Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UNIPROT:P04637 (p53)
77,613 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fine needle aspiration biopsy is an effective procedure for the diagnosis and biological characterization of carcinoma of the breast. The authors compared the immunocytochemical expression of oestrogen receptor and progesterone receptor, Ki67 antigen and p53 protein, evaluated in pre-surgical fine needle aspirates, with the immunohistochemical results observed in the corresponding histological sections. Fine needle aspirates and paraffin embedded sections obtained from 37 patients with primary carcinoma of the breast were studied by immunocytochemistry and immunohistochemistry, respectively. Percentage agreement between values obtained with cytology and histology was 89.6% for oestrogen receptor, 76.9% for progesterone receptor, 91.3% for Ki67 and 77.7% for p53. The data reported here suggest that the evaluation of biological parameters by fine needle aspiration biopsy may be useful to decide the best medical and surgical treatment for primary breast carcinoma.
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PMID:Primary breast carcinoma: immunocytochemical and immunohistochemical evaluation of biological parameters. 1119 98

CD31, an adhesion molecule expressed by endothelial cells, leukocytes, and platelets, is used in surgical pathology as a marker of normal and neoplastic vascularization. During the assessment of angiogenesis in breast carcinomas, CD31 expression was observed in a single case of large (5.2 cm diameter) high nuclear grade ductal carcinoma in situ (HG-DCIS) associated with poorly differentiated invasive ductal carcinoma (G3-IDC). Expression was limited to the cell membrane. This study focused on 32 HG-DCIS> or = 2 cm, either pure or associated with IDC. Cancer cells wereCD31(+) in 11 cases. Double staining using anti-CD31 monoclonal antibody (MAb) and anti-CD44 MAb, the anti-hyaluronate receptor, showed that foci of CD31(+) and CD44(-) tumour cells could be traced throughout the glandular tree, marking the intraductal diffusion of tumour up to Paget's cells at the nipple. The associated G3-IDC and their lymph node metastases were instead CD31(+) and CD44(+). CD31(+) tumours were oestrogen receptor (ER)(-), frequently p53(+) and c-erb-B2(+), and infiltrated by CD4(+) T lymphocytes. Normal and hyperplastic epithelia were constantly CD31(-). Other endothelial markers (e.g Factor VIII-RA and CD34) were not expressed by carcinoma cells, as was CD38, the CD31 ligand. In conclusion, CD31 expression is a feature acquired by breast cancer cells in the DCIS model. CD31 expression mainly correlates with tumour cells spreading within the ductal system. Finally, the invasive phenotype requires the co-expression of CD31 and CD44.
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PMID:Expression of CD31 by cells of extensive ductal in situ and invasive carcinomas of the breast. 1185 2

Chromosome 17p is among the most frequently deleted regions in a variety of human malignancies including breast cancer. This study has further refined the localization of a putative tumour suppressor gene (TSG) at 17p13 distal to the TP53 gene in breast carcinomas. It was found that 73% (37 of 51) of the breast tumours exhibited loss of heterozygosity (LOH) at one or more loci at 17p13. The allelic loss patterns of these tumours suggest the presence of at least seven commonly deleted regions on 17p13. The three most frequently deleted regions were mapped at chromosomal location 17p13.3-17p13.2 between the markers D17S831 and D17S1845 (56% LOH), at 17p13.1 between D17S1810 and D17S1832 (53% LOH), and at 17p13.1 between D17S938 and TP53 (55% LOH). A significant correlation was found between loss at 17p13 and tumour grade, size, proliferative activity, and oestrogen receptor (ER) status. Losses at 17p13 were seen more frequently in large and poorly differentiated tumours with high proliferative activity. These data support and extend previous reports on the presence of a putative TSG(s) at chromosomal region 17p13 distal to the TP53 gene and show that different subsets of LOH are associated with more aggressive tumour behaviour.
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PMID:Detailed deletion mapping in sporadic breast cancer at chromosomal region 17p13 distal to the TP53 gene: association with clinicopathological parameters. 1143 64

The association between tumour shrinkage and reduction in kinetic cell activity after primary chemotherapy in human breast cancer is still a matter of investigation. 157 patients with T2-4, N0-1, M0 breast cancer received primary chemotherapy consisting of either the CMF regimen + tamoxifen (the first consecutive 76 cases) or the single agent epirubicin (the subsequent 81). Ki67, p53, bcl2, c-erbB2 and steroid hormone receptors were evaluated immunohistochemically in tumour specimens obtained before chemotherapy and at surgery. Tumour shrinkage of >50% occurred in 72.4% of patients. Ki67 expression significantly decreased after chemotherapy; the reduction correlated with tumour response in both univariate (P < 0.005) and multivariate analysis (P = 0.02). p53, bcl-2, steroid hormone receptor and c-erbB2 immunostaining were scarcely affected. Baseline bcl2 (P = 0.04) and c-erbB2 (P = 0.02) were directly and inversely associated with the reduction in Ki67 immunostaining, respectively. Baseline p53 expression (P < 0.01) was directly related with Ki67 expression at residual tumour, whereas oestrogen receptor expression (P < 0.001) was inversely related. Ki67 at residual tumour was a better predictor for relapse-free survival (RFS) than baseline Ki67. Clinical response (P < 0.03), but not reduction in Ki67, was a significant independent predictor for disease recurrence. Chemotherapy was found to induce tumour shrinkage and to reduce the number of cells in the cell cycle, but its effect on tumour biology/aggressiveness was minimal. Reduction in Ki67 immunostaining correlated with clinical response but failed to be related to RFS. Ki67 expression at surgery rather than at baseline appears to be a better predictor for disease relapse.
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PMID:Relationship between tumour shrinkage and reduction in Ki67 expression after primary chemotherapy in human breast cancer. 1171 Aug 21

Known major mutations such as BRCA1/2 and TP53 only cause a small proportion of heritable breast cancers. Co-dominant genes of lower penetrance that regulate hormones have been thought responsible for most others. Incident breast cancer cases in the identical (monozygotic) twins of representative cases reflect the entire range of pertinent alleles, whether acting singly or in combination. Having reported the rate in twins and other relatives of cases to be high and nearly constant over age, we now examine the descriptive and histological characteristics of the concordant and discordant breast cancers occurring in 2310 affected pairs of monozygotic and fraternal (dizygotic) twins in relation to conventional expectations and hypotheses. Like other first-degree relatives, dizygotic co-twins of breast cancer cases are at higher than usual risk (standardised incidence ratio (SIR)=1.7, CI=1.1-2.6), but the additional cases among monozygotic co-twins of cases are much more numerous, both before and after menopause (SIR=4.4, CI=3.6-5.6), than the 100% genetic identity would predict. Monozygotic co-twin diagnoses following early proband cancers also occur more rapidly than expected (within 5 years, SIR=20.0, CI=7.5-53.3). Cases in concordant pairs represent heritable disease and are significantly more likely to be oestrogen receptor-positive than those of comparable age from discordant pairs. The increase in risk to the monozygotic co-twins of cases cannot be attributed to the common environment, to factors that cumulate with age, or to any aggregate of single autosomal dominant mutations. The genotype more plausibly consists of multiple co-existing susceptibility alleles acting through heightened susceptibility to hormones and/or defective tumour suppression. The resultant class of disease accounts for a larger proportion of all breast cancers than previously thought, with a rather high overall penetrance. Some of the biological characteristics differ from those of breast cancer generally.
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PMID:Heritable breast cancer in twins. 1217 98

Neoadjuvant/pre-surgical medical therapy of breast cancer provides a unique opportunity to derive biological information related to tumour response. Large clinical trials of neoadjuvant chemotherapy have established that pathological complete remission is an independent predictor of improved disease-free survival. Clinical response has been found to parallel substantial reductions in the proliferation of breast cancer cells. Increased apoptosis also occurs, but it is not closely associated with response. Numerous biological markers such as p53, bcl-2, oestrogen receptor (ER) and HER2 have been assessed for their possible role in chemoresistance/response, but the data are not clear at this stage. Continuing work using cDNA microarrays may yield new, more reliable indices of likely response and an improved insight into biological processes related to chemotherapeutic response.
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PMID:The biology of neoadjuvant chemotherapy for breast cancer. 1223 46

Two groups of patients were chosen from among 4,025 subjects examined in a breast screening program, one consisting of patients with stage I and the other of patients with stage IV breast cancer, characterized by neoplastic recurrence. In this comparison p53, HER and grading are of no direct help. We investigated receptor status at the time of the first operation and after complete surgical excision of the recurrence. The following variables were determined: oestrogen and progesterone receptor measures (ER, PR) in f.mol/ml, the 4 receptor phenotypes, the oestrogen-progesterone ratio and histological tumour grading in relation to oestrogen receptor positivity or negativity. Surgery consisted in quadrantectomy or total mastectomy, with axillary dissection or complete surgical excision of the recurrence. Adjuvant therapy was administered. The results show a different receptor percentage in recurrence compared to early breast cancer, which though not significant, indicates a reduced presence of ER+ PR+, ER- PR-, and an increase in the ER+PR- phenotype. Recurrence occurs more frequently when the lesion at the first operation is more advanced and if radiotherapy has not been included in the treatment. Histological grading shows a greater number of undifferentiated cells and a reduction in ER+ in recurrence, thus indicating a reduced target for the most widely used hormone treatments. The oestrogen-progesterone ratio is significantly increased (P < 0.01) in recurrence compared to stage I cancers. The cause of recurrence is a neoplastic embolism, often documented histologically. Recurrence does not necessarily mean a poor prognosis, because there is a survival rate after two years of 77% of the cases treated. These results obtained with widely used methods show the aggressiveness of some breast tumours, which can evolve and have a very poor prognosis even with the most complete therapy.
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PMID:The oestrogen-progesterone receptor ratio: an indicator of breast cancer evolution. 1223 50

The aim of this study was to evaluate the possible correlation between preoperative FDG-PET results in human breast cancer and the prognostic markers Ki-67, c- erb B2, p53, oestrogen/progesterone receptor status, axillary lymph node status, tumour size and tumour grading. Seventy-five female patients with breast cancer were included in this prospective study. Patient selection was independent of tumour size and the suspected clinical stage of disease. A high-resolution full-ring scanner (Siemens ECAT HR+) was used for PET imaging. The FDG uptake of breast tumours was calculated as the tumour to background ratio (TBR). In resected cancer tissue specimens, the proliferative fraction was evaluated by Ki-67 immunostaining. Additionally, immunostaining of the prognostic markers c-erb B2, p53, and progesterone and oestrogen receptors was performed. Haematoxylin and eosin-stained sections were used for tumour grading. Correlations between FDG uptake and prognostic markers were assumed to be significant at P<0.05 using the Mann-Whitney U test. In ductal breast cancer, mean TBR was 17.3 (median 7.7, range 1.6-122.7), while in lobular cancer it was 6.5 (median 3.7, range 1.4-22.7). Mean proliferative fraction (% Ki-67 positive tumour cells) was 15%+/-13.8% (median 10%, range 0%-60%). Twenty-three carcinomas showed <5% Ki-67 positive tumour cells. Statistical analysis indicated a positive correlation between FDG uptake and proliferative index in ductal breast cancer ( P<0.0001, r=0.63). By contrast, there was no correlation between FDG uptake and c- erb B2 ( P=0.79), p53 ( P=0.92), tumour grading ( P=0.09), oestrogen receptor status ( P=0.41), progesterone receptor status ( P=0.34), axillary lymph node status ( P=0.90) and tumour size ( P=0.3). It is concluded that FDG uptake is significantly higher in ductal breast cancer than in lobular cancer ( P<0.05). FDG uptake correlates with proliferative activity assessed by Ki-67 immunostaining ( P<0.05). A significant correlation with the other prognostic markers, however, could not be demonstrated.
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PMID:FDG uptake in breast cancer: correlation with biological and clinical prognostic parameters. 1227 13

Pivotal genetic information has been derived for a host of rare genetic disorders, but progress has been much slower in relation to the common causes of female infertility. In this chapter, we shall illustrate the approaches being applied in elucidating conditions causing infertility that are inherited in a polygenic/multifactorial fashion. The task is to determine the number of genes responsible and their chromosomal location(s). The first approach is to use genome-wide quantitative linkage analysis, searching throughout the genome with no prior expectation that a given gene or chromosomal region is casually involved. A second approach is to search across the genome for altered gene expression, for example comparing endometriosis and normal (non-endometriosis)cells. The third approach is less indiscriminate and more focused, depending upon identifying specific candidate genes. Aromatase, calhedrin, oestrogen receptor, galactose-1-phosphate uridyl transferase (GALT) and tumour suppressor genes such as p53 are attractive candidate genes for endometriosis. Endometriosis, which has long been suspected to possess a familial tendency, has been subjected to genome-wide linkage analysis in Oxford, UK, where sib-pair analysis uses polymorphic DNA markers and fluorescence-based automated analysis. Several regions of exclusion have been found, but no linkages have so far been reported. A candidate gene approach focuses on the presence of chromosomal aberrations, the assumption being that endometriosis parallels neoplasia. At Baylor College of Medicine, we thus began by showing chromosome alterations involving trisomy 11, monosomy 16 and monosomy 17 in late-stage endometriosis. A loss of only the p53 tumour suppressor gene, rather than a loss (monosomy) of chromosome 17 per se, however, seems to be the pivotal event. A second representative polygenic/multifactorial disorder causing female infertility is polycystic ovarian syndrome. Both quantitative linkage analysis and candidate gene approaches are being pursued. In the far more commonly observed 'idiopathic' variety (non-adrenal polycystic ovarian syndrome and hirsutism), consensus has long existed that one or more dominant genes causes the condition. Although the mode of inheritance in 'essential' polycystic ovarian syndrome remains uncertain, dominant tendencies are clearly more pertinent than recessive ones. Genes for adrenal biosynthetic enzymes, insulin receptors, leptin and leptin receptors, follistatin, activin and inhibins are attractive candidates for polycystic ovarian disease. A linkage to 37 candidate genes was sought using affected sib-pair analysis and transmission/disequilibrium methods.
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PMID:Molecular approach to common causes of female infertility. 1247 48

Breast cancer is the most common cancer in women worldwide and its incidence is increasing. Oestrogens and mitogenic growth factors may play an important role in the development of breast cancer, whereas inhibitory growth factors may prevent the development of breast cancer. Only about 5 to 10% of cases of breast cancer are due to inheritance of mutations in the BRCA1 or BRCA2 tumour suppressor genes. Mutations in the p53 tumour suppressor gene are commonly found in sporadic breast cancers. Retinoic acid and carotenoids may play a protective role in breast cancer since they inhibit the growth of the oestrogen receptor-positive MCF-7 breast cancer cell line. The presence of oestrogen and progesterone receptors predicts the likelihood of benefit from hormonal therapy. Amplification of the c-erbB2 oncogene in breast cancers is associated with a poor prognosis. It is now apparent that there is a complex, productive cross-talk between oestrogen-directed and growth factor-directed pathways which are believed to markedly reinforce their individual cellular effects on growth and gene responses.
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PMID:Role of steroid hormones and growth factors in breast cancer. 1247 34


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