Factors Associated With P53 Nuclear Accumulation in Prostatic Adenocarcinoma

Zf, Zhang; Aprikian, Armen; As, Sarkis; Zeng, Zs; Pollack, Daphna; Cordon‐Cardo, Carlos; Wr, Fair; Cb, Begg

doi:10.3892/ijo.4.4.897

Cited by 3 publications

(4 citation statements)

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“…Carcinogens present in tobacco smoke cause DNA damage and may influence TP53 pathways in many human cancers. Associations between p53 mutation/overexpression and tobacco smoking have been observed in tumour sites where this mutation is an early occurrence in the progression to carcinoma such as lung (Suzuki et al, 1992;Miller et al, 1992), head and neck (Field et al, 1991(Field et al, , 1994, oesophagus (Hollstein et al, 1991b) (Zhang et al, 1994b). Zhang et al (1995b recently reported no obvious association between tobacco smoking and p53 nuclear expression in colorectal cancer.…”

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confidence: 99%

The relationship between smoking exposure and p53 overexpression in colorectal cancer

Freedman

Michalek²,

Marshall³

et al. 1996

Br J Cancer

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SummaryAlthough epidemiological studies of the relationship between cigarette smoking and colorectal cancer risk have been equivocal, a positive association is consistently found for colorectal adenoma development. We performed an epidemiological study to determine whether p53 protein overexpression, in tumours obtained at the time of resection, is associated with cigarette exposure in colorectal cancer. A total of 163 colorectal cancer cases and 326 healthy controls responded to a standardised questionnaire on colorectal cancer risk factors including detailed information on their history of cigarette smoking. All patients' tumours were analysed immunohistochemically for p53 overexpression using an avidin -biotin immunoperoxidase procedure and polyclonal anti-p53 antibody CM 1. Comparison of colorectal cases with controls revealed an elevated risk for ex-smokers (OR= 1.34, 95% CI 0.85 -2.12) and current smokers (OR= 1.13, 95% CI 0.63-2.02) when compared with non-smokers. No dose-response relationship was found for total pack-years of smoking (trend test: P=0.19). However, a trend for total pack -years of smoking was found when p53-positive cases were compared with p53-negative cases suggesting aetiological, heterogeneity (trend test: P = 0.06). Estimating the individual relative risk of developing a p53-positive tumour relative to controls showed no associations for smoking status or total pack -years of smoking. However, when p53-negative cases were compared with controls, an elevated risk was found for ex-smokers (OR= 1.84, 95% CI 1.00 -3.37) and current smokers (OR= 1.78, 95% CI 0.88-3.61). A significant trend of increasing risk was also found for total packyears of smoking (trend test: P =0.03). Colorectal tumours developing through p53-positive dependent pathways were not associated with smoking exposure. A significant increase in risk was observed for the p53-negative independent pathway with smoking. p53 overexpression appears to be associated with smoking exposure in colorectal cancer.

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confidence: 99%

The relationship between smoking exposure and p53 overexpression in colorectal cancer

Freedman

Michalek²,

Marshall³

et al. 1996

Br J Cancer

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“…The fact that p53 expression was a rare event occurring at a late stage in the tumorigenesis suggests that other mech anisms may be of greater importance in the development of prostate cancer and that p53 mutation is only one of several pathways in malignant progression. Zhang et al [45] proposed in a recent article that p53 expression might be related to the aging process in prostatic carcinomas as they found a significant correlation between p53 immu noreactivity and patient age in a series of 48 patients of whom 9 were immunopositive. However, in the present study the mean age for the p53-positive patients (n = 19) was 71 years and the mean age for the p53 negative patients (n = 167) was 73 years, thus contradicting the proposed hypothesis.…”

Section: Discussionmentioning

confidence: 99%

p53 Immunoreactivity as Prognostic Marker for Cancer-Specific Survival in Prostate Cancer

Stattin

Bergh²,

Karlberg³

et al. 1996

Eur Urol

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“…TP53 mutational spectra can point to particular leads in the aetiology and carcinogenesis of cancer (Harris, 1993 (Field et al, 1991;Brachman et al, 1992), oesophageal (Hollstein et al, 1991) and bladder cancers (Spruck et al, 1993;Zhang et al, 1994a). It has also been related to the ageing in prostatic adenocarcinoma (Zhang et al, 1994b) and associated with exposures to ultraviolet light in squamous cell carcinoma (Brash et al, 1991), and to aflatoxin exposure and hepatitis B virus (Hsu et al, 1993) in hepatocellular carcinomas.Recent reports reveal that TP53 mutations occur commonly (40-70%) in colorectal cancer (Darmon et al, 1994). Mutations of the TP53 gene have been observed in the progression of colonic polyps to colon cancer (Vogelstein et al, 1988;Fearon and Vogelstein, 1990 al., 1986).…”

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confidence: 99%

“…TP53 mutational spectra can point to particular leads in the aetiology and carcinogenesis of cancer (Harris, 1993 (Kondo et al, 1992;Miller et al, 1992;Suzuki et al, 1992), head and neck (Field et al, 1991;Brachman et al, 1992), oesophageal (Hollstein et al, 1991) and bladder cancers (Spruck et al, 1993;Zhang et al, 1994a). It has also been related to the ageing in prostatic adenocarcinoma (Zhang et al, 1994b) and associated with exposures to ultraviolet light in squamous cell carcinoma (Brash et al, 1991), and to aflatoxin exposure and hepatitis B virus (Hsu et al, 1993) in hepatocellular carcinomas.…”

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confidence: 99%

Family history of cancer, body weight, and p53 nuclear overexpression in Duke's C colorectal cancer

Zhang

Zs²,

As³

et al. 1995

Br J Cancer

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Summary To examine the hypothesis that colorectal carcinomas with and without TP53 mutations may be characterised by aetiological heterogeneity, we analysed a group of 107 patients with primary Dukes' C colorectal cancer seen at the Memorial Sloan-Kettering Cancer Center (MSKCC) from 1986 to 1990. We assessed p53 overexpression using the monoclonal antibody PAb 1801, and identified 42 (39%) patients displaying p53-positive phenotype, defined as >25% of positive cells. Patients with two or more first-degree relatives with cancer had an odds ratio (OR) of 2.9 (95% CI 1.0-8.3) for p53 overexpression in comparison with those without a family history of cancer (trend test, P = 0.11). A possible association between body weight and p53 overexpression was observed. The ORs were 1.9 for the second quartile, 1.9 for the third quartile and 3.4 for the highest quartile in comparison with the lowest quartile (trend test, P = 0.06). No association between occupational physical activity, smoking, drinking, parity and p53 overexpression was identified. The results suggest that p53 overexpression may be related to genetic predisposition to colorectal cancer, and p53-positive and p53-negative colorectal cancers may be controlled by different aetiological pathways.Keywords: body weight; colorectal neoplasms; family history; p53/protein; risk factors Colorectal cancer (CRC) is the second most common malignancy of both sexes in developed countries . A total of 394 000 deaths are estimated to occur annually for colorectal cancer, making it the third most important cause of cancer mortality in the world . It is also a major public health problem in the United States, with an estimated 149000 new cases diagnosed in 1994, including 107 000 of colon cancer and 42 000 of rectum cancer. The incidence ranks the third in males and the second in females in the United States (American Cancer Society, 1994). Epidemiological studies show that increased risk of colorectal cancer may be associated with both genetic and environmental factors (Potter et al., 1993). For the genetic component of CRC, two major types of CRC predisposition have been identified: familial adenomatous polyposis (FAP), which is believed to account for 1% of CRC cases, and hereditary non-polyposis colorectal cancer (HNPCC), which is considered to explain about 4-15% of CRC cases (Peltomaki et al., 1993 (Marks et al., 1991;Cunningham et al., 1992;Vahakangas et al., 1992;Dalbagni et al., 1993;Cordon-Cardo et al., 1994;Jacquemier et al., 1994). TP53 mutational spectra can point to particular leads in the aetiology and carcinogenesis of cancer (Harris, 1993 (Field et al., 1991;Brachman et al., 1992), oesophageal (Hollstein et al., 1991) and bladder cancers (Spruck et al., 1993;Zhang et al., 1994a). It has also been related to the ageing in prostatic adenocarcinoma (Zhang et al., 1994b) and associated with exposures to ultraviolet light in squamous cell carcinoma (Brash et al., 1991), and to aflatoxin exposure and hepatitis B virus (Hsu et al., 1993) in hepatocellular carcinomas...

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Factors Associated With P53 Nuclear Accumulation in Prostatic Adenocarcinoma

Cited by 3 publications

References 0 publications

The relationship between smoking exposure and p53 overexpression in colorectal cancer

The relationship between smoking exposure and p53 overexpression in colorectal cancer

p53 Immunoreactivity as Prognostic Marker for Cancer-Specific Survival in Prostate Cancer

Family history of cancer, body weight, and p53 nuclear overexpression in Duke's C colorectal cancer

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