Abstract:
:Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs), such as gefitinib and erlotinib, are the first targeted therapy drugs approved for the treatment of advanced non-small-cell lung cancer (NSCLC). Interestingly, treatment with these small molecule, reversible EGFR-TKIs leads to more positive response rates in patients with adenocarcinoma, in females, Asians, and patients with no history of smoking. Positive responses to treatment in these populations may be due to the increased prevalence of mutations in the EGFR gene. Several distinct mutations in the EGFR gene have been identified in specimens from patients with NSCLC who responded to treatment with anilinoquinazoline EGFR inhibitors. However, despite the dramatic initial response to TKIs, most lung cancer patients relapse and subsequently become resistant to the drug, a process termed acquired resistance. The precise mechanisms underlying acquired resistance remain unclear. Resistance to EGFR-TKIs could result from several potential mechanisms, including development of a secondary mutation in EGFR (such as T790M), amplification of the MET receptor tyrosine kinase gene, or overexpression of other receptor tyrosine kinases.
journal_name
Cancer Biol Therjournal_title
Cancer biology & therapyauthors
Xu Y,Liu H,Chen J,Zhou Qdoi
10.4161/cbt.9.8.11881subject
Has Abstractpub_date
2010-04-15 00:00:00pages
572-82issue
8eissn
1538-4047issn
1555-8576pii
11881journal_volume
9pub_type
杂志文章,评审abstract::A right amount of oxygen and nutrients is essential for a tumor to develop. The role of oxygen dependent pathways and their regulators is therefore of utmost importance although little is known about the detailed impact they can have. Recently we have shown that inhibition of the oxygen sensor PHD2 in tumor cells bloc...
journal_title:Cancer biology & therapy
pub_type: 杂志文章
doi:10.4161/cbt.13.4.18830
更新日期:2012-02-15 00:00:00
abstract:INTRODUCTION:Malignant cells are capable of an unlimited number of cell divisions, either through production of telomerase, or through the alternate lengthening of telomere (ALT) mechanism. Yeast cells with genomic instability have been shown to survive in the absence of telomerase by increased recombination events. We...
journal_title:Cancer biology & therapy
pub_type: 杂志文章
doi:10.4161/cbt.3.12.1235
更新日期:2004-12-01 00:00:00
abstract::Ovarian cancer is a silent killer, and shows early extensive tumor invasion and peritoneal metastasis. The microcirculation of most tumors includes cooperation of pre-existing vessels, intussusceptive microvascular growth, postnatal vasculogenesis, glomeruloid angiogenesis and vasculogenic mimicry (VM). VM is critical...
journal_title:Cancer biology & therapy
pub_type: 杂志文章
doi:10.4161/cbt.7.5.5765
更新日期:2008-05-01 00:00:00
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journal_title:Cancer biology & therapy
pub_type: 杂志文章
doi:10.4161/cbt.12.12.18367
更新日期:2011-12-15 00:00:00
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journal_title:Cancer biology & therapy
pub_type: 杂志文章
doi:10.4161/cbt.4.12.2183
更新日期:2005-12-01 00:00:00
abstract::The mitochondrial production of reactive oxygen species has been implicated in the anticancer activity of furanonaphthoquinone. However, the mechanism of the activation remains elusive. In the current study, we found that treatment of HeLa cells with 2-methyl-5(or -8)-hydroxy-furanonaphthoquinone (FNQ13) induces mitoc...
journal_title:Cancer biology & therapy
pub_type: 杂志文章
doi:10.4161/cbt.5.11.3302
更新日期:2006-11-01 00:00:00
abstract::Hepatocellular carcinoma (HCC), characterized by a high rate of metastasis and recurrence after surgery, is caused by malignant proliferation of hepatocytes with epigenetic and/or genetic mutations. In particular, abnormal activation of the hepatocyte growth factor (HGF)-/c-mesenchymal-epithelial transition receptor (...
journal_title:Cancer biology & therapy
pub_type: 杂志文章
doi:10.1080/15384047.2019.1647051
更新日期:2019-01-01 00:00:00
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journal_title:Cancer biology & therapy
pub_type: 杂志文章
doi:10.4161/cbt.6.9.4546
更新日期:2007-09-01 00:00:00
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journal_title:Cancer biology & therapy
pub_type: 杂志文章
doi:10.4161/cbt.9.3.11143
更新日期:2010-02-01 00:00:00
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journal_title:Cancer biology & therapy
pub_type: 杂志文章,多中心研究
doi:10.4161/cbt.23625
更新日期:2013-04-01 00:00:00
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journal_title:Cancer biology & therapy
pub_type: 杂志文章,评审
doi:10.4161/cbt.2.4.448
更新日期:2003-07-01 00:00:00
abstract::Expression of the heparanase gene is associated with invasive, angiogenic and metastatic potential of diverse malignant tumors and cell lines. Here we used RNA interference strategies to evaluate the role of human heparanase in breast malignancy and to explore the therapeutic potential of its specific targeting. The s...
journal_title:Cancer biology & therapy
pub_type: 杂志文章
doi:10.4161/cbt.6.4.3888
更新日期:2007-04-01 00:00:00
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journal_title:Cancer biology & therapy
pub_type: 杂志文章,评审
doi:10.4161/cbt.9.1.10905
更新日期:2010-01-01 00:00:00
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journal_title:Cancer biology & therapy
pub_type: 杂志文章
doi:10.1080/15384047.2020.1806643
更新日期:2020-09-01 00:00:00
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journal_title:Cancer biology & therapy
pub_type: 杂志文章
doi:10.1080/15384047.2020.1779005
更新日期:2020-09-01 00:00:00
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journal_title:Cancer biology & therapy
pub_type: 杂志文章
doi:10.1080/15384047.2017.1345393
更新日期:2017-12-02 00:00:00
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journal_title:Cancer biology & therapy
pub_type: 杂志文章
doi:10.4161/cbt.1.1.35
更新日期:2002-01-01 00:00:00
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journal_title:Cancer biology & therapy
pub_type: 杂志文章
doi:10.1080/15384047.2016.1139266
更新日期:2016-04-02 00:00:00
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journal_title:Cancer biology & therapy
pub_type: 杂志文章
doi:10.4161/cbt.8.19.9650
更新日期:2009-10-01 00:00:00
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journal_title:Cancer biology & therapy
pub_type: 杂志文章
doi:10.4161/cbt.6.7.4340
更新日期:2007-07-01 00:00:00
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journal_title:Cancer biology & therapy
pub_type: 杂志文章
doi:10.4161/cbt.9.6.10894
更新日期:2010-03-15 00:00:00
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journal_title:Cancer biology & therapy
pub_type: 杂志文章
doi:10.4161/cbt.12.8.15978
更新日期:2011-10-15 00:00:00
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journal_title:Cancer biology & therapy
pub_type: 杂志文章
doi:10.4161/cbt.6.11.4852
更新日期:2007-11-01 00:00:00
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journal_title:Cancer biology & therapy
pub_type: 杂志文章
doi:10.1080/15384047.2018.1450113
更新日期:2018-08-03 00:00:00
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journal_title:Cancer biology & therapy
pub_type: 评论,杂志文章
doi:10.4161/cbt.5.6.2939
更新日期:2006-06-01 00:00:00
abstract::The chemotherapeutic agents doxorubicin (dox) or 5-fluorouracil (5FU) are used to treat cancer cells as they cause irreparable DNA damage, inducing these aberrant cells to undergo cell death. The mediator of this process is presumed to be in part the tumor suppressor p53 which regulates genes involved in DNA repair an...
journal_title:Cancer biology & therapy
pub_type: 杂志文章
doi:10.4161/cbt.29112
更新日期:2014-08-01 00:00:00
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journal_title:Cancer biology & therapy
pub_type: 杂志文章
doi:10.1080/15384047.2015.1046650
更新日期:2015-01-01 00:00:00
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journal_title:Cancer biology & therapy
pub_type: 杂志文章
doi:10.4161/cbt.1.1.41
更新日期:2002-01-01 00:00:00
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journal_title:Cancer biology & therapy
pub_type: 杂志文章
doi:10.4161/cbt.10.5.12533
更新日期:2010-09-01 00:00:00
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journal_title:Cancer biology & therapy
pub_type: 杂志文章
doi:10.1080/15384047.2015.1026507
更新日期:2015-01-01 00:00:00