Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001418 (adenocarcinoma)
 68,496 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to investigate the role of tumor proliferation in patients with nonurachal bladder adenocarcinoma. Samples were obtained from 16 patients (12 men and 4 women, mean age 62 years) with primary nonrurachal bladder adenocarcinoma. The 16 formalin-fixed specimens were stained immunohistochemically for Ki-67 antigen and PCNA using MIB-1 and PC-10 antibodies. In addition, the AgNOR quantity was assessed using the colloid silver nitrate staining technique in all cases. The Ki-67, PCNA and AgNOR proliferation indices were found to be significantly higher in high-grade and invasive tumors. The higher the grade (p<0.01) and stage (p<0.01), the higher were the proliferation indices. Patients whose tumor samples had a high Ki-67, PCNA and AgNOR proliferation index showed a higher incidence of local recurrence (p<0.01) and distant metastasis (p<0.01). In conclusion, our results suggest that Ki-67, PCNA and AgNOR proliferation scores may be important prognostic indices in nonurachal bladder adenocarcinomas.
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PMID:The prognostic importance of the nucleolar organizer region (AgNOR), Ki-67 and proliferating cell nuclear antigen (PCNA) in primary nonurachal bladder adenocarcinoma. 1150 74

Non-small cell lung cancer is associated with approximately 85% mortality due to its high metastatic potential. Therapeutic efforts have failed to produce a significant improvement in prognosis. In this situation, a better understanding of the key factors of metastasis may be useful for designing new molecular targets of therapy. In order to identify these factors, we compared the expression profiles of two subpopulations of an adenocarcinoma cell line with a high metastatic potential, PC9/f9 and PC9/f14, with the parent cell line, PC9, using a cDNA array. The expression of 15 genes was found to be significantly enhanced or reduced in the highly metastatic subpopulations. The expression of matrix metalloproteinase-2 (MMP-2), plasminogen activator inhibitor-1 (PAI-1) and interleukin-1 (IL-1 alpha) were upregulated in the highly metastatic subpopulations, while the expression of carcinoembryonic antigen (CEA), caspase-5, Fas ligand, Prk/FNK, cyclin E, cyclin B1, Ki-67, proliferating cell nuclear antigen (PCNA), Smad4, macrophage proinflammatory human chemokine-3 alpha (MIP-3 alpha)/LARC, Met and CD44 were downregulated. Data from the literature suggest that the altered expression of MMP-2, PAI-1, IL-1 alpha, CEA, caspase-5, Fas ligand, Prk/FNK and Smad4 promotes the highly metastatic phenotype. The differential expression of these genes was confirmed by Northern blot analysis, standard reverse transcription-polymerase chain reaction (RT-PCR) and real-time quantitative RT-PCR. This analysis in subpopulations of a lung cancer cell line indicated that the highly metastatic potential of lung cancer may be induced not by an alteration in the expression of a single gene, but by the accumulation of alterations in the expression of several genes involved in extracellular matrix (ECM) adhesion disruption, ECM degradation, escape from apoptosis, and resistance to transforming growth factor-beta(1) (TGF-beta(1)). Strategies for inhibiting metastasis of pulmonary adenocarcinoma should be designed accordingly.
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PMID:Altered expression of several genes in highly metastatic subpopulations of a human pulmonary adenocarcinoma cell line. 1150 65

A histopathology study of 22 pancreatic adenocarcinoma cases revealed that 13 of the patients presented with hyperplastic lesions (atypical and non-atypical hyperplasia, mucous cell hypertrophy, focal epithelial hyperplasia, and ductal papillary hyperplasia), and 9 exhibited fibrosis adjacent to the carcinoma. All lesions expressed high levels of epidermal growth factor receptor (EGF-R) (p<0.0001 and p=0.0008, respectively) as compared with normal ductal epithelium. Non-atypical and atypical hyperplastic lesions also had a higher proliferating cell nuclear antigen (PCNA) labeling index (p<0.001 and p=0.0008, respectively) than normal ductal epithelium. A gradient in PCNA+ nuclei was found in acinar cells adjacent to the tumors. In 16 cases with marked fibrosis, we observed a significant increase of PCNA+ nuclei in stromal fibroblasts (p=0.0041) and significant upregulation of basic fibroblast growth factor (bFGF) mRNA expression in adjacent tumor cells (p=0.0213). These data suggest that the production of bFGF by pancreatic cancer cells induces ductal and stromal hyperplasia of the pancreas.
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PMID:Induction of ductal and stromal hyperplasia by basic fibroblast growth factor produced by human pancreatic carcinoma. 1156 41

To investigate the cell kinetics of human endometrial disorders immunolocation of PCNA (proliferating cell nuclear antigen) was performed in 69 specimens of normal, hyperplastic, or malignant endometrial tissue that had been fixed in formalin and embedded in paraffin. Immunoreactivity of PCNA was observed in all specimens examined. In the proliferative phase, PCNA positive cells were present in both the glands and stroma. In the secretory phase PCNA positive cells were seen principally in the stromal cells. A PCNA labeling index was obtained by counting one thousand cells per case. PCNA positivity in the proliferative phase was significantly higher than in the secretory phase (P < 0.01), but lower than in moderately differentiated (P < 0.01) or poorly differentiated (P < 0.05) adenocarcinoma. No significant differences in the PCNA labeling index were observed between hyperplasia and adenocarcinoma. These findings indicate that possible biologic differences between these proliferative endometrial lesions are probably not due to differences in cell proliferative activity, but rather to factors other than proliferation such as their ability to invade.
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PMID:Immunohistochemical study of PCNA (proliferating cell nuclear antigen) in normal and abnormal endometrium. 1157 32

Ten cases of gynecologic malignancies, including three endometrial, two ovarian and four cervical carcinomas, were studied for the expression of a 185 kDa protein (ErbB-2), coded by a proto-oncogene, c-erbB-2, in primary lesions as well as in metastatic lesions. Positive immunoreactivity was observed in all primary adenocarcinomas but not from squamous cell carcinomas. Many adenocarcinoma cells in distant metastatic sites or in tertiary lymph nodes were strongly stained for ErbB-2. These metastatic cells also showed an expression of proliferating cell nuclear antigen (PCNA). Detection of ErbB-2 mRNA by a reverse-transcription polymerase chain reaction showed that the transcription occurred exclusively in adenocarcinomas. To our knowledge, this is the first report demonstrating ErbB-2 expression in distant metastatic lesions of gynecologic cancers.
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PMID:ErbB-2, a c-erbB-2-coded protein, is expressed in metastatic cells of adenocarcinoma of endometrium, cervix and ovaries. 1157 13

Normal alveolar capillary endothelium is quiescent in nature and displays anticoagulant thrombomodulin (TM) on its surface. The cytoplasms of these endothelial cells are ultrastructurally non-fenestrated type, and they barely express von Willebrand factor (vWf). Alveolar fibrosis is accompanied by a capillary endothelium reactive for vWf, and a loss of TM expression. In primary lung adenocarcinoma, neovascularization occurs in association with alveolar fibrosis. In order to study basic factors related to angiogenesis and phenotypic changes of the capillaries located in tumor-bearing alveolar walls, we examined 37 primary lung adenocarcinomas with electron microscopy and confocal laser scanning microscopy with antibodies for TM, vWf, vascular endothelial growth factor (VEGF), and its receptors (KDR and Flt-1), and proliferating markers (Ki-67/proliferating cell nuclear antigen). Tissues microdissected specifically from alveolar walls were used for reverse transcription-polymerase chain reaction (RT-PCR) to assess expressions of mRNA isoforms of VEGF and its receptors. New capillary branching was found by ultrastructural study in the alveolar walls in 12% of the patients. Nuclei of the capillary endothelial cells were reactive for proliferating cell markers. Endothelial fenestrae were developed in 65% of the patients, TM reactivity was lost in the alveolar capillaries, and their cell cytoplasms obtained a reactivity for vWf through a transitional mosaic-like distribution pattern of both antigens. Besides cytoplasmic VEGF expression in neoplastic cells, tumor-bearing alveolar walls showed significant expression of mRNA of VEGF165 and KDR. These findings imply that angiogenesis and phenotypic changes of the alveolar capillaries are closely related to a higher expression of tumor-associated VEGF165 and of KDR in the alveolar walls in primary lung adenocarcinoma.
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PMID:Angiogenesis and phenotypic alteration of alveolar capillary endothelium in areas of neoplastic cell spread in primary lung adenocarcinoma. 1169 72

Recent evidence suggests that K-ras protooncogene protein p21 may have a tumor-suppressive role in the context of development of lung adenocarcinoma. Levels of K-ras p21, raf-1, mitogen-activated protein kinases Erk 1 and 2, the phosphorylated-activated forms of Erk 1 and 2 (Erk 1P and 2P), and proliferating cell nuclear antigen (PCNA) were measured by immunoblotting in mouse lung tumors (5 to 9 mm in size) caused by N-nitrosodimethylamine (NDMA) and in control lungs. In tumors compared with normal lung, cell membrane-associated K-ras p21 was significantly decreased and cytosolic K-ras p21 increased. Total, membrane, and cytosolic raf-1 and Erk 1P and 2P were increased in tumors compared with normal lung. A single dose of 5 nmol/kg 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) given after NDMA resulted in a significant 2.4-fold increase in tumor multiplicity. A significantly greater decrease in membrane-associated K-ras p21 and increase in total and membrane associated raf-1 occurred in the NDMA/TCDD tumors compared with the NDMA-only tumors. PCNA levels increased in tumors, a finding confirmed by immunohistochemistry, and correlated with tumor size after NDMA/TCDD treatment but not after NDMA only. The increase in raf-1 in the tumors was confirmed by immunohistochemistry, which also revealed an increase in raf-1-positive alveolar macrophages specifically associating with tumors from the earliest stages. These results suggest a possible tumor-suppressive function for K-ras p21 in lung and a positive role for raf-1 and Erk 1/2 in lung tumorigenesis. TCDD may promote tumors by contributing to downregulation of K-ras and stimulation of raf-1.
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PMID:Decrease in K-ras p21 and increase in Raf1 and activated Erk 1 and 2 in murine lung tumors initiated by N-nitrosodimethylamine and promoted by 2,3,7,8-tetrachlorodibenzo-p-dioxin. 1188 34

A 14-year-old female cougar died from gastroduodenal adenocarcinomas and rectal adenoma. At necropsy, polypoid tumor masses of various sizes were scattered on the mucosal surfaces of the stomach, duodenum, and rectum. Histologically, the gastric tumor was diagnosed as an intestinal type adenocarcinoma and the tumor cells metastasized to the mesenteric lymph nodes, spleen, and lung. Helicobacter-like organisms were detected in the lumina lined by foveolar epithelium. In the duodenum, the carcinoma cells were localized in the limina propria and many of them were intensely positive for proliferating cell nuclear antigen (PCNA). In contrast, the rectal adenoma had a lower number of PCNA-positive cells. In the rectum, chronic inflammation with numerous spirochetes was also noted. These results indicated that the occurrence of the gastrointestinal tumors might be associated with the bacterial infection described above.
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PMID:Gastroduodenal adenocarcinomas and rectal adenoma in a cougar (Felis concolor) infected with Helicobacter-like organisms and spirochetes. 1191 52

The modifying effects of dietary feeding of estrogenic compounds, 4-nonylphenol (4-NP) and genistein (GS), on 7,12-dimethylbenz[a]anthracene (DMBA)-induced ovarian carcinogenesis were investigated in female Sprague-Dawley rats. We also assessed the effects of test compounds on proliferating cell nuclear antigen (PCNA) index and the expression of estrogen receptor (ER)-alpha and -beta and androgen receptor (AR) in induced neoplasms. Rats were given a single injection of DMBA (0.01 ml of 0.5- DMBA suspended in olive oil) into their left ovary to induce ovarian neoplasms. They also received the experimental diet containing 25 to 250 ppm 4-NP or GS for 50 weeks, starting one week after the dosing of DMBA. DMBA exposure produced ovarian adenocarcinoma with an incidence of 35% at the end of the study (Week 51). Dietary administration of 4-NP or GS caused significant reduction in the incidence of ovarian adenocarcinoma: 86% reduction (P=0.0218) by feeding of 25 or 250 ppm 4-NP and 25 ppm GS, and 100% reduction (P=0.0042) by feeding of 250 ppm GS. The PCNA index in adenocarcinomas was higher than that of surface ovarian epithelium. ER-alpha, beta and AR were expressed in a variable percentage of moderately and poorly differentiated adenocarcinoma cell nuclei, but not in well-differentiated adenocarcinoma cells. These results might suggest that dietary feeding of estrogenic compounds either synthetic (4-NP) or natural (GS) could act as an inhibitor of DMBA-induced rat ovarian carcinogenesis.
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PMID:Inhibitory effects of estrogenic compounds, 4-nonylphenol and genistein, on 7,12-dimethylbenz[a]anthracene-induced ovarian carcinogenesis in rats. 1205 6

Salivary duct carcinoma (SDC) was first described by Kleinsesser in 1968 and was classified as an independent entity by the 1991 Revised World Health Organization. It is a rare but highly malignant tumor. We reviewed pathology in 49 cases of salivary adenocarcinoma, and diagnosed 6 cases as SDC. All had a rapidly enlarged mass in the parotid gland. All were men, and 4 involved facial palsy and metastasis to cervical lymph nodes. Fine needle aspiration biopsy was conducted in 3 cases, but none was diagnosed as SDC. Two had chemotherapy, but showed no effect. All underwent surgery, but only 1 survived more than 4 years. Immunohistochemically, none showed s-100 protein. Four showed PCNA and p53 protein. Highly positive cells of PCNA and p53 were found around comedo necrosis.
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PMID:[Clinicopathological study of salivary duct carcinoma]. 1213


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