carcinogenesis/tyrosine

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The role of T-cell protein tyrosine phosphatase in epithelial carcinogenesis.

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T-cell protein tyrosine phosphatase (TC-PTP, encoded by PTPN2) is a nonreceptor PTP that is most highly expressed in hematopoietic tissues. TC-PTP modulates a variety of physiological functions including cell cycle progression, cell survival and proliferation, and hematopoiesis through tyrosine

Ron tyrosine kinase receptor regulates papilloma growth and malignant conversion in a murine model of skin carcinogenesis.

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Recent studies demonstrate that the receptor tyrosine kinase (TK) Ron is tumorigenic when overexpressed and plays a role in regulating skin homeostasis. We hypothesized that Ron signaling promotes skin carcinogenesis. To test this hypothesis, mice deficient in the TK domain of Ron (TK(-/-) mice)

Treatment of Wistar rats with a renal carcinogen, ferric nitrilotriacetate, causes DNA-protein cross-linking between thymine and tyrosine in their renal chromatin.

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Ferric nitrilotriacetate (Fe-NTA) induces renal proximal tubular damage associated with lipid peroxidation and oxidative DNA base modifications that finally leads to a high incidence of renal adenocarcinoma in rodents. In the present study, we report on the in vivo formation of DNA-protein

The repression and derepression of hepatic tyrosine aminotransferase by carcinogens.

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Like hydrocortisone, a single carcinogenic dose of dimethylnitrosamine (50 mg/kg) initiates the induction cycle for hepatic tyrosine aminotransferase in adrenalectomized rats. However, following this initial induction in the presence of dimethylnitrosamine, the enzyme becomes refractory to

Protein tyrosine kinase expression during the estrous cycle and carcinogenesis of the mammary gland.

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The susceptibility of the mammary epithelium to neoplastic transformation is linked to the exposure to estrogen during the estrous cycle. The effects of the estrous cycle on the mouse mammary gland have been investigated by analyzing 3H-thymidine incorporation, milk protein gene expression and DNA

The effect of carcinogens on the accumulation of tyrosine aminotransferase by foetal rat hepatocytes in culture.

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The hepatocarcinogen 3'-methyl-4-dimethyl-aminoazobenzene (MDAB) suppresses the accumulation of tyrosine aminotransferase in cultured foetal hepatocytes. Experiments involving liver derived from foetuses of various ages reveals that a response is only obtained with rats older than 16-day gestation.

Enhancement by tyrosine methyl ester of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

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The effect of tyrosine methyl ester (TME) on the incidence, number, and histological types of gastric cancers induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) was investigated in male Wistar rats. Rats were subcutaneously given TME, 512 mg/kg body weight, every other day after 20 weeks of oral

Characterization of the timing and prevalence of receptor tyrosine kinase expression changes in oesophageal carcinogenesis.

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Despite being common in epithelial malignancies, the timing of receptor tyrosine kinase (RTK) up-regulation is poorly understood and therefore hampers the identification of the receptor to target for effective treatment. We aimed to determine if RTK expression changes were early events in

Hormone-dependent nuclear localization of the tyrosine kinase iyk in the normal human breast epithelium and loss of expression during carcinogenesis.

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iyk, a member of the frk family of non-receptor tyrosine kinases, was originally isolated from normal mouse mammary glands and is characterized by a nuclear localizing signal within the SH2 domain. We have investigated the expression and subcellular localization of iyk in the normal human breast and

Modulating effect of amount and types of dietary fat on ornithine decarboxylase, tyrosine protein kinase and prostaglandins production during colon carcinogenesis in male F344 rats.

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Epidemiological and laboratory animal model studies suggest that the effect of dietary fat on colon carcinogenesis depends on the amount and its type. In the present study, we investigated the modulating effect of high-fat diets rich in omega-3, omega-6 and omega-9 fatty acids on liver, colon and

Implications of tyrosine phosphoproteomics in cervical carcinogenesis.

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BACKGROUND Worldwide cervical cancer remains a leading cause of mortality from gynecologic malignancies. The link between cervical cancer and persistent infection with HPV has been established. At a molecular level little is known about the transition from the precancerous state to invasive cancer.

Syk tyrosine kinase expression during multistep mammary carcinogenesis.

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OBJECTIVE To analyze the expression of Syk tyrosine kinase, recently implicated as a tumor suppressor in mammary carcinogenesis, during the multi step development of human breast carcinoma. METHODS Syk expression was examined in invasive carcinomas of the breast and in corresponding premalignant

Novel tyrosine phosphorylations accompany the activation of pp60c-src during chemical carcinogenesis.

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Treatment of normal Syrian hamster embryo (SHE) cells in vitro with various chemical carcinogens results in transformed preneoplastic cell lines. Continued passage of these preneoplastic cells gives rise to rare variant cells with enhanced capacity for tumorigenic growth. We have previously shown

Chemoprevention of 7,12-dimethylbenz[a]anthracene (DMBA)-induced oral carcinogenesis in hamster cheek pouch by topical application of a dual inhibitor of epidermal growth factor receptor (EGFR) and ErbB2 tyrosine kinases.

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Oral cancer is a common neoplasm worldwide with tobacco and alcohol being the major etiological factors contributing to its pathogenesis. Epidermal growth factor receptor (EGFR) and ErbB2 are known to be involved in the development of oral cancer with the former up-regulated in up to 90% human

Disruption of EphA2 receptor tyrosine kinase leads to increased susceptibility to carcinogenesis in mouse skin.

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EphA2 receptor tyrosine kinase is frequently overexpressed in different human cancers, suggesting that it may promote tumor development and progression. However, evidence also exists that EphA2 may possess antitumorigenic properties, raising a critical question on the role of EphA2 kinase in

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