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)

Intraductal mucin-hypersecreting neoplasm of the pancreas (IMHN) is a unique tumor that is composed of tumor cells with different cell atypia. K-ras and p53 alterations have been shown to occur in pancreatic duct cell carcinoma (PDC), but they have not been well documented in the individual lesion of IMHN. The aim of this study was to examine the relation of the genetic alterations of K-ras and p53 in IMHN to the tumorigenesis of the pancreas. In 32 microscopically dissected lesions of seven cases of IMHN, the K-ras mutation was investigated by primer-mediated, mutant-enriched, polymerase chain reaction-restriction fragment length polymorphism. Mutant p53 expression was examined in the adjacent serial sections by immunohistochemistry. In IMHN, alterations of K-ras and p53 were frequently observed (71.9 and 50%, respectively). The frequency became higher as the grade of cell atypia increased. Simultaneous alterations of the two genes were detected in carcinoma and its accompanying hyperplastic and dysplastic lesions. It is suggested that alterations of K-ras and p53 may be early events in the tumorigenesis of IMHN and may cooperate to produce neoplastic transformation of the pancreatic duct epithelium.
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PMID:K-ras mutation and p53 protein accumulation in intraductal mucin-hypersecreting neoplasms of the pancreas. 874 Apr 3

In a comparative study, the expression of p53 protein was investigated in intestinal- and gastric-type adenomas of the stomach. The former is a conventional type, which is well known to be a premalignant lesion of the stomach, but the latter is a rare, more recently noted entity. Of 28 intestinal-type adenomas, 17 (60.7%) contained more than 5% of p53 immunoreactive cells. In these adenomas, the extent of positivity for p53 protein was significantly higher in high-grade dysplasia than in low-grade dysplasia (P < 0.05), suggesting that p53 alteration plays a part in the dysplastic progression of intestinal-type adenomas. Among 18 gastric-type adenomas in which most of the tumour cells displayed gastric-type mucin, substantial expression of p53 protein was found only in the 3 tumours with high-grade dysplasia. Thus, the incidence of p53 expression was significantly higher in intestinal-type adenomas than in gastric-type adenomas (P < 0.01). These results suggest that p53 gene alteration is an earlier event in the gastric carcinogenetic sequence with the intestinal phenotype than in that with the gastric phenotype.
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PMID:Differential p53 protein expression in stomach adenomas of gastric and intestinal phenotypes: possible sequences of p53 alteration in stomach carcinogenesis. 876 30

The detection and elimination of minimal systemic disease in patients with solid tumors is one of the main current topics in clinical oncology. The present review focuses, therefore, on new diagnostic approaches to identify minimal disease in peripheral blood, bone marrow, and lymph nodes of patients with epithelial cancer as the major type of solid tumors in Western industrialized countries. These approaches may be used to improve tumor staging and monitoring of adjuvant therapies, as well as to detect tumor cell contamination in autologous stem cell grafts. Most investigators have developed either immunocytochemical assays with monoclonal antibodies to a variety of epithelial-specific cytoskeleton and membrane antigens or molecular methods based on the extensive amplification of a specific (c)DNA sequence by the polymerase-chain reaction (PCR). In immunocytochemical assays, antibodies to cytokeratins can be regarded as the most specific and sensitive probes to detect isolated epithelial tumor cells in bone marrow and blood. Molecular methods are based on the detection of either mutations in oncogenes and tumor suppressor genes (e.g., ki-ras and p53 genes) or the mRNA expression of tissue-specific and tumor-associated genes. mRNA species targeted in these assays encode cytokeratins, prostate-specific antigen, prostate-specific membrane antigen, carcinoembryonic antigen, and polymorphic-epithelial mucin. To introduce the available methods into clinical practice, standardized protocols need to be developed and validated in multi-center studies.
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PMID:Detection of minimal disease in patients with solid tumors. 887 11

A case of adenocarcinoma of the renal pelvis is presented. The patient was an 84-year-old man suffering from long-standing right-sided nephrolithiasis. Surgical resection of the right kidney revealed adenocarcinoma with slight stromal invasion. A tubulovillous adenoma, which was morphologically similar to an adenoma of the large intestine, was also found adjacent to the adenocarcinoma. The pelvic epithelium neighboring the lesion revealed intestinal metaplasia. Histochemical studies revealed that the tumor in the patient and adenocarcinomas or adenomas of the large intestine have similar properties of cytoplasmic mucin. These findings suggest that the epithelium with intestinal metaplasia may have developed into the adenoma and finally transformed into the adenocarcinoma. In addition, only tumor cells with severe atypia, most of which morphologically corresponded to adenocarcinoma, demonstrated positive nuclear staining for anti-p53. This suggests that p53 may play an important role in the malignant transformation of adenomas into adenocarcinomas, as is the case in the large intestine.
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PMID:Primary adenocarcinoma of the renal pelvis with special reference to histochemical observations. 891 51

Given the plethora of well-documented breast carcinoma-associated antigens in humans including MAGE-1, -2 and -3, mutated p53, p21ras, HER-2/neu and DF3/MUC-1, coupled with evidence that humoral and cytotoxic T-cell responses against these antigens exist, the central dilemma facing tumor immunologists is why the host immune response is so inefficient. One possibility is that tumor cells themselves are either inefficient or ineffective antigen-presenting cells (APCs). The failure of tumor cells to function as APCs may be due to their inability to process and present the antigen, the absence or insufficient numbers of adhesion and costimulatory molecules or, potentially, the secretion of inhibitory cytokines. Therefore, we sought to determine whether human breast cancer cell lines could function as APCs and, if not, to identify mechanism(s) responsible for this defect. Here, we show that human breast cancer cell lines fail to present alloantigen. This defect does not reside in their inherent capacity to present antigen but rather is due to apoptosis of activated T cells induced by exposure to the breast carcinoma-associated mucin antigen, DF3/MUC1. These results support the hypothesis that DF3/MUC1 may contribute to the paucity of clinically significant anticarcinoma-specific immune responses.
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PMID:Breast cancer-associated antigen, DF3/MUC1, induces apoptosis of activated human T cells. 894 37

Microglandular adenocarcinoma of the endometrium may cause diagnostic problems because of its bland cytologic appearance and its histologic similarity to benign microglandular hyperplasia of the cervix. We present two cases of microglandular adenocarcinoma and discuss the clinical, pathologic, and immunohistochemical findings. Both patients were postmenopausal women, one of whom was taking exogenous hormones. Endometrial biopsy specimens contained polypoid tissue fragments, within which were microcystic spaces lined by flattened, cuboidal, or columnar cells. Solid nests or sheets of tumor cells surrounded glands in some tissue fragments. The nuclei were uniform and bland, and mitotic figures, although readily identifiable, were infrequent (1 per 10 high-power fields). A majority of tumor cells contained intracytoplasmic mucin. Numerous neutrophils were present in gland lumens and tissues. Immunohistochemical stains for carcinoembryonic antigen and TAG72 (B72.3) revealed focal moderate to intense apical and cytoplasmic staining; immunostains for p53 protein were negative. One carcinoma was confined to the endometrium, whereas the other invaded into the inner one-third of the myometrium. Both patients were well after a limited follow-up of 1 year. Microglandular adenocarcinoma is a distinctive variant of endometrial carcinoma that is most likely a form of mucinous adenocarcinoma.
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PMID:Microglandular adenocarcinoma of the endometrium: a form of mucinous adenocarcinoma that may be confused with microglandular hyperplasia of the cervix. 898 33

Five cases of intraductal papillary-mucinous neoplasm (IPMN) of the pancreas are here described. This group of tumors represents a distinct clinicopathological entity with characteristic endoscopic, radiological, gross and microscopic appearances. Our five cases all showed marked dilatation of the main pancreatic duct which contained mucin and papillary tumor, sometimes filling and sometimes lining the lumen. The papillae were lined by columnar epithelium showing varying degrees of dysplasia. In one case there was adjacent invasive adenocarcinoma. Immunohistochemical staining for p53 protein was strongly positive in a majority of cells in the three cases with severe epithelial dysplasia and in the invasive adenocarcinoma, while weaker staining in a minority of cells was seen in the remaining two cases. A small proportion of tumor cells expressed PCNA and Ki-67 immunohistochemically in four cases, while the case with severe dysplasia and invasive carcinoma showed positivity for these proliferation markers in most cells. The four cases of exclusively intraductal tumor showed no evidence of disease recurrence at follow-up (median 55 months). The patient with IPMN and associated invasive adenocarcinoma died 21 months post-operatively. In view of its relatively favourable prognosis, it is important that IPMN is recognised.
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PMID:Intraductal papillary-mucinous neoplasm of the pancreas: a report of five cases with immunohistochemical findings. 909 70

Mucin production, when heavily sialylated, can promote cancer cell invasion and metastasis, and modulate the immune recognition system of the host. To explore the prognostic implication of sialomucin expression in lung cancer, we studied 116 patients with non-small-cell lung cancer (NSCLC). Tumor specimens were stained immunohistochemically with monoclonal antibodies (mAbs) against mucin glycoprotein (17Q2, HMFG2, SM3), and histochemically with periodic acid-Schiff/alcian blue to differentiate neutral mucin from acid mucin, and with high-iron diamine/alcian blue to differentiate sialomucin from sulfomucin. The expression status of two established molecular prognostic factors, the p53 and erbB-2 oncoproteins, were evaluated immunohistochemically. The staining was performed on two separately archived, paraffin-embedded tumor blocks for each patient, with normal lung as a control. Correlations were subsequently made among stains and various clinicopathologic factors. All analyses were blinded, and included Kaplan-Meier survival estimates with Cox proportional hazards regression modeling. Associations were established among adenocarcinoma histotype and erbB-2 overexpression, sialomucin expression, and 17Q2 and HMFG2 immunohistochemical positivity (p < 0.05). Sialomucin expression was closely linked to erbB-2 overexpression (p = 0.01). Significant univariate predictors (p < 0.05) of recurrence and cancer death were surgical stage, p53 expression, erbB-2 overexpression, and sialomucin expression. These four factors remained as independent predictors of early recurrence (p < 0.05) after multivariate analysis. For cancer death prediction, p53 and sialomucin expression had a marginal effect. We concluded that sialomucin expression is also a poor indicator of prognosis, which is associated with erbB-2 oncoprotein overexpression, early postoperative recurrence, and cancer death in NSCLC.
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PMID:Sialomucin expression is associated with erbB-2 oncoprotein overexpression, early recurrence, and cancer death in non-small-cell lung cancer. 910 88

Because patients with longstanding ulcerative colitis are at an increased risk for developing colorectal cancer, surveillance colonoscopy and colectomy for dysplasia or asymptomatic cancer is advised as a method of reducing cancer-related mortality. Generally, the use of dysplasia as a criterion for a positive test in cancer surveillance has performed poorly. The emerging field of colon cancer genetics has identified several important tumor markers that have the potential to improve sensitivity for the detection of early neoplasia. Specifically, p53 tumor suppressor gene mutations, aneuploidy, and mucin-associated sialosyl-Tn expression appear most promising for future use in surveillance programs.
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PMID:Cancer biology in ulcerative colitis and potential use in endoscopic surveillance. 917 46

To investigate the expression of a simple mucin-type carbohydrate antigen (Sialyl-Tn/STn) and its putative relationship with established or potentially useful clinico-pathologic prognostic parameters in breast cancer, we studied forty-six cases of invasive breast carcinoma in formalin-fixed, paraffin-embedded tissue sections. STn antigen was detected by the HB-STn antibody using an avidin-biotin-peroxidase method. The parameters studied were tumour size, histologic grade, nodal status, proliferative index (with MIB-1), ER expression, ploidy, c-erbB-2 and p53 expression. STn expression was observed in 18 cases (39%) of breast cancer. The expression of STn was associated with axillary node metastasis, ER negativity and c-erbB-2 expression. A tendency towards an association between STn immunoreactivity and high histologic grade was also found. No correlation was observed between STn immunoreactivity and age, tumour size, proliferative index, ploidy and p53 expression. We conclude that the detection of STn immunoreactivity may be useful for predicting the likelihood of lymph node metastasis and that the outcome of patients with breast cancer should be further investigated in order to find whether or not the data of the present study are confirmed in larger series.
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PMID:Expression of sialyl-Tn in breast cancer. Correlation with prognostic parameters. 918 86


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