Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vaginal and vulvar scrapes from 30 patients which have HPV types 16 or 18 positive cervical neoplasia (13 of mild dysplasia, 5 of moderate dysplasia, 4 of severe dysplasia, 3 of carcinoma in situ, and 5 of invasive carcinoma) were examined by the polymerase chain reaction (PCR), to detect amplified E7 gene of HPV types 16 and 18 DNA sequences. In 24 vaginal and 15 vulvar scrapes, the same type of HPV as in cervical scrapes was detected. The frequencies of HPV DNA in vaginal and vulvar scrapes for histological diagnosis of cervical neoplasia were 84.6% (11/13) and 53.8% (7/13) in mild dysplasias, both were 100% (5/5) in moderate dysplasias, 75% (3/4) and 25% (1/4) in severe dysplasias, 66.7% (2/3) and 33.3% (1/3) in CISs, and 60% (3/5) and 20% (1/5) in invasive carcinomas, respectively. The results of vulvar scrapes showed that the frequency of HPV DNA in mild and moderate dysplasias was significantly higher than that in severe dysplasias, CISs and invasive carcinomas (p < 0.05). We suggest that, in addition to the investigation for the natural history of HPV infection, cell dynamics, local immunological status and any other factors in the HPV-infected lesion must be investigated to clarify the carcinogenesis of HPV in the uterine cervix. Furthermore, HPVs detected in the vagina and vulva were thought to have disappeared without reaching an integrated form during the follow-up of cervical neoplasia with HPV infection over a long period.
 ...
PMID:[Molecular biological study on multifocal infection of HPV in uterine cervix, vagina and vulva]. 133 14

Most adenocarcinomas of the colorectum arise in a visible benign precursor lesion, the adenoma, which is a monoclonal proliferation of dysplastic nonmalignant epithelial cells. The resultant adenoma-adenocarcinoma sequence represents the predominant pathogenetic pathway, in contrast to de novo carcinoma. Therefore, the adenoma is a tempting endpoint for chemoprevention trials. The adenoma-adenocarcinoma sequence occurs in diverse clinical settings. In familial adenomatous polyposis (FAP) syndrome, autosomal dominant inheritance of the mutated APC (adenomatous polyposis coli) gene on chromosome 5q21 typically results in thousands of adenomas in the colorectum and in lesser numbers in the proximal small bowel. Adenocarcinoma usually develops in only a few of these adenomas, typically in the left colon and duodenum. In hereditary nonpolyposis colorectal cancer (HNPCC) syndrome, autosomal dominant inheritance of an unidentified gene appears to result in small numbers of adenomas which progress frequently to adenocarcinoma, predominantly in the right or transverse colon. In familial aggregation of colorectal cancer without a recognizable syndrome, cancer and/or adenomas occur in pedigree members. In "sporadic" cancers and adenomas, family history is absent and the tumors are mainly in the left colon. Colorectal adenomas have variable characteristics including size, shape (polypoid vs. flat), villous architecture, and dysplasia. A variety of oncogenes and tumor suppressor genes are altered during progression. Epigenetic factors are important as evidenced by the disappearance of adenomas in FAP patients after ileorectal anastomosis or treatment with the nonsteroidal antiinflammatory drug sulindac. Several variations on the theme of the adenoma-carcinoma sequence are evident. Identification of the inherited and acquired genetic alterations as well as the interacting environmental factors will provide a rational basis for chemoprevention.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:The adenoma-adenocarcinoma sequence in the large bowel: variations on a theme. 133 99

The detection of human papillomavirus (HPV) type 16 early genes: E7, E5, and the late gene: L1 was attempted in 42 uterine cervical neoplasia (35 cervical carcinomas and 7 cervical dysplasias) using the polymerase chain reaction (PCR) method. Consequently, E7 gene was detected in 19 (54.3%) of 35 carcinomas and in 5 (71.4%) of 7 dysplasias, E5 gene was detected in 7 (20.0%) of 35 carcinomas and in 5 (71.4%) of 7 dysplasias, L1 gene was detected in 18 (51.4%) of 35 carcinomas and in 5 (71.4%) of 7 dysplasias, respectively. In order to elucidate the transcriptional pattern of HPV type 16 in each of the clinical stages, the expression of mRNA for E7, E5 and L1 genes was examined in HPV DNA positive cases using the reverse transcriptase polymerase chain reaction (RT-PCR) method. E7 gene mRNA was detected in 18 (94.7%) of 19 cervical carcinomas, whereas E5 and L1 genes mRNAs were detected in only 4 (57.1%) of 7 and in one (5.6%) of 18 carcinomas respectively. In cervical dysplasias, E7, E5 and L1 genes mRNA were detected in all cases. E7, E5 and L1 genes were transcriptionally active in all dysplasias, whereas E5 and L1 genes were not always transcriptionally active in carcinomas. These results suggest that the HPV type 16 early gene E7 is present preferentially as integrated form and transcriptionally active in the carcinoma cell, and plays an important role in the development of malignancy. On the other hand, E5 and L1 genes are present and transcribed in the dysplasia cell but their transcriptional activity is less frequent in the carcinoma cell.
 ...
PMID:Occurrence and expression of human papillomavirus type 16 genes in uterine cervical carcinomas. 133 65

Two patients, members of one family, with Peutz-Jeghers syndrome are described who underwent surgery for bowel obstruction. Both had multiple polyps in the gastrointestinal tract. Severe dysplasia and adenomatous change were present in two hamartomatous polyps adjacent to a stenosing colonic carcinoma in one patient and moderate dysplasia and adenomatous change were observed in two hamartomatous rectal polyps in his son. These changes support recent reports in the literature of progression towards neoplasia in these lesions.
 ...
PMID:Do dysplastic and adenomatous changes in large bowel hamartomas predispose to malignancy?--A report of two cases. 133 70

Twenty-eight cases of transitional cell carcinomas, (19 papillary cell carcinomas, 9 nonpapillary invasive carcinomas) with concomitant mucosal biopsies are reported. Multiple biopsies were obtained cystoscopically at diagnosis (during resection or biopsy of the main tumor) or afterwards, during post-operative evaluation. Fifteen patients (53.6%) were positive for dysplasia, carcinoma "in situ" or micro-invasive carcinoma in the biopsies. These lesions were correlated with the primary neoplasm in regard to: 1) histological grade. Atypical lesions were more frequent the higher the grade (0.01 < p < 0.05); 2) clinical staging. The possibility of finding atypical lesions was higher in cases with more advanced staging (0.01 < p < 0.05) and 3) presence of one or more tumors visible cystoscopically. The results were not statistically significant (0.10 < p < 0.50) but there was a trend toward a higher incidence of atypical lesions among patients with more than one tumor at cystoscopy. Performance of multiple mucosal biopsies is the only means of diagnosing for atypical lesions of the bladder because, due to their plane configuration, they are not detected cystoscopically. The presence of these lesions is very important because they influence the prognosis and the therapeutic measures.
 ...
PMID:Multiple biopsies in bladder urothelial carcinomas. Correlation of atypical lesions with histological grade, clinical staging and number of tumors. 134 6

Growth patterns in prostatic cancer can reduce detectability of genetic alterations. Tumors show histologic grade heterogeneity, multifocality, interdigitation of benign and malignant glands, and varying amounts of stroma. These characteristics introduce sampling errors when one uses traditional methods for genetic analysis that depend on disaggregated cells [metaphase or interphase chromosome studies] or on tissue extracts [Southern blotting or polymerase chain reaction (PCR)] to detect molecular events. To circumvent these problems, we used two approaches to study paraffin-embedded tumors, which permit focused analysis of critical tissue components. Serial 4- to 5-microns sections are applied to slides in groups of three. Every second slide is hematoxylin and eosin stained to visualize areas of carcinoma, dysplasia, hyperplasia, and stroma; tumor-rich areas are circled with ink and used as templates to examine or excise the same areas from adjacent nonstained sections. PCR methods for quantitative and qualitative gene assay are effective in evaluating samples when alteration at a particular locus is suspected. Fluorescence in situ hybridization with chromosome-specific paracentromeric probes for detection of copy number of the relevant chromosome is applied to the adjacent section. Normal chromosome controls for both methods were demonstrated. This protocol enables us to correlate genetic alterations precisely with tumor extent and morphology.
 ...
PMID:An approach to definition of genetic alterations in prostate cancer. 134 66

Qualitative and quantitative changes in secretion of goblet cells of large bowel mucosa in adenomatous polyps (60), adenocarcinoma (30) and bioptates of adjacent transitional mucosa (30) were studied. As neoplasia progressed, mucin profile appeared to follow a certain pattern: it reached its peak in moderate dysplasia in polyps containing predominantly sulphomucins; subsequently both sulphomucin and sialomucin levels decreased. Adenocarcinomas showed a sharp drop in glycoprotein level, and an insignificant build-up of sialomucins was registered in some cases only. Enhanced abnormal secretion was observed in mucinous carcinoma and adenocarcinoma characterized by the presence of large mucinous areas. Also, qualitative changes were identified in transitional mucosa adjacent to tumor.
 ...
PMID:[The mucin profile in the mucosa of the large intestine in neoplasms]. 134 58

We have investigated whether monoclonal antibody (PC10) of proliferating cell nuclear antigen (PCNA) could be useful as a marker of proliferating cells within formalin-fixed, paraffin-embedded tissue sections of 140 gynecological tumors and their related lesions. There was a positive correlation (r = 0.76) between the labelling index for PCNA and that for Ki67. Immunohistochemical staining for PC10 was confined to the nucleus and showed a diffuse or granular pattern or a mixture of both. The distribution of PC10 staining in non-neoplastic tissues was localized to proliferating cell compartments. In malignant tissues, the localization of the distribution of PCNA-positive cells came to be lost and the proportion of positive cells varied from case to case as well as from field to field within the same tissue section. The cases in which more than 31% of cells were positive for PCNA were as follows: Cervical squamous dysplasia 2/3, squamous carcinoma in situ 2/5, microinvasive squamous carcinoma 2/2, invasive squamous carcinoma 9/13, adenocarcinoma in situ 4/4, microinvasive adenocarcinoma 3/3, invasive adenocarcinoma 6/7, endometrial adenocarcinoma 6/25, ovarian epithelial malignant tumors 11/17, sex cord stromal tumors 2/14, and germ cell tumors 3/22. It is concluded that immunohistochemical staining for PC10 may be useful as a marker for proliferating activity of the cells both in normal and tumor tissues rather than for malignancy.
 ...
PMID:[Immunohistochemical study of proliferating cell nuclear antigen (PCNA) in gynecological tumors and their related lesions]. 134 57

The expression of multidrug resistance (mdr) genes was investigated in the livers of transgenic mice that express the human hepatitis B virus large envelope polypeptide under the transcriptional control of a liver-specific promoter. These mice develop a storage disease due to the accumulation of a nonsecretable form of hepatitis B surface antigen in the hepatocyte. Liver cell injury is followed by a hepatocellular proliferative response, dysplasia, microscopic nodular hyperplasia, and finally hepatocellular carcinoma. The expression of mdr1, mdr2, and mdr3 genes was analyzed in livers at different stages of the disease by RNase protection assay, Western blot, and immunohistochemistry. RNase protection assay revealed that mdr3 mRNA expression was moderately increased in tissue with microscopic nodular hyperplasia and significantly overexpressed in hepatocellular carcinoma but undetectable in earlier stages of the disease. Western blot using isoform-specific anti-mdr3 antibody demonstrated that the expression of mdr3 protein reflected the steady-state level of mdr3 mRNA. Immunohistochemical analyses using anti-mdr3 isoform-specific antibody and monoclonal antibody C219, which recognizes all the three mdr isoforms, demonstrated selective overexpression in preneoplastic foci during the stage of microscopic nodular hyperplasia as well as in neoplastic hepatocytes in hepatocellular carcinoma. No consistent activation of mdr1 and mdr2 (but occasional coactivation with mdr1) genes during hepatocarcinogenesis was observed. Our results suggest that the hepatocellular mdr3-specific activation mechanism is associated with the late events of hepatocarcinogenesis in this model. The predictable kinetics of mdr gene expression in this transgenic tumor model suggest that it is suitable for future studies of the mechanism of mdr gene activation and the possible pharmacological consequences for mdr3 gene expression of hepatocellular carcinoma.
 ...
PMID:Activation of multidrug resistance (P-glycoprotein) mdr3/mdr1a gene during the development of hepatocellular carcinoma in hepatitis B virus transgenic mice. 135 18

Neoplastic progression in patients with chronic ulcerative colitis (UC) is characterized by the development of epithelial dysplasia, which is accompanied by genetic abnormalities that can be detected by flow cytometric and molecular biologic methods. Distribution of and correlation between histologic abnormalities, DNA content, and loss of heterozygosity for a p53 allele (p53 LOH) in the colons of nine UC patients were analyzed. Loss of a p53 allele was found in 85% (22/26) of biopsy specimens classified histologically as carcinoma, 63% (25/40) of biopsy specimens with high grade dysplasia, and 33% (7/21) of biopsy specimens with low grade dysplasia. Loss of heterozygosity for p53 was also found in 9% (5/57) of biopsy specimens indefinite for dysplasia and in 1/18 biopsy specimens negative for dysplasia, showing that this genetic change may occur early in the histological progression towards carcinoma. Aneuploid DNA contents were more common than p53 LOH in regions with negative, indefinite or low grade dysplastic histology; moreover, p53 LOH was detected only in aneuploid cells and not in diploid epithelium. Aneuploidy alone was not as specific a marker for the concomitant presence of dysplasia or carcinoma in a biopsy sample as aneuploidy combined with p53 LOH. These findings show that aneuploidy may precede both p53 LOH and epithelial dysplasia. Two UC patients' colons contained geographically separated clones of cells with different aneuploidies that also showed loss of different p53 alleles, suggesting that neoplasia may arise within different populations of cells in separate areas of the same colon.
 ...
PMID:Neoplastic progression in ulcerative colitis: histology, DNA content, and loss of a p53 allele. 850 Jul 56


<< Previous 1 2 3 4 5 6 7 8 9 10