Association of Phosphorylated Epidermal Growth Factor Receptor with Survival in Patients with Locally Advanced Non-small Cell Lung Cancer Treated with Radiotherapy

Tsakiridis, Theodoros; Cutz, Jean‐Claude; Singh, Gurmit; Hirte, Hal W.; Okawara, Gordon; Corbett, Tom; Sur, Ranjan; Cai, Wenjie; Whelan, Timothy J.; Wright, James R.

doi:10.1097/jto.0b013e31817c6094

Cited by 18 publications

(19 citation statements)

References 21 publications

(29 reference statements)

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“…Tsakiridis et al have stated the presence of the activated membrane EGFR in NSCLC [78]. Hirish et al showed that the over expression occurred in 62% of NSCLCs [16].…”

Section: Resultsmentioning

confidence: 99%

“…For the first time we simultaneously analyze the mutation in both EGFR and PTEN and over-expression of PI3K, EGFR, Akt, STAT3 and Ras in NSCLC EGFR signaling in one study. Various studies have shown that EGFR signaling plays a very important role in NSCLCs [6], [7], [16]–[22], [68], [69], [78]–[81]. Since, EGFR signaling is crucial for cell survival and proliferation; it might be the main reason for tumor progression in NSCLC.…”

Section: Resultsmentioning

confidence: 99%

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Modeling of Tumor Progression in NSCLC and Intrinsic Resistance to TKI in Loss of PTEN Expression

2012

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EGFR signaling plays a very important role in NSCLC. It activates Ras/ERK, PI3K/Akt and STAT activation pathways. These are the main pathways for cell proliferation and survival. We have developed two mathematical models to relate to the different EGFR signaling in NSCLC and normal cells in the presence or absence of EGFR and PTEN mutations. The dynamics of downstream signaling pathways vary in the disease state and activation of some factors can be indicative of drug resistance. Our simulation denotes the effect of EGFR mutations and increased expression of certain factors in NSCLC EGFR signaling on each of the three pathways where levels of pERK, pSTAT and pAkt are increased. Over activation of ERK, Akt and STAT3 which are the main cell proliferation and survival factors act as promoting factors for tumor progression in NSCLC. In case of loss of PTEN, Akt activity level is considerably increased. Our simulation results show that in the presence of erlotinib, downstream factors i.e. pAkt, pSTAT3 and pERK are inhibited. However, in case of loss of PTEN expression in the presence of erlotinib, pAkt level would not decrease which demonstrates that these cells are resistant to erlotinib.

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“…Tsakiridis et al have stated the presence of the activated membrane EGFR in NSCLC [78]. Hirish et al showed that the over expression occurred in 62% of NSCLCs [16].…”

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Modeling of Tumor Progression in NSCLC and Intrinsic Resistance to TKI in Loss of PTEN Expression

2012

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“…To check if the Runx1 cKO skin responded differently at the molecular level to TPA treatment, we checked for expression of several selected markers previously reported to be regulated during tumorigenesis (2,60). The differentiation markers keratin 1, 5, and 15 and ␣6-integrin, Loricrin, and E-cadherin were expressed in both WT and cKO skin and revealed consistently lower stratification and expansion of the epidermis and the infundibulum in cKO skin (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…(Mice analyzed at 2 weeks of TPA treatment were not initiated with DMBA.) We checked for Runx1 expression, the progress of epidermal stratification and differentiation as shown by expression of several markers (previously described [60]), and the level of several well-known tumorigenic markers (1) (Fig. 12 and 13).…”

Section: Resultsmentioning

confidence: 99%

Runx1 Directly Promotes Proliferation of Hair Follicle Stem Cells and Epithelial Tumor Formation in Mouse Skin

Hoi

Lee

et al. 2010

Molecular and Cellular Biology

105

135

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Runx1/AML1 is a transcription factor implicated in tissue stem cell regulation and belongs to the small Runx family of cancer genes. In the hair follicle (HF), Runx1 epithelial deletion in morphogenesis impairs normal adult hair homeostasis (cycle) and blocks adult hair follicle stem cells (HFSCs) in quiescence. Here, we show that these effects are overcome later in adulthood. By deleting Runx1 after the end of morphogenesis, we demonstrate its direct role in promoting anagen onset and HFSC proliferation. Runx1 deletion resulted in cyclin-dependent kinase inhibitor Cdkn1a (p21) upregulation. Interfering with Runx1 function in cultured HFSCs impaired their proliferation and normal G 0 /G1 and G 1 /S cell cycle progression. The proliferation defect could be rescued by Runx1 readdition or by p21 deletion. Chemically induced skin tumorigenesis in mice turned on broad Runx1 expression in regions of the skin epithelium, papillomas, and squamous cell carcinomas. In addition, it revealed reduced rates of tumor formation in the absence of Runx1 that were accompanied by decreased epithelial levels of phospho-Stat3. Runx1 protein expression was similar in normal human and mouse hair cycles. We propose that Runx1 may act as a skin oncogene by directly promoting proliferation of the epithelial cells.

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“…27 Accumulating evidences indicate that c-Src-mediated phosphorylation of EGFR Tyr 845 is involved in regulation of receptor function, as well as in tumor progression. 28,29 Src is overexpressed in a high percentage of human neoplasms, including head and neck cancer, and its deregulation is identified as one of the major oncogenic signatures found in cancer. 30,31 Early studies on cells show that cells transiently expressing EGFR baring a Tyr to Phe mutation at Tyr 845 are impaired in their ability to synthesize DNA in response to of negative patients (Fig.…”

Section: Abstract: Egfr Oscc Phosphorylated Egfr Targeted Therapymentioning

confidence: 99%

pEGFR-Tyr 845 expression as prognostic factors in oral squamous cell carcinoma

Aquino

Pannone

Santoro

et al. 2012

Cancer Biology & Therapy

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Association of Phosphorylated Epidermal Growth Factor Receptor with Survival in Patients with Locally Advanced Non-small Cell Lung Cancer Treated with Radiotherapy

Cited by 18 publications

References 21 publications

Modeling of Tumor Progression in NSCLC and Intrinsic Resistance to TKI in Loss of PTEN Expression

Modeling of Tumor Progression in NSCLC and Intrinsic Resistance to TKI in Loss of PTEN Expression

Runx1 Directly Promotes Proliferation of Hair Follicle Stem Cells and Epithelial Tumor Formation in Mouse Skin

pEGFR-Tyr 845 expression as prognostic factors in oral squamous cell carcinoma

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