Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:A9QXG9 (bcl-2)
 7,497 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The stomach is the most frequent site of extranodal lymphoma and primary gastric lymphoma might be distinguished from the nodal lymphoma by its different pathogenesis and prognosis. Based on the Isaacson's classification, clinico-pathologic reviews of 38 resected primary gastric lymphomas were done. Immunohistochemical stainings for PCNA, B and T cell markers, bcl-2 and p53 were performed. Eighteen were of low grade and 20 were of high grade. There were significant differences between low and high graders in the aspect of the size, depth of lesion, gross type, immunophenotype, staining intensity for PCNA, expressions of bcl-2 and p53. The overall 2-year survival rate was 85.3%. Factors with prognostic significance on survival by univariate analyses included immunophenotype, histologic grading and PCNA staining pattern. After multivariate analyses, immunophenotype proved to be a significant factor. We think that the histologic grading by Isaacson's classification and the immunohistochemical stainings performed were useful in pathologic and/or clinical aspects. The excellent survival rate in this study was partly due to the selection of resectable cases. However, earlier diagnosis and appropriate treatment might have contributed to the improved prognosis of gastric lymphoma in recent years.
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PMID:Primary malignant lymphomas of the stomach. Pathological and clinical analyses of 38 resected cases. 900 96

Human granulocytic ehrlichiosis (HGE) is an emerging and occasionally fatal human infectious disease whose pathogenesis is largely unknown. Goodman et al. (1) recently described the successful cultivation of the HGE infectious agent in human promyelocytic HL-60 leukemic cells. It was reported in the same study that infectivity invariably led to host cell death, although the mechanism by which HGE infection triggers cellular self-destruction is as yet undetermined. In this communication, we show that in vitro passage of HGE pathogen-infected blood elicits a significantly dysfunctional G1-to-S transition. Moreover, we provide evidence that the cytopathic properties of the HGE pathogen are attributed to its ability to induce apoptosis in host HL-60 cells. Determination of specific protein expression changes by Western blot analysis showed that HGE infection resulted in reduced expression of PCNA and pRB, both of which play a role in cell cycling. Moreover, the steady state level of bcl-2, which protects eukaryotic cells against apoptosis, is suppressed by exposure to the HGE agent. These results suggest that this pathogen HGE induces apoptosis in HL-60 cells by a mechanism involving the shut-off of multiple cell cycle and apoptosis regulatory events.
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PMID:Cellular changes and induction of apoptosis in human promyelocytic HL-60 cells infected with the agent of human granulocytic ehrlichiosis (HGE). 912 68

This study evaluated whether the increased risk of development of gastric carcinoma due to chronic Helicobacter pylori infection could be linked with elevated cell proliferative activity and expression of p53 and bcl-2. Forty-eight patients undergoing therapy for H pylori-positive gastroduodenal ulcers were separated into not eradicated (NE; n = 23) and eradicated (E; n = 25) groups 6 months after the treatment. Serum pepsinogen (PG) I:II ratios and histologic changes in the gastric corpus and the antrum, assessed according to the modified Sydney System, as well as epithelial cell proliferation (mitosis, Ki67, and proliferating cell nuclear antigen [PCNA]), and expression of oncoproteins (p53 and bcl-2) were examined before and at 3 months and 6 months after treatment for H pylori. Chronic persistent H pylori infection was associated with a low PG I:II ratio, increased inflammation and activity score, and elevated cell proliferation, as evidenced by the Ki67 and PCNA labeling indexes and the mitotic index in the NE group. Scattered accumulation of p53 protein continued to be observed in the NE group after treatment but was significantly decreased in the E group. We conclude that persistent H pylori infection causes gastritis, with epithelial degeneration and regeneration that result in accentuation of epithelial cell proliferation and accumulation of p53 protein, presumably heightening the genetic instability consistent with the development of carcinoma.
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PMID:Enhanced cellular proliferation and p53 accumulation in gastric mucosa chronically infected with Helicobacter pylori. 920 75

Prognostic factors in oligodendrogliomas are not well defined, even considering the labeling index of proliferation markers. As in other neuroepithelial tumors, the difficulty in calculating cell loss may contribute to this uncertainty. Proliferation markers Ki-67/MIB.1 and PCNA, mitoses, apoptotic nuclei, p53 and bcl-2 expression were investigated in 98 oligodendrogliomas. Apoptosis was assessed by the aspect of nuclei, by in situ end-labeling (ISEL) technique and by c-Jun immunohistochemical demonstration. The Bcl-2 also was immunohistochemically studied for its anti-apoptotic role. Mitotic index (MI), labeling index (LI) for MIB.1 and PCNA and apoptotic index (AI) were calculated and compared among themselves and with histology and survival. It was found that AI correlated with MI (p = 0.001) and was significantly higher in anaplastic than in classic oligodendrogliomas (p = 0.001). Apoptosis occurred only slightly more frequently in cases with high LIs for proliferation markers (MIB.1 and PCNA) (p = non-significant) and it was definitely higher in p53-positive cases (p = 0.008). It did not correlate with bcl-2 which was poorly expressed in oligodendrogliomas, with the exception of cells with astrocytic features. Apoptotic index correlated very weakly with survival (p = 0.05); therefore, it cannot be considered a highly reliable prognostic factor in oligodendrogliomas.
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PMID:Role of apoptosis in the prognosis of oligodendrogliomas. 922 Apr 57

Tissue homeostasis and the maintenance of cell populations depend on a delicate balance between the rates of cell proliferation and cell death. Programmed cell death or apoptosis is believed to play a major role in physiological processes which, when defective, could contribute to the pathogenesis and progression of tumors. A role for altered programmed cell death in cancer stems from the description of alterations on tumor-associated genes involved in the regulation of apoptosis such as p53 and bcl-2. The p53 gene promotes apoptosis in cells with genetic damage, while bcl-2 is an antiapoptotic gene. It is therefore possible that the balance between p53 and bcl-2 may have significant implications for the pathobiology of breast cancer. This study was therefore undertaken to evaluate the expression of these two proteins with opposite functions and their relation to the total growth fraction of the tumor as measured by PCNA immunoreactivity. A significant correlation was observed between expression of p53 and PCNA. In contrast, bcl-2 expression did not correlate with the expression of p53. There was also no correlation observed between expression of bcl-2 and PCNA. A significant correlation was observed between expression of p53 and the grade of the tumor and stage of the disease. Our results thus support the hypothesis that accumulation of p53 is associated with a high tumor proliferation rate, an association that might be expected in view of the role of wild-type p53 as a negative regulator of cell proliferation. Another important observation was the lack of relationship between bcl-2 expression and PCNA immunoreactivity, supporting the hypothesis that bcl-2 is not a major regulator of proliferation.
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PMID:Expression of the antiapoptotic protein bcl-2 is not dependent on the tumor suppressor p53 protein in Indian breast carcinoma. 925 35

An organotypic, tridimensional cell culture, also called a raft system, was used to study the influence of fibroblasts on epithelial carcinogenesis in a cell line derived from laryngeal squamous cell carcinoma and harboring a mutated p53. Differences between the effects of normal fibroblasts and those of tumor-derived fibroblasts were compared by means of fibroblasts taken from the normal skin and from the tumor of a cancer patient and cultivated with epithelial carcinoma cells in an organotypic culture. To study cell contact-mediated changes, the fibroblasts were either simply embedded in collagen matrix or additionally brought into direct contact with epithelial cells. Control epithelial cells were cultivated without any fibroblasts in an organotypic model. A protein panel [p53, p21, PCNA, bcl-2, Ki67, total cytokeratin (CK), CK 8, CK 10, CK 17, CK 18, CK 19, vimentin] involved in cell cycling and epithelial differentiation was assessed immunocytochemically in all organotypic cultures with fibroblasts, in tumor cells cultivated as a monolayer, and in the original tumor sample. The most dysplastic phenotype was obtained when tumor-derived fibroblasts were used in direct contact with epithelial cells, whereas the most benign phenotype was seen when skin fibroblasts had no contact with them. The intensive staining seen for p53 can be explained by p53 mutations also reflecting the weak expression of p21 and abundant expression of PCNA. The intensive Ki67 staining seen in all sections paralleled that of PCNA and marked active cellular proliferation. The CK staining pattern seen in cultured epithelia toward embryonic CKs, CK 8 and CK 18, suggested a simple epithelial phenotype. CK 19 was found only in the epithelium where no direct contacts had occurred. Vimentin expression increased when the raft epithelium was shifting toward a more benign phenotype. The results stress the importance of the origin of fibroblasts as well as the role of direct cellular contacts in modifying the epithelial phenotype even when the epithelial cells are malignant.
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PMID:Fibroblasts can modulate the phenotype of malignant epithelial cells in vitro. 928 67

Eighty patients with primary intraoral squamous cell carcinomas of the head and neck, with a follow-up of 4-14 years were analysed for clinical outcome in relation to immunohistochemical expression of PCNA, Ki-67, p53, bcl-2 and presence of mutations in the p53 gene. The tumor site was not associated with the different parameters calculated. PCNA and Ki-67 labelling showed median values of 56% and 32%, respectively, and neither antigen was of predictive value. Fifty-five percent of the tumours expressed p53, and 38 (48%) had mutations in the p53 gene. No association between the presence of p53 protein or mutations in the p53 gene and clinical outcome was found. Bcl-2 positivity was detected in a minor fraction (10%) of the tumours.
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PMID:PCNA, Ki-67, p53, bcl-2 and prognosis in intraoral squamous cell carcinoma of the head and neck. 931 25

We have demonstrated that induction of transgene expression in the v-Ha-ras-transgenic TG.AC mouse is a critical event in skin tumorigenesis and that cutaneous papillomas arise from follicular epidermis after treatment with chemical carcinogens. The sensitivity of TG.AC mice to skin tumorigenesis, coupled with their low incidence of spontaneous skin tumors, makes this strain a good model for identifying carcinogens and for investigating the roles that other genes may play in the development of skin neoplasia. To investigate the possible involvement of the bcl-2 gene in skin tumorigenesis in the TG.AC mouse, we crossed heterozygous bcl-2-knockout mice (C57BI/6, 129 background) with TG.AC mice (FVB/N background). Female mice were genotyped by using a neo cassette to identify bcl-2-deficient mice. In addition, homozygous TG.AC mice were bred with FVB/N mice to generate hemizygous TG.AC mice on an FVB/N background to serve as a gene-dosage control. The F1 progeny consisted of FVB/N(v-Ha-ras+/-):C57BI/6,129(bcl-2+/+),FVB/N(v-Ha-ra s+/-):C57BI/6,129(bcl-2+/-), and FVB/N(v-Ha-ras+/-,bcl-2+/+). Ten-week-old mice were dosed twice weekly for 10 wk with acetone, 1.25 microg of 7,12-tetradecanoylphorbol-13-acetate (TPA), or 2.5 microg of TPA, and papillomas were counted weekly. Papillomas were analyzed for ras transgene and bcl-2 expression by reverse transcription-polymerase chain reaction, v-Ha-ras expression by in situ hybridization, and proliferating cell nuclear antigen expression by immunohistochemical analysis. Fewer papillomas (P < 0.05) were observed at the low dose of TPA (1.25 microg) in mice carrying the bcl-2 knockout allele than in the wild-type mice, suggesting that reduction of the bcl-2 gene product affects the susceptibility of TG.AC mice to TPA-induced papillomas. However, at the high dose of TPA (2.5 microg), there was no difference in papilloma response between knockout and wild-type mice, regardless of strain background. This suggests that at the higher dose of TPA, the effect of reduction in bcl-2 gene product was obscured. These results support the hypothesis that bcl-2 plays a limited role in skin tumorigenesis in the TG.AC mouse.
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PMID:Decreases in phorbol ester-induced papilloma development in v-Ha-ras transgenic TG.AC mice during reduced gene dosage of bcl-2. 932 37

Disordered balance between proliferation and apoptosis may contribute to carcinogenesis. Thirty-two oral biopsies were collected prospectively: 10 normal (N), 10 leukoplakia (dysplasia, D = 5; hyperplasia, H = 5) and 12 squamous cell carcinoma (C: 11). Distant normal tissue was also collected (HN, DN, CN). Based on counts of 1000 cells/slide, mitotic (MI), apoptotic (AI) and proliferating cell nuclear antigen (PCNA: PI) indices were calculated and bcl-2 expression recorded. AI correlated with MI (P < 0.001), but not PI or bcl-2 expression. PCNA was higher in H and HN than other groups (P < 0.0001). bcl-2 was reduced in C and CN (P < 0.001). Peak mitosis shifted basally in dysplasia, whilst peak apoptosis remained unaltered. These data confirm topographical alterations in proliferation relative to apoptosis in dysplasia of the oral cavity. Reduced bcl-2 in carcinoma and related 'normal' epithelium was unexpected, and may contribute to the high incidence of metachronous carcinomas in these patients.
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PMID:Apoptosis, mitosis, PCNA and bcl-2 in normal, leukoplakic and malignant epithelia of the human oral cavity: prospective, in vivo study. 950 26

Gonadotropin-releasing hormone (GnRH) agonists are commonly used in the treatment of uterine leiomyomas, but little is known about their histological and cellular effects on these neoplasms. We examined a cellular proliferation index as determined by the nuclear antigen Ki-67 and proliferating cell nuclear antigen (PCNA) expression, estrogen receptor (ER), and progesterone receptor (PR) expression in 27 leiomyomas from patients treated with the GnRH agonist leuprolide acetate (LA) and compared them with 33 untreated controls. All leiomyomas were removed by myomectomies from premenopausal woman after 2 to 6 months of LA treatment or in the follicular phase of the menstrual cycle in the untreated controls. Histological features examined included cellularity, nuclear atypia, vascular changes (dilated, thickened, or thrombosed vessels), edema, calcification, hemorrhage, necrosis, hyalinization, and mitotic activity. Although no difference was found between GnRH-treated and nontreated groups with respect to most histological features examined, immunohistochemical studies showed a significant decrease in the cellular proliferation index, ER, and PR expression in the LA-treated cases compared with nontreated controls. The cellular proliferation index, ER, and PR expression decreased by 85%, 49%, and 36%, respectively, in the LA-treated group as compared with controls (P < .001). A subset of cases from the LA-treated and nontreated groups were also analyzed with respect to bcl-2 (an inhibitor of apoptosis) expression, and no significant difference between the LA-treated and nontreated groups was observed with both groups showing a strong (> 75% of cells) cytoplasmic staining pattern. Results of this study show that LA treatment of leiomyomas results in a decrease in number of cycling cells.
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PMID:Cellular proliferation, estrogen receptor, progesterone receptor, and bcl-2 expression in GnRH agonist-treated uterine leiomyomas. 956 85


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