Vlašić, I., Rinneburger, M., Klümper, N., Spiro, J., Vogel, W., Offermann, A., Kümpers, C., Fritz, C. & Schmitt, A. (2016) Ercc1 Deficiency Promotes Tumorigenesis and Increases Cisplatin Sensitivity in a TP53 Context-specific Manner. Molecular cancer research, 14 (11), 1110-1123 doi:10.1158/1541-7786.MCR-16-0094.
@article{article, author = {Joki\'{c}, Mladen and Vla\v{s}i\'{c}, Ignacija and Rinneburger, Miriam and Kl\"{u}mper, Niklas and Spiro, Judith and Vogel, Wenzel and Offermann, Anne and K\"{u}mpers, Christiane and Fritz, Christian and Schmitt, Anna and Riabinska, Arina and Wittersheim, Maike and Michels, Sebastian and Ozreti\'{c}, Luka and Florin, Alexandra and Welcker, Daniela and Akyuz, Mehmet Deniz and Nowak, Michael and Erkel, Martin and Wolf, J\"{u}rgen and B\"{u}ttner, Reinhard and Schumacher, Bj\"{o}rn and Thomale, J\"{u}rgen and Persigehl, Thorsten and Maintz, David and Perner, Sven and Reinhardt, Hans Christian}, year = {2016}, pages = {1110-1123}, DOI = {10.1158/1541-7786.MCR-16-0094}, keywords = {Ercc1, TP53, lung adenocarcinoma, cisplatin}, journal = {Molecular cancer research}, doi = {10.1158/1541-7786.MCR-16-0094}, volume = {14}, number = {11}, issn = {1541-7786}, title = {Ercc1 Deficiency Promotes Tumorigenesis and Increases Cisplatin Sensitivity in a TP53 Context-specific Manner}, keyword = {Ercc1, TP53, lung adenocarcinoma, cisplatin} }
@article{article, author = {Joki\'{c}, Mladen and Vla\v{s}i\'{c}, Ignacija and Rinneburger, Miriam and Kl\"{u}mper, Niklas and Spiro, Judith and Vogel, Wenzel and Offermann, Anne and K\"{u}mpers, Christiane and Fritz, Christian and Schmitt, Anna and Riabinska, Arina and Wittersheim, Maike and Michels, Sebastian and Ozreti\'{c}, Luka and Florin, Alexandra and Welcker, Daniela and Akyuz, Mehmet Deniz and Nowak, Michael and Erkel, Martin and Wolf, J\"{u}rgen and B\"{u}ttner, Reinhard and Schumacher, Bj\"{o}rn and Thomale, J\"{u}rgen and Persigehl, Thorsten and Maintz, David and Perner, Sven and Reinhardt, Hans Christian}, year = {2016}, pages = {1110-1123}, DOI = {10.1158/1541-7786.MCR-16-0094}, keywords = {Ercc1, TP53, lung adenocarcinoma, cisplatin}, journal = {Molecular cancer research}, doi = {10.1158/1541-7786.MCR-16-0094}, volume = {14}, number = {11}, issn = {1541-7786}, title = {Ercc1 Deficiency Promotes Tumorigenesis and Increases Cisplatin Sensitivity in a TP53 Context-specific Manner}, keyword = {Ercc1, TP53, lung adenocarcinoma, cisplatin} }

Časopis indeksira:


  • Current Contents Connect (CCC)
  • Web of Science Core Collection (WoSCC)
    • Science Citation Index Expanded (SCI-EXP)
    • SCI-EXP, SSCI i/ili A&HCI
  • Scopus
  • MEDLINE

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