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https://www.readbyqxmd.com/read/28546520/-omic-approach-in-non-smoker-female-with-lung-squamous-cell-carcinoma-pinpoints-to-germline-susceptibility-and-personalized-medicine
#1
Margherita Baldassarri, Chiara Fallerini, Francesco Cetta, Marco Ghisalberti, Cristiana Bellan, Simone Furini, Ottavia Spiga, Sergio Crispino, Giuseppe Gotti, Francesca Ariani, Piero Paladini, Alessandra Renieri, Elisa Frullanti
Purpose: Lung cancer is strongly associated to tobacco smoking. However, global statistics estimate that in females the proportion of lung cancer cases that is unrelated to tobacco smoking reaches fifty percent, making questionable the etiology of the disease. Materials and Methods: A never-smoker female with primary EGFR/KRAS/ALK-negative squamous cell carcinoma of the lung and their normal sibs were subjected to a novel integrative "omic" approach using a pedigree-based model for discovering genetic factors leading to cancer in the absence of well-known environmental trigger...
May 26, 2017: Cancer Research and Treatment: Official Journal of Korean Cancer Association
https://www.readbyqxmd.com/read/28544061/survival-difference-according-to-mutation-status-in-a-prospective-cohort-study-of-australian-patients-with-metastatic-non-small-cell-lung-carcinoma-nsclc
#2
Lavinia Tan, Marliese Alexander, Ann Officer, Michael MacManus, Linda Mileshkin, Ross Jennens, Dishan Herath, Richard de Boer, Stephen B Fox, David Ball, Benjamin Solomon
BACKGROUND AND OBJECTIVE: Non-small cell lung cancer (NSCLC) is a heterogeneous disease comprising not only different histologic subtypes but also different molecular subtypes. Our objective is to describe the frequency of oncogenic drivers in patients with metastatic NSCLC, the proportion of patients tested and survival difference according to mutation status in a single-institution study. METHODS: Metastatic NSCLC patients enrolled onto a prospective Thoracic Malignancies Cohort (TMC) Study between July 2012 and August 2016 were selected...
May 24, 2017: Internal Medicine Journal
https://www.readbyqxmd.com/read/28539837/ezh2-acts-as-a-tumor-suppressor-in-kras-driven-lung-adenocarcinoma
#3
Yanxiao Wang, Ning Hou, Xuan Cheng, Jishuai Zhang, Xiaohong Tan, Chong Zhang, Yuling Tang, Yan Teng, Xiao Yang
Previous studies have suggested that enhancer zeste homolog 2 (Ezh2), a histone methyltransferase subunit of polycomb repressive complex 2 (PRC2), acts as an oncogene in lung adenocarcinoma (ADC) development. However, we found that in human lung ADC samples, deletion and mutations of EZH2 were also frequently present, with 14% of patients harboring loss-of-function EZH2 alterations. To explore the effect of Ezh2 loss on lung tumor formation, lung epithelial Ezh2 gene was deleted in Kras-driven lung ADC mouse model...
2017: International Journal of Biological Sciences
https://www.readbyqxmd.com/read/28538732/cps1-maintains-pyrimidine-pools-and-dna-synthesis-in-kras-lkb1-mutant-lung-cancer-cells
#4
Jiyeon Kim, Zeping Hu, Ling Cai, Kailong Li, Eunhee Choi, Brandon Faubert, Divya Bezwada, Jaime Rodriguez-Canales, Pamela Villalobos, Yu-Fen Lin, Min Ni, Kenneth E Huffman, Luc Girard, Lauren A Byers, Keziban Unsal-Kacmaz, Christopher G Peña, John V Heymach, Els Wauters, Johan Vansteenkiste, Diego H Castrillon, Benjamin P C Chen, Ignacio Wistuba, Diether Lambrechts, Jian Xu, John D Minna, Ralph J DeBerardinis
Metabolic reprogramming by oncogenic signals promotes cancer initiation and progression. The oncogene KRAS and tumour suppressor STK11, which encodes the kinase LKB1, regulate metabolism and are frequently mutated in non-small-cell lung cancer (NSCLC). Concurrent occurrence of oncogenic KRAS and loss of LKB1 (KL) in cells specifies aggressive oncological behaviour. Here we show that human KL cells and tumours share metabolomic signatures of perturbed nitrogen handling. KL cells express the urea cycle enzyme carbamoyl phosphate synthetase-1 (CPS1), which produces carbamoyl phosphate in the mitochondria from ammonia and bicarbonate, initiating nitrogen disposal...
May 24, 2017: Nature
https://www.readbyqxmd.com/read/28538213/prediction-of-egfr-and-kras-mutation-in-non-small-cell-lung-cancer-using-quantitative-18f-fdg-pet-ct-metrics
#5
Ryogo Minamimoto, Mehran Jamali, Olivier Gevaert, Sebastian Echegaray, Amanda Khuong, Chuong D Hoang, Joseph B Shrager, Sylvia K Plevritis, Daniel L Rubin, Ann N Leung, Sandy Napel, Andrew Quon
This study investigated the relationship between epidermal growth factor receptor (EGFR) and Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations in non-small-cell lung cancer (NSCLC) and quantitative FDG-PET/CT parameters including tumor heterogeneity. 131 patients with NSCLC underwent staging FDG-PET/CT followed by tumor resection and histopathological analysis that included testing for the EGFR and KRAS gene mutations. Patient and lesion characteristics, including smoking habits and FDG uptake parameters, were correlated to each gene mutation...
May 10, 2017: Oncotarget
https://www.readbyqxmd.com/read/28525386/prognostic-value-of-kras-mutation-in-advanced-non-small-cell-lung-cancer-treated-with-immune-checkpoint-inhibitors-a-metaanalysis-and-review
#6
Jung Han Kim, Hyeong Su Kim, Bum Jun Kim
Immune checkpoint inhibitors (ICIs) have emerged as a promising treatment option in the fight against advanced non-small-cell lung cancer (NSCLC). KRAS is the most frequently mutated oncogene in NSCLC. We performed this meta-analysis to investigate if KRAS mutation status affects survival benefits of ICIs in patients with advanced NSCLC. Electronic databases were searched for eligible studies. We included randomized trials with the data of overall survival stratified by KRAS mutation status. From 3 eligible studies, 138 patients with KRAS mutant NSCLC and 371 with KRAS wild-type tumor were included in the meta-analysis...
May 3, 2017: Oncotarget
https://www.readbyqxmd.com/read/28523147/micrornas-a-new-tool-in-the-complex-biology-of-kras-mutated-non-small-cell-lung-cancer
#7
EDITORIAL
Stéphane Renaud, Joseph Seitlinger, Gilbert Massard
No abstract text is available yet for this article.
April 2017: Journal of Thoracic Disease
https://www.readbyqxmd.com/read/28513466/non-small-cell-lung-cancer-mutations-targeted-and-combination-therapy
#8
Justyna Kutkowska, Irena Porębska, Andrzej Rapak
Year after year, a growing number of cases of non-small cell lung cancer (NSCLC), mostly caused by smoking, have been noted. Most patients die because of the late detection of cancer and tumor resistance to treatment with cytostatics. Treatment of patients with advanced NSCLC is impeded by the low sensitivity of the tumor to cytostatic agents and the co-existence of many diseases, which substrate is, like lung cancer, cigarette smoking. Along with the development of molecular biology, targeted therapy has started to be used, affecting specific signaling pathways involved in the processes of oncogenesis...
May 17, 2017: Postȩpy Higieny i Medycyny Doświadczalnej
https://www.readbyqxmd.com/read/28507793/composite-biomarkers-defined-by-multiparametric-immunofluorescence-analysis-identify-alk-positive-adenocarcinoma-as-a-potential-target-for-immunotherapy
#9
Hélène Roussel, Eléonore De Guillebon, Lucie Biard, Marion Mandavit, Laure Gibault, Elisabeth Fabre, Martine Antoine, Paul Hofman, Michèle Beau-Faller, Hélène Blons, Claire Danel, Françoise Le Pimpec Barthes, Alain Gey, Clémence Granier, Marie Wislez, Pierre Laurent-Puig, Stéphane Oudard, Patrick Bruneval, Cécile Badoual, Jacques Cadranel, Eric Tartour
Anaplastic lymphoma kinase (ALK) inhibitors have been successfully developed for non-small cell lung carcinoma (NSCLC) displaying chromosomal rearrangements of the ALK gene, but unfortunately resistance invariably occurs. Blockade of the PD-1-PD-L1/2 inhibitory pathway constitutes a breakthrough for the treatment of NSCLC. Some predictive biomarkers of clinical response to this therapy are starting to emerge, such as PD-L1 expression by tumor/stromal cells and infiltration by CD8(+) T cells expressing PD-1...
2017: Oncoimmunology
https://www.readbyqxmd.com/read/28504652/a-smap-in-the-face-for-cancer
#10
Shirish Shenolikar
Observed deficits in protein phosphatase 2A (PP2A) function in a variety of human cancers have stimulated drug discovery efforts aimed at restoring PP2A function to inhibit tumor growth. Work published by Sangodkar et al. in this issue of the JCI describes the characterization of orally available small molecule activators of PP2A (SMAPs). These SMAPs attenuated mitogenic signaling and triggered apoptosis in KRAS-mutant lung cancer cells and inhibited tumor growth in murine models. Tumors with mutations in the SMAP-binding site of the PP2A A subunit displayed resistance to SMAPs...
May 15, 2017: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/28504649/activation-of-tumor-suppressor-protein-pp2a-inhibits-kras-driven-tumor-growth
#11
Jaya Sangodkar, Abbey Perl, Rita Tohme, Janna Kiselar, David B Kastrinsky, Nilesh Zaware, Sudeh Izadmehr, Sahar Mazhar, Danica D Wiredja, Caitlin M O'Connor, Divya Hoon, Neil S Dhawan, Daniela Schlatzer, Shen Yao, Daniel Leonard, Alain C Borczuk, Giridharan Gokulrangan, Lifu Wang, Elena Svenson, Caroline C Farrington, Eric Yuan, Rita A Avelar, Agnes Stachnik, Blake Smith, Vickram Gidwani, Heather M Giannini, Daniel McQuaid, Kimberly McClinch, Zhizhi Wang, Alice C Levine, Rosalie C Sears, Edward Y Chen, Qiaonan Duan, Manish Datt, Shozeb Haider, Avi Ma'ayan, Analisa DiFeo, Neelesh Sharma, Matthew D Galsky, David L Brautigan, Yiannis A Ioannou, Wenqing Xu, Mark R Chance, Michael Ohlmeyer, Goutham Narla
Targeted cancer therapies, which act on specific cancer-associated molecular targets, are predominantly inhibitors of oncogenic kinases. While these drugs have achieved some clinical success, the inactivation of kinase signaling via stimulation of endogenous phosphatases has received minimal attention as an alternative targeted approach. Here, we have demonstrated that activation of the tumor suppressor protein phosphatase 2A (PP2A), a negative regulator of multiple oncogenic signaling proteins, is a promising therapeutic approach for the treatment of cancers...
May 15, 2017: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/28502721/met-exon-14-skipping-mutations-in-lung-adenocarcinoma-clinicopathologic-implications-and-prognostic-values
#12
Geun Dong Lee, Seung Eun Lee, Doo-Yi Oh, Dan-Bi Yu, Hae Min Jeong, Jooseok Kim, Sungyoul Hong, Hun Soon Jung, Ensel Oh, Ji-Young Song, Mi-Sook Lee, Mingi Kim, Kyungsoo Jung, Jhingook Kim, Young Kee Shin, Yoon-La Choi, Hyeong Ryul Kim
INTRODUCTION: Response to MET inhibitors in non-small cell lung cancer with MET exon 14 (METex14) skipping has fueled molecular screening efforts and search for optimal therapies. However, further work is needed to refine the clinicopathologic and prognostic implications of METex14 skipping METHODS: Among 795 East-Asian patients who underwent surgery for non-small cell lung cancer, we screened 45 patients with quintuple-negative (EGFR-/KRAS-/ALK-/ROS1-/RET-) lung adenocarcinomas using RT-PCR, and found 17 patients (37...
May 10, 2017: Journal of Thoracic Oncology
https://www.readbyqxmd.com/read/28492898/selumetinib-plus-docetaxel-compared-with-docetaxel-alone-and-progression-free-survival-in-patients-with-kras-mutant-advanced-non-small-cell-lung-cancer-the-select-1-randomized-clinical-trial
#13
Pasi A Jänne, Michel M van den Heuvel, Fabrice Barlesi, Manuel Cobo, Julien Mazieres, Lucio Crinò, Sergey Orlov, Fiona Blackhall, Juergen Wolf, Pilar Garrido, Artem Poltoratskiy, Gabriella Mariani, Dana Ghiorghiu, Elaine Kilgour, Paul Smith, Alexander Kohlmann, David J Carlile, David Lawrence, Karin Bowen, Johan Vansteenkiste
Importance: There are no specifically approved targeted therapies for the most common genomically defined subset of non-small cell lung cancer (NSCLC), KRAS-mutant lung cancer. Objective: To compare efficacy of the mitogen-activated protein kinase kinase (MEK) inhibitor selumetinib + docetaxel with docetaxel alone as a second-line therapy for advanced KRAS-mutant NSCLC. Design, Setting, and Participants: Multinational, randomized clinical trial conducted at 202 sites across 25 countries from October 2013 through January 2016...
May 9, 2017: JAMA: the Journal of the American Medical Association
https://www.readbyqxmd.com/read/28492885/treatment-of-kras-mutant-non-small-cell-lung-cancer-the-end-of-the-beginning-for-targeted-therapies
#14
Jacob Kaufman, Thomas E Stinchcombe
No abstract text is available yet for this article.
May 9, 2017: JAMA: the Journal of the American Medical Association
https://www.readbyqxmd.com/read/28490719/realities-of-kras-mutated-non-small-cell-lung-cancer
#15
Young Joo Min
No abstract text is available yet for this article.
May 2017: Korean Journal of Internal Medicine
https://www.readbyqxmd.com/read/28489822/traf2-and-otud7b-govern-a-ubiquitin-dependent-switch-that-regulates-mtorc2-signalling
#16
Bin Wang, Zuliang Jie, Donghyun Joo, Alban Ordureau, Pengda Liu, Wenjian Gan, Jianping Guo, Jinfang Zhang, Brian J North, Xiangpeng Dai, Xuhong Cheng, Xiuwu Bian, Lingqiang Zhang, J Wade Harper, Shao-Cong Sun, Wenyi Wei
The mechanistic target of rapamycin (mTOR) has a key role in the integration of various physiological stimuli to regulate several cell growth and metabolic pathways. mTOR primarily functions as a catalytic subunit in two structurally related but functionally distinct multi-component kinase complexes, mTOR complex 1 (mTORC1) and mTORC2 (refs 1, 2). Dysregulation of mTOR signalling is associated with a variety of human diseases, including metabolic disorders and cancer. Thus, both mTORC1 and mTORC2 kinase activity is tightly controlled in cells...
May 10, 2017: Nature
https://www.readbyqxmd.com/read/28484014/selective-targeting-of-point-mutated-kras-through-artificial-micrornas
#17
Mario Acunzo, Giulia Romano, Giovanni Nigita, Dario Veneziano, Luigi Fattore, Alessandro Laganà, Nicola Zanesi, Paolo Fadda, Matteo Fassan, Lara Rizzotto, Raleigh Kladney, Vincenzo Coppola, Carlo M Croce
Mutated protein-coding genes drive the molecular pathogenesis of many diseases, including cancer. Specifically, mutated KRAS is a documented driver for malignant transformation, occurring early during the pathogenesis of cancers such as lung and pancreatic adenocarcinomas. Therapeutically, the indiscriminate targeting of wild-type and point-mutated transcripts represents an important limitation. Here, we leveraged on the design of miRNA-like artificial molecules (amiRNAs) to specifically target point-mutated genes, such as KRAS, without affecting their wild-type counterparts...
May 8, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28483607/interleukin-17a-promotes-lung-tumor-progression-through-neutrophil-attraction-to-tumor-sites-and-mediating-resistance-to-pd-1-blockade
#18
Esra A Akbay, Shohei Koyama, Yan Liu, Ruben Dries, Lauren E Bufe, Michael Silkes, Md Maksudul Alam, Dillon M Magee, Robert Jones, Masahisa Jinushi, Meghana Kulkarni, Julian Carretero, Xiaoen Wang, Tiquella Warner-Hatten, Jillian D Cavanaugh, Akio Osa, Atsushi Kumanogoh, Gordon J Freeman, Mark M Awad, David C Christiani, Raphael Bueno, Peter S Hammerman, Glenn Dranoff, Kwok-Kin Wong
HYPOTHESIS: Proinflammatory cytokine Interleukin (IL)-17A (IL-17A) is overexpressed in a subset of patients with lung cancer. We hypothesized that IL-17A promotes a pro-tumorigenic inflammatory phenotype, and inhibits anti-tumor immune responses. EXPERIMENTAL DESIGN: We generated bi-transgenic mice expressing a conditional IL-17A allele along with conditional Kras(G12D) and performed immune phenotyping of mouse lungs, survival analysis, and treatment studies with antibodies either blocking PD-1 or IL6, or depleting neutrophils...
May 5, 2017: Journal of Thoracic Oncology
https://www.readbyqxmd.com/read/28475299/consistency-and-reproducibility-of-next-generation-sequencing-and-other-multigene-mutational-assays-a-worldwide-ring-trial-study-on-quantitative-cytological-molecular-reference-specimens
#19
Umberto Malapelle, Clara Mayo-de-Las-Casas, Miguel A Molina-Vila, Rafael Rosell, Spasenija Savic, Michel Bihl, Lukas Bubendorf, Manuel Salto-Tellez, Dario de Biase, Giovanni Tallini, David H Hwang, Lynette M Sholl, Rajyalakshmi Luthra, Birgit Weynand, Sara Vander Borght, Edoardo Missiaglia, Massimo Bongiovanni, Daniel Stieber, Philippe Vielh, Fernando Schmitt, Alessandra Rappa, Massimo Barberis, Francesco Pepe, Pasquale Pisapia, Nicola Serra, Elena Vigliar, Claudio Bellevicine, Matteo Fassan, Massimo Rugge, Carlos E de Andrea, Maria D Lozano, Fulvio Basolo, Gabriella Fontanini, Yuri E Nikiforov, Suzanne Kamel-Reid, Gilda da Cunha Santos, Marina N Nikiforova, Sinchita Roy-Chowdhuri, Giancarlo Troncone
BACKGROUND: Molecular testing of cytological lung cancer specimens includes, beyond epidermal growth factor receptor (EGFR), emerging predictive/prognostic genomic biomarkers such as Kirsten rat sarcoma viral oncogene homolog (KRAS), neuroblastoma RAS viral [v-ras] oncogene homolog (NRAS), B-Raf proto-oncogene, serine/threonine kinase (BRAF), and phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit α (PIK3CA). Next-generation sequencing (NGS) and other multigene mutational assays are suitable for cytological specimens, including smears...
May 5, 2017: Cancer
https://www.readbyqxmd.com/read/28472989/circulating-mutational-portrait-of-cancer-manifestation-of-aggressive-clonal-events-in-both-early-and-late-stages
#20
Meng Yang, Umit Topaloglu, W Jeffrey Petty, Matthew Pagni, Kristie L Foley, Stefan C Grant, Mac Robinson, Rhonda L Bitting, Alexandra Thomas, Angela T Alistar, Rodwige J Desnoyers, Michael Goodman, Carol Albright, Mercedes Porosnicu, Mihaela Vatca, Shadi A Qasem, Barry DeYoung, Ville Kytola, Matti Nykter, Kexin Chen, Edward A Levine, Edgar D Staren, Ralph B D'Agostino, Robin M Petro, William Blackstock, Bayard L Powell, Edward Abraham, Boris Pasche, Wei Zhang
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...
May 4, 2017: Journal of Hematology & Oncology
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