UMLS:C0027627 - FACTA Search

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Query: UMLS:C0027627 (metastases)
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Actinic keratoses (AKs) are primarily induced by ultraviolet (UV) radiation and are often identified as premalignant lesions. In our opinion, AKs are proliferations of transformed, neoplastic keratinocytes confined to the epidermis that may eventually extend into the dermis, at which point they are termed squamous cell carcinoma (SCC). In contrast to AKs, SCCs have the potential to metastasize and kill. This process is analogous to that of evolving carcinoma of the uterine cervix that has been termed cervical intraepithelial neoplasia (CIN), a time-tested and reliable classification that provides clinicians with accurate information on which to base treatment decisions regarding cervical neoplasms following biopsy testing. A similar classification scheme could provide guidance to clinicians for the diagnosis and treatment of evolving SCC of the skin and as such, we propose a similar classification using the terminology keratinocytic intraepidermal neoplasia (KIN). This system is more reflective of the histology and natural history of SCC and eliminates ambiguity in the terminology of lesions currently referred to as AKs. The KIN classification defines features by which individual specimens can be objectively graded and specific treatment recommendations are made based on the grade of the lesion. We propose that the term keratinocytic intraepidermal neoplasia (KIN) be used to define and describe evolving SCC of the skin and that the term actinic (solar) keratosis be eliminated.
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PMID:Incipient intraepidermal cutaneous squamous cell carcinoma: a proposal for reclassifying and grading solar (actinic) keratoses. 1018 37

Women with both a history of high grade cervical intraepithelial neoplasia (CIN III) and breast carcinoma as second primary cancer were selected for studying the presence of HPV in breast carcinomas. Paraffin embedded material from 38 patients with 41 breast carcinoma cases after CIN III were examined by polymerase chain reaction (PCR) and in situ hybridization. By PCR we detected HPV 16 DNA in 19 out of 41 cases (46%) of the breast carcinomas. One case proved to be HPV 16 positive also by in situ hybridization. HPV 16 was also detected in 32 out of the 38 patients with CIN III (84%). All HPV 16 positive breast carcinomas were HPV 16 positive in their corresponding CIN III lesions. Eight patients with diagnosed breast cancer before the CIN III lesions were used as controls. None of these had HPV positive breast carcinomas. No cases were positive for HPV 11, 18, or 33. HPV 16 was detected in the primary tumours, in local metastases from HPV 16 positive tumours, in a distant HPV 16 positive breast carcinoma metastasis to the colon, and in other primary cancers in patients with HPV 16 positive breast carcinomas and HPV 16 positive CIN III. Estrogen and progesterone receptors were quantified in the HPV positive and HPV negative breast carcinomas, and there was no significant difference in the fraction positive in the two groups. Oncogenic HPV DNA might be transported from an original site of infection to other organs by blood or lymph, and possibly be a factor in the development of cancer in different organs.
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PMID:Human papillomavirus 16 in breast cancer of women treated for high grade cervical intraepithelial neoplasia (CIN III). 1032 89

A significant higher incidence of some cancers, especially lung cancer, has been found in women with previous HPV-related (human papillomavirus) urogenital and anal neoplasias than in individuals without this particular clinical history. The aim of our study was to investigate whether HPV is present in both CIN III (cervical intraepithelial neoplasia) lesions and bronchopulmonary second primary cancers in women with a clinical history of both diseases. Paraffin-embedded tumour tissue from 75 patients with bronchopulmonary carcinomas was examined using the polymerase chain reaction (PCR) technique and in situ hybridization for the presence of human HPV. In total, 51 primary tumours without metastases, 11 primary tumours with metastases and 13 lymph node metastases without available tissue from primary tumours were analysed. In our study 37/75 primary bronchopulmonary tumours (49%) were identified as HPV positive by the PCR method: 18 cases were purely HPV 16 positive (49%), 12 were purely HPV 6 positive (32%), 5 cases were HPV 16/6 positive (14%), 1 case was HPV 16/11 positive (2%) and 1 case was HPV 16/18 positive (2%). Fourteen metastases were HPV positive, and HPV 16, 11 and 6 were detected in both regional and distant metastases. Two of the HPV 16-positive metastases were brain metastases from two separate HPV 16-positive primary tumours; 35% of the HPV-positive cases were adenocarcinomas, 30% squamous cell carcinomas, 22% oat cell carcinomas, 5% large cell carcinomas, 3% anaplastic carcinoma, 3% low-differentiated carcinoma, and 3% malignant cylindroma. The CIN III lesions from 34 of the 37 HPV-positive bronchopulmonary carcinomas were analysed by PCR. The overall HPV positivity in the CIN III lesions was 74% (25/34 cases): 48% were purely HPV 16 positive, 24% purely HPV 6 positive, 24% HPV 16/6 positive and 4% were HPV 18 positive. Our results indicate that HPV is also involved in the development of bronchopulmonary cancers in women with a history of CIN III lesions.
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PMID:HPV positive bronchopulmonary carcinomas in women with previous high-grade cervical intraepithelial neoplasia (CIN III). 1042 55

Most cervical carcinomas appear to arise from cervical intraepithelial neoplasia (CIN) lesions. In addition to infection with high-risk human papilloma viruses, which is indicative of an increased risk of progression, alterations of oncogenes and tumor suppressor genes play a role. Genetic studies of CIN lesions, primary cervical carcinoma, and metastases may shed light on the relative importance of various genetic alterations involved in the progression of CIN to invasive carcinoma. We examined tumor material from 10 patients with squamous cell carcinoma of the uterine cervix and synchronous CIN lesions and lymph node metastases. The CIN component, invasive carcinoma, and lymph node metastases were analyzed separately for loss of heterozygosity (LOH) on the following loci: VHL (3p21), HLA region (6p22-23), PGL (11q 22-24), E6 associated protein (15q11-13), TP53 (17p13), DCC (18q21.1), and chromosomes 1, 2, 4, 9, 20, and X. Using immunohistochemistry, the expression of the EGF receptor, ERBB2, and TP53 was determined. In CIN lesions, frequent LOH was found at chromosome arms 3p, 6p, and 11q. Primary invasive carcinoma showed additional LOH at chromosome arms 6q, 17p, and 18q. In lymph node metastases, an additional locus on the X chromosome displayed LOH. All carcinomas and synchronous lesions but one showed high expression levels of the EGF receptor. TP53 staining, when present, was found in all synchronous lesions. Focal staining of ERBB2 was found in one CIN lesion, two invasive carcinomas, and four metastases. The molecular alterations accumulated in a fashion that paralleled the progression of the tumors. These results indicate that cervical tumorigenesis occurs in a stepwise fashion, including infection and integration of oncogenic HPV and several specific genetic alterations. Genes Chromosomes Cancer 26:346-354, 1999.
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PMID:Genetic alterations during the progression of squamous cell carcinomas of the uterine cervix. 1053 70

The aim of this study was to define the clinical implications of semi-quantitative telomerase activity in gynecological tumors by comparing the telomerase activity of cancerous lesion and the adjacent non-cancerous lesion. In 118 cases of gynecologic tumors, including 41 uterine cervical tumors, 43 uterine body tumors and 34 ovarian tumors, telomerase activities were determined using TRAPeze telomerase detection kit for the extension reaction of the telomere sequence and the PCR reaction for amplification of the sequence, and using fluorecence-based telomere repeat amplification protocol (F-TRAP) method for the detection. In all gynecologic cancers examined, telomerase activity of the cancerous lesion was significantly higher than that of the non-cancerous lesion. Telomerase activity in the uterine cervix increased in the following order of the normal uterine cervix, cervical dysplasia and cervical cancer. Regarding the endometrial cancer, telomerase activity at the primary lesion in patients with lymph node metastases was significantly higher than that in patients without lymph node metastases. When telomerase activity was compared by histologic subtypes of the ovarian cancer, clear cell adenocarcinoma showed significantly lower telomerase activity than the other subtypes, especially endometrioid adenocarcinoma. In all gynecologic cancers examined, there was no clear correlation between the telomerase activity and age at diagnosis or age of menopause. Although all tumors with 100 units or more telomerase activity were cancerous, the sensitivity was 39% in cervical cancer, 41% in endometrial cancer and 21% in ovarian cancer, respectively. Cervical intraepithelial neoplasia (CIN) had already increased telomerase activity and endometrial cancer with lymph node metastases had also greater activity than that without lymph node metastases. Although telomerase activity in ovarian cancer tended to increase as stage advances, it is noteworthy that clear cell adenocarcinoma showed significantly lower telomerase activity than endometrioid adenocarcinoma.
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PMID:Telomerase activity in gynecological tumors. 1094 30

Histopathology is the bedrock and cornerstone in the management of malignant tumors. Careful macroscopic description with selection of representative tissue for histologic examination is required for quality assurance and quality improvement and for assessing prognostic factors in cervical cancer specimens. The pathology report in cervical cancer (CX) should include three-dimensional tumor measurement, the exact measurement of depth of infiltration of the cervical wall, tumor grading, the presence of lymphatic space as well as blood vessel involvement. The statement for resection margins should include the vaginal, parametrane, rectal and vesical direction. All resected lymph node should be counted, measured and processed completely in step sections. If lymph node metastases are diagnosed, the report should include the size and count of metastatic nodes in relation to resected nodes. Pelvic and para-aortal nodes should be reported separately. Lymph nodes in the parametrane tissue represent regional nodes; and metastatic involvement should be stated as pN1 and not as pT2b. The tumor typing and staging should be conform with WHO-classification of malignant tumors and the TNM-classification system. The last one should be used in all cases which were surgically treated. Konizations and LOOP-excision specimens should be processed completely in step sections. The pathology report must include the severity of CIN-lesion, changes caused by HPV-infection, according to colposcopic localisation.
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PMID:[Pathologic-anatomic description and basic morphological information for management of dysplasias and carcinomas of the cervix uteri]. 1144 18

Loss of chromosome 18q21 is well documented in colorectal cancer, and it has been suggested that this loss targets the DCC, DPC4/SMAD4, and SMAD2 genes. Recently, the importance of SMAD4, a downstream regulator in the TGF-beta signaling pathway, in colorectal cancer has been highlighted, although the frequency of SMAD4 mutations appears much lower than that of 18q21 loss. We set out to investigate allele loss, mutations, protein expression, and cytogenetics of chromosome 18 copy number in a collection of 44 colorectal cancer cell lines of known status with respect to microsatellite instability (MSI). Fourteen of thirty-two MSI(-) lines showed loss of SMAD4 protein expression; usually, one allele was lost and the other was mutated in one of a number of ways, including deletions of various sizes, splice site changes, and missense and nonsense point mutations (although no frameshifts). Of the 18 MSI(-) cancers with retained SMAD4 expression, four harbored missense mutations in the 3' part of the gene and showed allele loss. The remaining 14 MSI(-) lines had no detectable SMAD4 mutation, but all showed allele loss at SMAD4 and/or DCC. SMAD4 mutations can therefore account for about 50-60% of the 18q21 allele loss in colorectal cancer. No MSI(+) cancer showed loss of SMAD4 protein or SMAD4 mutation, and very few had allelic loss at SMAD4 or DCC, although many of these MSI(+) lines did carry TGFBIIR changes. Although SMAD4 mutations have been associated with late-stage or metastatic disease, our combined molecular and cytogenetic data best fit a model in which SMAD4 mutations occur before colorectal cancers become aneuploid/polyploid, but after the MSI(+) and MSI(-) pathways diverge. Thus, MSI(+) cancers may diverge first, followed by CIN(+) (chromosomal instability) cancers, leaving other cancers to follow a CIN(-)MSI(-) pathway.
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PMID:SMAD4 mutations in colorectal cancer probably occur before chromosomal instability, but after divergence of the microsatellite instability pathway. 1148 57

Colorectal cancer affected approximately 135,000 people in the United States in 2001, resulting in 57,000 deaths. At the cellular level, colorectal cancer results from the progressive accumulation of genetic and epigenetic alterations that lead to the transformation of normal colonic epithelial cells to colon adenocarcinoma cells. The loss of genomic stability appears to be a key molecular and pathogenetic step that occurs early in the tumorigenesis process and serves to create a permissive environment for the occurrence of alterations in tumor suppressor genes and oncogenes. At least three forms of genomic instability have been identified in colon cancer: (1) microsatellite instability (MSI), (2) chromosome instability (i.e. aneusomy, gains and losses of chromosomal regions) (CIN), and (3) chromosomal translocations. Microsatellite instability occurs in approximately 15% of colon cancers and results from inactivation of the mutation mismatch repair (MMR) system by either MMR gene mutations or hypermethylation of the MLH1 promoter. MSI promotes tumorigenesis through generating mutations in target genes that possess coding microsatellite repeats, such as TGFBR2 and BAX. CIN is found in the majority of colon cancers and leads to a different pattern of gene alterations that contribute to tumor formation. CIN appears to result primarily from deregulation of the DNA replication checkpoints and mitotic-spindle checkpoints. The mechanisms that induce and influence genomic instability in cancer in general and more specifically in colon cancer are only partly understood and are consequently under intense investigation. These studies have revealed mutation of the mitotic checkpoint regulators BUB1 and BUBR1 and amplification of STK15 in a subset of CIN colon cancers. The etiology of CIN in the other unexplained cases of colon cancer remains to be determined. Hopefully, discovery of the cause and specific role of genomic instability in colon cancer will yield more effective chemotherapy strategies that take advantage of this unique characteristic of cancer cells.
Cancer Metastasis Rev
PMID:Genomic instability and colon cancer. 1500 Jan 46

We reviewed recent cytological reporting of abnormal glandular cells on cervical smears in order to assess the predictive value of these reports and the contribution of colposcopy in the assessment of these abnormalities. The study consisted of a 5-year retrospective review of the clinical management of 80 women with abnormal glandular cells on a cervical smear, with clinical and histopathological data available for review in the interval 1992-1996. There were two groups of women: (i) those referred with gynaecological symptoms and (ii) those with screen detected abnormalities who were asymptomatic and significantly younger than the first group. The predictive value of a glandular smear for malignancy was 42.5% and for premalignancy 28.8%. The most common lesions detected were cervical intraepithelial neoplasia (CIN) (13), endometrial cancer (13), cervical adenocarcinoma (10) and cervical intraepithelial glandular neoplasia (CIGN) (8). Four cases of endometrial carcinoma presented through screening. In the remainder a variety of benign conditions were identified as responsible for the abnormal smear. Failure to find an explanation for the abnormal smear only occurred in 8.8%. In developing a protocol for abnormal glandular smears, our observations indicate that: (a) those with abnormal bleeding require endometrial sampling; (b) for those with screen detected abnormality, colposcopy is valuable as it is a sensitive predictor of early invasion and can predict glandular abnormality; (c)diseases of the entire genital tract, non-gynaecological viscera and metastatic cancer can generate cytological abnormality; (d) screen detected borderline abnormality in endocervical cells is associated with CIN III.
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PMID:The abnormal glandular smear: cytologic prediction, colposcopic correlation and clinical management. 1551 97

Altered sialylation observed during oncogenic transformation, tumor metastases and invasion, has been associated with enhanced sialyltransferases (STs) transcription. Increased mRNA expression of STs (ST6Gal I, ST3Gal III) has been detected in invasive cervical squamous cell carcinoma. A study of the sialic acid concentration in local tissue of cervix and in serum showed a slight elevation in benign inflammatory lesions and a moderate elevation in severe neoplasia, but to date, altered expression of STs in cervical intraepithelial neoplasia has not yet been evaluated. This study investigates the changes in mRNA expression of three STs (ST6Gal I, ST3Gal III, and ST3Gal IV) in cervical intraepithelial lesions (CIN). Alterations of these STs mRNA expression were examined in 35 cervix specimens classified as normal, CIN 1, CIN 2 and CIN 3, by semiquantitative reverse transcription-polymerase chain reaction, mRNA expression of the three STs was enhanced in CIN 1, CIN 2 and CIN 3 with respect to normal tissue, with a significant difference of p < 0.001 (Mann-Whitney U test) for all the enzymes. Our results suggest that altered expression of ST3Gal III, ST3Gal IV and ST6Gal I in CIN could play an important role during malignant transformation and could be related with the enhanced sialic acid expression detected in neoplasic tissues.
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PMID:Enhanced sialyltransferases transcription in cervical intraepithelial neoplasia. 1941 26

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