Expression of oncoproteins in primary human non-small cell lung cancer and incidence of metastases

Volm, M; Drings, P.; Wodrich, W; G, van Kaick

doi:10.1007/bf00058052

Cited by 36 publications

(20 citation statements)

References 19 publications

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“…58 Following activation of PKC, the c-jun/c-fos heterodimer (AP-1) binds to the antioxidant response element (ARE) and enhances transcription of a variety of proteins. Overexpression of jun has been associated with lung cancer [59][60][61][62][63] and provides evidence of another mechanism through which inflammatory mechanisms contribute to a greater risk for cancer.…”

Section: Mechanisms Of Inflammation and Carcinogenesismentioning

confidence: 99%

“…In addition, the enhanced production of ROS increases the activation of molecular pathways, leading to enhanced DNA-binding of the oncogenes jun and fos. [54][55][56][57][58][59][60][61][62][63] Activation of jun/fos (AP-1) appears to lead to enhanced rates of cell proliferation by inhibiting expression of P21, leading to release from G2/M arrest and progression into mitosis. 73,74 P21 also binds to cyclin-dependent kinases responsible for inhibiting progression from G0 arrest into G1 as well as progression from G1 to S phase.…”

Section: (Continued)mentioning

confidence: 99%

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Inflammation as Cause for Scar Cancers of the Lung

Ardies

2003

Integr Cancer Ther

111

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The molecular and cellular basis of inflammation has become a topic of great interest of late because of the association between mechanisms of inflammation and risk for cancer. Inflammatory-mediated events, such as the production of reactive oxygen species (ROS), the activation of growth factors (for wound repair), and the altering of signaltransduction processes to activate cell-proliferation (to replace necrotic/apoptotic tissue cells), events that also can occur independently of inflammation, are all considered to be components of risk for a variety of cancers. Using scar cancer of the lung as an example, mechanisms of inflammation associated with recurring infections with Mycobacterium tuberculosis are discussed in the context that they may, in fact, be the major or sole cause of a cancer. Production of ROS, prostaglandins, leukotrienes, and cytokines in pulmonary tissues is greatly enhanced due to a cell-mediated immune response against macrophages infected with M. tuberculosis. These responses lead to the extensive fibrosis associated with recurring infections, possibly leading to decreased clearance of lymph and lymph-associated particles from the infected region. They also will enhance rates of cell division by inhibiting synthesis of P21, leading to enhanced progression from G0 arrest to G1 phase, from G1 to S phase, and from G2 to M phase of the cell cycle. By increasing rates of oxidative DNA damage and inhibiting apoptosis by enhancing synthesis of BCL-2, mutagenesis of progeny cells is enhanced, and these effects coupled with enhanced angiogenesis stimulated by COX-2 products lead to an environment that is highly conducive to tumorigenesis. Based on the evidence, it appears that but for an inflammatory response to recurring infections, some cases of scar cancer would not exist. By making appropriate lifestyle and dietary changes, a variety of anti-inflammatory effects can be produced, which should attenuate inflammation-induced risk for cancer.

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Section: Mechanisms Of Inflammation and Carcinogenesismentioning

confidence: 99%

Section: (Continued)mentioning

confidence: 99%

Inflammation as Cause for Scar Cancers of the Lung

Ardies

2003

Integr Cancer Ther

111

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“…12,18,19,[23][24][25] The procedures are summarized in Figure 2. Although the cells treated with Cytokeep retained strong p53 staining for as long as one month, the intensity of the staining gradually diminished and was almost lost within six months.…”

Section: Discussionmentioning

confidence: 99%

Freeze Substitution and Freeze Drying for Stable, Long-Term Preservation of Cytologic Specimens for Immunostaining

Takahashi¹,

Okuyama²,

Matsuo³

et al. 1996

Acta Cytologica

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“…Activation of c-myc has been associated with tumours of the breast (Watson et al, 1993), colon , ovary (Tashiro et al, 1992) and squamous cell carcinomas (Ogunbiyi et al, 1993). Significantly, c-myc gene activation has been correlated with poor clinical prognosis for aggressive tumours including bladder cancer (Kotake et al, 1990) and human non-small-cell lung carcinoma (Volm et al, 1993).…”

mentioning

confidence: 99%

Tumour cells surviving in vivo cisplatin chemotherapy display elevated c-myc expression

Walker

White²,

Esdale³

et al. 1996

Br J Cancer

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Summary The c-myc oncogene has been extensively implicated in cell proliferation, cell differentiation and programmed cell death. Aberrant expression of the c-myc gene product has been observed in a range of tumours and has also been implicated in cisplatin (cis-dichlorodiammineplatinum)-mediated chemoresistance. A solid transplantable tumour model in syngeneic DA rats was subjected to treatment with cisplatin to determine the impact of such therapy on endogenous c-myc gene expression. Serially

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Expression of oncoproteins in primary human non-small cell lung cancer and incidence of metastases

Cited by 36 publications

References 19 publications

Inflammation as Cause for Scar Cancers of the Lung

Inflammation as Cause for Scar Cancers of the Lung

Freeze Substitution and Freeze Drying for Stable, Long-Term Preservation of Cytologic Specimens for Immunostaining

Tumour cells surviving in vivo cisplatin chemotherapy display elevated c-myc expression

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