[HTML][HTML] mTOR signaling in cancer and mTOR inhibitors in solid tumor targeting therapy
T Tian, X Li, J Zhang - International journal of molecular sciences, 2019 - mdpi.com
The mammalian or mechanistic target of rapamycin (mTOR) pathway plays a crucial role in
regulation of cell survival, metabolism, growth and protein synthesis in response to upstream …
regulation of cell survival, metabolism, growth and protein synthesis in response to upstream …
mTOR signaling in disease
E Dazert, MN Hall - Current opinion in cell biology, 2011 - Elsevier
The target of rapamycin (TOR) is a highly conserved serine/threonine kinase and a central
controller of cell growth, metabolism and aging. Mammalian TOR (mTOR) is activated in …
controller of cell growth, metabolism and aging. Mammalian TOR (mTOR) is activated in …
LKB1 and KEAP1/NRF2 Pathways Cooperatively Promote Metabolic Reprogramming with Enhanced Glutamine Dependence in KRAS-Mutant Lung …
A Galan-Cobo, P Sitthideatphaiboon, X Qu, A Poteete… - Cancer research, 2019 - AACR
In KRAS-mutant lung adenocarcinoma, tumors with LKB1 loss (KL) are highly enriched for
concurrent KEAP1 mutations, which activate the KEAP1/NRF2 pathway (KLK). Here, we …
concurrent KEAP1 mutations, which activate the KEAP1/NRF2 pathway (KLK). Here, we …
Systematic RNA interference reveals that oncogenic KRAS-driven cancers require TBK1
The proto-oncogene KRAS is mutated in a wide array of human cancers, most of which are
aggressive and respond poorly to standard therapies. Although the identification of specific …
aggressive and respond poorly to standard therapies. Although the identification of specific …
[HTML][HTML] KrasG12D-induced IKK2/β/NF-κB activation by IL-1α and p62 feedforward loops is required for development of pancreatic ductal adenocarcinoma
J Ling, Y Kang, R Zhao, Q Xia, DF Lee, Z Chang, J Li… - Cancer cell, 2012 - cell.com
Constitutive Kras and NF-κB activation is identified as signature alterations in pancreatic
ductal adenocarcinoma (PDAC). However, how NF-κB is activated in PDAC is not yet …
ductal adenocarcinoma (PDAC). However, how NF-κB is activated in PDAC is not yet …
KRAS Mutation: Should We Test for It, and Does It Matter?
PJ Roberts, TE Stinchcombe - Journal of clinical oncology, 2013 - ascopubs.org
Lung cancer is the leading cause of cancer mortality in the United States and worldwide.
Previously, lung cancer was simplistically divided into non–small-cell lung cancer (NSCLC) …
Previously, lung cancer was simplistically divided into non–small-cell lung cancer (NSCLC) …
Targeted therapy in non-small-cell lung cancer—is it becoming a reality?
F Janku, DJ Stewart, R Kurzrock - Nature reviews Clinical oncology, 2010 - nature.com
Abstract Treatment outcomes in advanced or metastatic non-small-cell lung cancer (NSCLC)
remain unsatisfactory, with low long-term survival rates. Palliative chemotherapy offers a …
remain unsatisfactory, with low long-term survival rates. Palliative chemotherapy offers a …
Targeting the KRAS pathway in non-small cell lung cancer
P Tomasini, P Walia, C Labbe, K Jao… - The oncologist, 2016 - academic.oup.com
Lung cancer remains the leading cause of cancer-related deaths worldwide. However,
significant progress has been made individualizing therapy based on molecular aberrations …
significant progress has been made individualizing therapy based on molecular aberrations …
Mutant KRAS conversion of conventional T cells into regulatory T cells
S Zdanov, M Mandapathil, R Abu Eid… - Cancer immunology …, 2016 - AACR
Constitutive activation of the KRAS oncogene in human malignancies is associated with
aggressive tumor growth and poor prognosis. Similar to other oncogenes, KRAS acts in a …
aggressive tumor growth and poor prognosis. Similar to other oncogenes, KRAS acts in a …
Cellular senescence and the immune system in cancer
LI Prieto, DJ Baker - Gerontology, 2019 - karger.com
In response to a variety of cancer-inducing stresses, cells may engage a stable cell cycle
arrest mechanism, termed cellular senescence, to suppress the proliferation of preneoplastic …
arrest mechanism, termed cellular senescence, to suppress the proliferation of preneoplastic …