Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P43146 (tumour suppressor)
 5,935 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Partial sequence determinations were performed on exon 8 of tumour suppressor gene p53 of cattle, sheep, goat, horse and pig. High sequence homology between these species and other species including dog, cat, chicken and man is demonstrated. A mutation CGG-->TGG (arginine-->tryptophan) was detected in a feline solid carcinoma of the mammary gland.
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PMID:Sequence of an exon of tumour suppressor p53 gene--a comparative study in domestic animals: mutation in a feline solid mammary carcinoma. 764 Sep 60

Ductal carcinoma in situ (DCIS) of the breast is commonly described as a premalignant lesion. Using PCR to amplify DNA from areas of tumour cells which have been microdissected from fixed material, we have studied the involvement of chromosome 1 in 19 cases of DCIS. A series of microsatellite repeat polymorphisms has been used to define regions of allelic imbalance and this has confirmed the involvement in DCIS of six of the regions previously implicated in studies of invasive breast tumours. This suggests that these regions may harbour tumour suppressor genes, the inactivation of which is important for the early stages of breast tumour development. Analysis of separate ducts from within the same tumour has revealed that the same genetic alterations are not necessarily present throughout the lesion. In addition we have found that in three cases where frank invasive carcinoma is also present, similar alterations can be detected in the in situ and invasive component.
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PMID:Frequent alterations of chromosome 1 in ductal carcinoma in situ of the breast. 773 21

This study investigates whether a reciprocal association occurs between HPV infection and somatic mutation of the tumour suppressor gene p53 in laryngeal carcinomas. Using immunohistochemical techniques, 87 tumours were examined for expression of the mutant form of p53 phosphoprotein using the monoclonal antibody PAB 1801. The prevalence of different HPV types in these tumours was determined by using the polymerase chain reaction and restriction enzyme analysis. Over-expression of p53 was noted in 50/87 (57.5%) of the tumours investigated but not in any of the non-neoplastic laryngeal mucosa (controls). There was no statistical correlation between p53 immunoreactivity and the clinicopathological parameters of laryngeal carcinomas. HPV DNA was detected in 8/36 (22.2%) of the tumours: HPV-6 in three, HPV-11 in one, HPV-16 in two, and unknown HPV type in two. In p53-mutant tumours, HPV was present in 4/20 tumours but none of these were high risk HPV types. In p53-normal tumours, on the other hand, HPV was present in 4/16 tumours but two of these were definitely high risk HPV-16. These results imply the reciprocal association between HPV and somatic mutations of p53 found in the case of cervical carcinoma.
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PMID:The prevalence of different human papillomavirus types and p53 mutations in laryngeal carcinomas: is there a reciprocal relationship? 778

The tumour suppressor gene p53 codes for a transcription factor which is thought to play a critical role in the induction of G1 cell cycle arrest and programmed cell death (apoptosis) following DNA damage by ionizing radiation. The aim of this investigation was to determine whether a p53 independent radiation-induced apoptosis pathway exists in human colon epithelial cell lines. This report describes the induction, by gamma-radiation, of apoptosis in the colorectal adenoma cell line S/RG/C2, and in the colorectal carcinoma cell line PC/JW, both of which lack wild type p53. In addition, flow cytometry revealed that both cell lines failed to arrest in G1 after radiation. Thus, although loss of wild type p53 may abrogate G1 arrest, radiation-induced apoptosis can still occur in human colonic tumour cell lines through a p53 independent mechanism.
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PMID:Gamma-radiation-induced apoptosis in human colorectal adenoma and carcinoma cell lines can occur in the absence of wild type p53. 778 88

From a human breast carcinoma cell line, HMT-3909, a tumorigenic and a non-tumorigenic subline have previously been described. Cells of both sublines have been characterised as carcinoma cells. In the present work we examined whether differences in growth factor requirements or oncogene expression may explain the difference in tumorigenicity. We found that exogenous growth factor dependence discriminated between the two sublines. No alterations in oncogenes or tumour suppressor genes were demonstrated that could explain the differences in tumorigenicity. The lower growth factor requirement and the higher growth rate of the tumorigenic subline indicates that, in these cells, growth potential may determine the outcome of the tumorigenicity assay.
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PMID:Growth factor requirement, oncogene expression and TP53 mutations of a tumorigenic and a non-tumorigenic subline of the human breast carcinoma cell line, HMT-3909. 778 3

p53 is a nuclear phosphoprotein which acts as a tumour suppressor factor, regulating cell growth and division. Mutations in the p53 gene appear to be the most common genetic alterations in human cancer. The aim of this study was to investigate p53 expression in laryngeal squamous cell carcinomas and to assess its role as a marker of prognostic significance. Using immunohistochemical staining techniques, a series of laryngeal carcinomas (n = 87) were examined for expression of the mutant form of p53 phosphoprotein using the monoclonal antibody PAB 1801. p53 over-expression was noted in 50 biopsies of laryngeal carcinomas (57.5%) but not in any of the non-neoplastic laryngeal mucosa which were used as the control. There was no statistical correlation between p53 immunoreactivity and the clinicopathological parameters of the cancers including: site of tumour, TNM staging, differentiation grading and tumour recurrence. These findings indicate that p53 expression is strongly associated with carcinoma cells and not with normal cells in the larynx. However, p53 expression is probably unrelated to the biological aggressiveness of these tumours.
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PMID:Over-expression of tumour suppressor gene p53 in laryngeal squamous cell carcinomas and its prognostic significance. 778 34

The series of genetic changes leading to malignancy in colorectal cancer is well reported. This includes mutational activation of the proto-oncogene Ki-ras and mutation/deletion of the p53 tumour suppressor gene. The frequency of these mutations was investigated in a panel of 52 colorectal cancer patients using a combination of immunocytochemistry and non-radioactive, digoxigenin-labelled in situ hybridisation. Sixty two per cent (32 of 52) of the study population were positive for p53 overexpression and 36% (19 of 52) positive for Ki-ras mutation. Twenty seven per cent (14 of 52) of the patients expressed both mutations. Mutation of either the p53 or the Ki-ras gene did not correlate with Dukes's stage, tumour differentiation or 5 year survival rate of the patients. Most of the rectal carcinoma specimens (11 of 15) showed p53 over-expression but the significance of this was not supported statistically. Thus detection of molecular changes is becoming more amenable to incorporation into routine histological carcinoma assessment because of the advent of non-radioactive labelling in in situ hybridisation and antibodies suitable for paraffin wax embedded specimens. The significance of these mutations in disease prognosis, however, remains questionable.
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PMID:Mutations of Ki-ras and p53 genes in colorectal cancer and their prognostic significance. 782 87

Although the aetiology of common skin cancer, basal cell carcinoma (BCC), is unknown, epidemiological findings suggest that, in addition to genetic predisposition, excessive exposure to UV-light, especially in the form of episodes of intensive sunburn, is a crucial aetiological factor. Biologically, BCC may vary from superficial, relatively benign tumours to aggressive infiltrating tumours. Hereditary BCC (Gorlin's syndrome) is most probably caused by inactivation of a tumour suppressor gene on chromosome 9q, and recent findings suggest that this gene may also be involved in common sporadic cases of BCC.
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PMID:[Basal cell cancer--current research sheds new light]. 789 23

Thyroid tumorigenesis is discussed in the context of the thyroid as a stable tissue, composed of differentiated cells, with a greater dissociation of control of growth from control of differentiation than is found in stem cell tissues. Experimental thyroid carcinogenesis regimes usually use mutagen exposure followed by induced growth. The normal thyroid follicle cell has a limited growth capacity, so loss of one tumour suppressor gene followed by growth-associated loss of heterozygosity would allow escape from this growth limitation, and the formation of a neoplastic clone. In man, there are two pathways of tumour formation, one through follicular adenoma to follicular carcinoma, and one to papillary carcinoma. These two pathways show differing aetiology, and differing oncogene involvement. In the follicular carcinoma pathway TSH-induced growth is relevant as it is in experimental animals. Mutagenesis is important for both papillary and follicular carcinomas. Radiation mutagenesis is of particular current importance because of the occurrence of thyroid carcinoma in children exposed to fallout from Chernobyl. The greater capacity for post-mutagen growth in children than adults is likely to explain the increased radiosensitivity of children, both to external and internal radiation.
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PMID:Thyroid tumorigenesis. 795 31

Mutations in the p53 tumour suppressor gene, with consequent accumulation of the p53 protein, are frequently observed in non-small cell lung cancer (NSCLC). Little is known, however, about the timing of their appearance or their maintenance through cancer progression and metastatic spread. We have examined the normal epithelium and a panel of bronchial lesions, including dysplastic, neoplastic, and metastatic lesions, for p53 immunoreactivity and for expression of proliferating cell nuclear antigen (PCNA). No p53 immunoreactivity was found in normal and hyperplastic epithelium, nor in squamous metaplastic lesions. Twenty out of 30 invasive tumours and 13 out of 17 in situ carcinomas adjacent to an invasive tumour showed p53 immunoreactivity. There was a strict correlation between the level of p53 expression in the non-invasive and the invasive components of the tumours. Five out of eight pairs of primary tumours and matching metastases expressed p53, at identical levels in both compartments. These data indicate that p53 overexpression can occur in the earliest recognized phase of NSCLC and that the alteration is maintained during progression from in situ to invasive carcinoma and metastatic spread. PCNA expression increased from early to advanced phases of NSCLC. High PCNA immunoreactivity was observed in tumours expressing high p53 levels. A significant association was observed for PCNA expression between preinvasive and invasive lesions.
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PMID:Human non-small cell lung cancer: p53 protein accumulation is an early event and persists during metastatic progression. 767 94


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