Zobrazeno 1 - 10
of 16
pro vyhledávání: '"Raymond M. Paranal"'
Autor:
Hirokazu Kimura, Raymond M Paranal, Neha Nanda, Laura D Wood, James R Eshleman, Ralph H Hruban, Michael G Goggins, Alison P Klein, The Familial Pancreatic Cancer Genome Sequencing Project, Nicholas J Roberts
Publikováno v:
eLife, Vol 11 (2022)
Pathogenic germline CDKN2A variants are associated with an increased risk of pancreatic ductal adenocarcinoma (PDAC). CDKN2A variants of uncertain significance (VUSs) are reported in up to 4.3% of patients with PDAC and result in significant uncertai
Externí odkaz:
https://doaj.org/article/9d870a3f89c84fea8ab4363964ed5f55
Autor:
Pasi A. Jänne, Michael J. Eck, Geoffrey R. Oxnard, Magda Bahcall, Amanda J. Redig, Dalia Ercan, Antonio Calles, Atsuko Ogino, Jihyun Choi, Claire E. Repellin, Marzia Capelletti, Christine Lydon, Hideki Endoh, Raymond M. Paranal, Junko Tanizaki, Takayuki Kosaka
Supplemental Table 1.
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::3b5e626b1ac775abd73df8a4c49b8e41
https://doi.org/10.1158/0008-5472.22413624.v1
https://doi.org/10.1158/0008-5472.22413624.v1
Autor:
Pasi A. Jänne, Michael J. Eck, Geoffrey R. Oxnard, Magda Bahcall, Amanda J. Redig, Dalia Ercan, Antonio Calles, Atsuko Ogino, Jihyun Choi, Claire E. Repellin, Marzia Capelletti, Christine Lydon, Hideki Endoh, Raymond M. Paranal, Junko Tanizaki, Takayuki Kosaka
Figure S1. Fifty percent (50%) inhibitory concentration of neratinib, afatinib and dacomitinib in Ba/F3 cells expressing different EGFR or HER2 exon 20 insertion mutations and the EGFR exon 20 insertion patient derived cell lines. to second generatio
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::3ceaa64700eac137dd5c17fb2cb4e1a6
https://doi.org/10.1158/0008-5472.22413630
https://doi.org/10.1158/0008-5472.22413630
Autor:
Pasi A. Jänne, Michael J. Eck, Geoffrey R. Oxnard, Magda Bahcall, Amanda J. Redig, Dalia Ercan, Antonio Calles, Atsuko Ogino, Jihyun Choi, Claire E. Repellin, Marzia Capelletti, Christine Lydon, Hideki Endoh, Raymond M. Paranal, Junko Tanizaki, Takayuki Kosaka
Figure legends for all supplemental figures
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::01189ff230a53dd8340d35d803df423d
https://doi.org/10.1158/0008-5472.22413627.v1
https://doi.org/10.1158/0008-5472.22413627.v1
Autor:
Pasi A. Jänne, Michael J. Eck, Geoffrey R. Oxnard, Magda Bahcall, Amanda J. Redig, Dalia Ercan, Antonio Calles, Atsuko Ogino, Jihyun Choi, Claire E. Repellin, Marzia Capelletti, Christine Lydon, Hideki Endoh, Raymond M. Paranal, Junko Tanizaki, Takayuki Kosaka
Insertion mutations in EGFR and HER2 both occur at analogous positions in exon 20. Non–small cell lung cancer (NSCLC) patients with tumors harboring these mutations seldom achieve clinical responses to dacomitinib and afatinib, two covalent quinazo
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::8728e626a2c5528a5a479a0d8e3cea87
https://doi.org/10.1158/0008-5472.c.6508770.v1
https://doi.org/10.1158/0008-5472.c.6508770.v1
Publikováno v:
Cancer Research. 83:6511-6511
Pancreatic Ductal Adenocarcinoma (PDAC) is a lethal disease with a five-year survival rate of 11%. PDAC develops from pancreatic precursor lesions, including intraductal papillary mucinous neoplasm (IPMN); studying these lesions is important to under
Autor:
Pınar Özden, Eser, Raymond M, Paranal, Jieun, Son, Elena, Ivanova, Yanan, Kuang, Heidi M, Haikala, Ciric, To, Jeffrey J, Okoro, Kshiti H, Dholakia, Jihyun, Choi, Yoonji, Eum, Atsuko, Ogino, Pavlos, Missios, Dalia, Ercan, Man, Xu, Michael J, Poitras, Stephen, Wang, Kenneth, Ngo, Michael, Dills, Masahiko, Yanagita, Timothy, Lopez, Mika, Lin, Jeanelle, Tsai, Nicolas, Floch, Emily S, Chambers, Jennifer, Heng, Rana, Anjum, Alison D, Santucci, Kesi, Michael, Alwin G, Schuller, Darren, Cross, Paul D, Smith, Geoffrey R, Oxnard, David A, Barbie, Lynette M, Sholl, Magda, Bahcall, Sangeetha, Palakurthi, Prafulla C, Gokhale, Cloud P, Paweletz, George Q, Daley, Pasi A, Jänne
Publikováno v:
Science translational medicine
The clinical efficacy of epidermal growth factor receptor (EGFR)–targeted therapy in EGFR-mutant non–small cell lung cancer is limited by the development of drug resistance. One mechanism of EGFR inhibitor resistance occurs through amplification
Autor:
Emily S. Chambers, Alwin Schuller, Stephen Wang, Dalia Ercan, Mika Lin, Pınar Özden Eser, Raymond M. Paranal, Nicolas Floc'h, Sangeetha Palakurthi, Alison D. Santucci, Jeffrey J. Okoro, Geoffrey R. Oxnard, Man Xu, Kenneth H. Ngo, Jeanelle Tsai, Ciric To, Lynette M. Sholl, George Q. Daley, Michael Dills, Pavlos Missios, Kesi Michael, Paul D. Smith, Yoonji Eum, Magda Bahcall, Yanan Kuang, David A. Barbie, Masahiko Yanagita, Jennifer C. Heng, Rana Anjum, Prafulla C. Gokhale, Elena Ivanova, Jieun Son, Kshiti Dholakia, Heidi M. Haikala, Darren Cross, Jihyun Choi, Michael J. Poitras, Pasi A. Jänne, Timothy Lopez, Cloud P. Paweletz, Atsuko Ogino
Publikováno v:
Science Translational Medicine. 13
A subset of drug-resistant EGFR -mutant MET -amplified lung cancer switches oncogenic dependence to MET and is treatable with MET inhibitor monotherapy.
Autor:
Atsuko Ogino, T. Kosaka, Marzia Capelletti, Jihyun Choi, Hideki Endoh, Junko Tanizaki, Michael J. Eck, Dalia Ercan, Magda Bahcall, Raymond M. Paranal, Geoffrey R. Oxnard, Pasi A. Jänne, Amanda J. Redig, Antonio Calles, Claire E. Repellin, Christine A. Lydon
Publikováno v:
Cancer Research. 77:2712-2721
Insertion mutations in EGFR and HER2 both occur at analogous positions in exon 20. Non–small cell lung cancer (NSCLC) patients with tumors harboring these mutations seldom achieve clinical responses to dacomitinib and afatinib, two covalent quinazo
Autor:
Kenneth D. Westover, Raymond M. Paranal, David Santamaría, Chiara Ambrogio, Sudershan R. Gondi, Haiyun Wang, John C. Hunter, Shuai Li, Pasi A. Jänne, Cristina Caffarra, Roberto Chiarle, Jia Lu, Zhi Wei Zhou, Jiaqi Li, Jens Köhler, Marzia Capelletti, Qi Lv
Publikováno v:
Cell. 172(4)
The mechanism by which the wild-type KRAS allele imparts a growth inhibitory effect to oncogenic KRAS in various cancers, including lung adenocarcinoma (LUAD), is poorly understood. Here, using a genetically inducible model of KRAS loss of heterozygo