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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the U.S. oral cancer accounts for 2.1% of all cancers and 1% of cancer deaths. Two to three times as many males as females are affected. Blacks have more intra-oral cancer than whites, and their incidence and mortality rates have increased in recent years. The etiologic process very likely involves several factors. The major etiologic agents are tobacco (all types) and alcoholic beverages. Herpes simplex virus, human papilloma virus, and Candida have been implicated. Host factors include poor state of dentition, nutritional aberrations, cirrhosis of liver, lichen planus, and immunologic impairmant. Cellular changes include amplification of some oncogenes, alterations in antigen expression, production of gamma-glutamyl transpeptidase, and disturbance of keratin and involucrin production. Experimentally, cancer is readily produced on the hamster cheek pouch and rat oral mucosa. Unlike oral cancer in humans, most experimental lesions are exophytic, and they rarely metastasize.
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PMID:Oral cancer. 212 24

Thirty-six cases of vulvar squamous cell carcinoma 5 mm or less in thickness were studied, and potential predictors of lymph node metastases were evaluated. Tumor thickness and depth of stromal invasion were measured. Inguinal lymph node metastases were present in six (17%) cases, all of which had primary neoplasms more than 3 mm thick. The most superficial lesion to have lymph node metastasis was 3.2 mm thick and had 1.6 mm of stromal invasion. Nonetheless, depth of stromal invasion of less than 3 mm was associated with statistically fewer lymph node metastases (7%) than that of neoplasms with 3 mm or more of stromal invasion (50%). Although lymphatic or blood capillary invasion was present in four (11%) cases, this feature had no statistically significant association with lymph node metastasis. There was no relationship between clinical stage, surface diameter, or histological grade of the lesion and lymph node metastasis. A significant percentage of cases had either carcinoma in situ (31%) or atypical hypertrophic dystrophy (19%) in the epithelium adjacent to the infiltrating carcinoma. Koilocytotic atypia suggestive of human papilloma virus infection was present in the adjacent epithelium in 47% of the cases. This study suggests that thickness of the neoplasm is a valid predictor for the presence or absence of lymph node metastasis in vulvar squamous cell carcinoma; it may be more useful than neoplastic depth of invasion in this regard.
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PMID:The pathology of superficially invasive, thin vulvar squamous cell carcinoma. 651 Nov 60

In this study we investigated 56 renal cell carcinomas immunohistochemically for the expression of proliferating cell nuclear antigen (PCNA) and tumour suppressor protein p53. We also analyzed for the presence of human papilloma virus (HPV) DNA subtypes 6, 11, 16, 18, 31 and 33 by in situ hybridization. In carcinomas which showed more than 10% of PCNA positive nuclei there were significantly more cases with invasion (P = 0.032) or metastatic disease (P = 0.047). Nine out of 22 grade III-IV tumours (40.9%) but only six out of 30 grade I-II tumours (20%) showed more than 10% of PCNA positive cells (P = 0.097). Patients with 10% or more PCNA positive cells in kidney tumours had more advanced disease at the time of diagnosis than those showing less PCNA positive cells (P = 0.05). Six p53 positive cases were found among 56 tumours (11%), but only one case had more than 10% positive cell nuclei. The presence of HPV DNA was found in 29 out of 56 cases (52%). Multiple subtypes were found in 19 cases (34%). The most commonly occurring subtypes were 18 and 33. There was no association between PCNA, p53 and the presence of HPV DNA subtypes. Because of the association of PCNA with invasion and metastatic disease, it would be worth while to study PCNA further as a possible marker for aggressiveness of renal carcinomas. Both this study and those concentrated on mutational analysis suggest that p53 is generally not important for the development of renal cell carcinoma. On the other hand, the presence of HPV DNA in these tumours implicates HPV viral infection in the aetiology of renal cancer.
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PMID:Proliferating cell nuclear antigen but not p53 or human papillomavirus DNA correlates with advanced clinical stage in renal cell carcinoma. 783 39

The study aimed to verify the probable correlation between the incidence of cervical cancer and the presence of human papilloma virus (HPV) in relation to a state of folic acid hypovitaminosis. In this context, however, it is important not to overlook the important protective role played by vitamins A and C in cancer prevention, as mentioned in the paper. Numerous authors agree that this is a real finding in cervical pathology, as shown in our research, even if folic acid therapy does not alter the course and prognosis of disease. On the contrary, low blood levels of folic acid appear to increase the risk of contracting the disease. Extensive and radical surgery therefore appears to be even more justified in order to increase the probability of recovery on the operating table in view of the irrational and inexorable progress of this pathology, especially if metastases are already present.
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PMID:[Correlations between folic acid, human papilloma virus (HPV) and cervix neoplasms]. 793 74

Two different characteristic patterns of human papilloma virus (HPV) type 16 DNA were found by Southern blot hybridization in four pelvic and paraaortic lymph node metastases in a patient with FIGO stage IIIb cervical cancer. Both patterns added up to give the HPV 16 DNA pattern of the primary tumor. This strongly suggests that the tumor was composed of two distinct compartments, each spawning its own lymph node metastases. A second patient presented with a vaginal tumor 4 years after stage IIb cervical cancer had been treated with hysterectomy only. The vaginal tumor was removed and pelvic lymphadenectomy performed. Integrated HPV 16 DNA was found in the vaginal tumor whereas one involved and one free lymph node contained episomal HPV 16 DNA with a characteristic deletion. The apparent heterogeneity of the cancer cell population may indicate that the metastasis is not related to the vaginal tumor but that it is a late sequel of the cervical cancer. Alternatively the metastasis could have originated from an unsampled portion of the vaginal tumor.
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PMID:Specific rearrangements of human papillomavirus DNA provide molecular evidence for genetic heterogeneity of primary cervical cancers, recurrencies, and lymph node metastases in two patients. 827 8

To date over 60 different human papilloma virus (HPV) types have been described and novel HPV genomes are still being identified. The identification and taxonomy of papilloma viruses has become increasingly complex However, some types, especially HPV-16, -18 and to a lesser extent HPV-31 and -33, which are found in a high proportion of invasive cervical cancers and their metastases, are classified as high risk types For preventive reasons it is important to identify and classify the different HPV types in clinical specimens. Many of the methods used until recently are cumbersome. In this paper we use molecular biology techniques which permit a rapid screening and typing of high risk HPVs in clinical specimens. The screening procedure is based on the very sensitive method of polymerase chain reaction. Using a set of general primers derived from the E1 open reading frame, which anneal to a large variety of human papilloma virus DNA, we can classify samples into positive or negative for the presence of HPV sequences in a single step. The typing of the high risk HPV types is achieved by restriction enzyme analysis using the endonuclease Alu I which cleaves each high risk HPV type at different sites, thus permitting the easy identification of each type after agarose gel electrophoresis.
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PMID:A rapid method for the screening and typing of high risk HPVs using molecular biology techniques. 857

Cancer is a progressive multigenic disorder characterized by defined changes in the transformed phenotype that culminates in metastatic disease. Determining the molecular basis of progression should lead to new opportunities for improved diagnostic and therapeutic modalities. Through the use of subtraction hybridization, a gene associated with transformation progression in virus- and oncogene-transformed rat embryo cells, progression elevated gene-3 (PEG-3), has been cloned. PEG-3 shares significant nucleotide and amino acid sequence homology with the hamster growth arrest and DNA damage-inducible gene gadd34 and a homologous murine gene, MyD116, that is induced during induction of terminal differentiation by interleukin-6 in murine myeloid leukemia cells. PEG-3 expression is elevated in rodent cells displaying a progressed-transformed phenotype and in rodent cells transformed by various oncogenes, including Ha-ras, v-src, mutant type 5 adenovirus (Ad5), and human papilloma virus type 18. The PEG-3 gene is transcriptionally activated in rodent cells, as is gadd34 and MyD116, after treatment with DNA damaging agents, including methyl methanesulfonate and gamma-irradiation. In contrast, only PEG-3 is transcriptionally active in rodent cells displaying a progressed phenotype. Although transfection of PEG-3 into normal and Ad5-transformed cells only marginally suppresses colony formation, stable overexpression of PEG-3 in Ad5-transformed rat embryo cells elicits the progression phenotype. These results indicate that PEG-3 is a new member of the gadd and MyD gene family with similar yet distinct properties and this gene may directly contribute to the transformation progression phenotype. Moreover, these studies support the hypothesis that constitutive expression of a DNA damage response may mediate cancer progression.
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PMID:Subtraction hybridization identifies a transformation progression-associated gene PEG-3 with sequence homology to a growth arrest and DNA damage-inducible gene. 925 46

Squamous cell carcinoma is the most common tumour of the penis. It is a rare disease in Western countries, and it is often associated with phimosis, poor hygiene or human papilloma virus infection. It could be prevented or diagnosed early in most cases, but, due to cultural and educational reasons, it is often diagnosed late. Nodal metastases are relatively common, but distant dissemination is very rare. Radical surgery gives the best control of the primary tumour, but it is mutilating. Laser surgery for limited superficial lesions and sophisticated radiotherapy for relatively small infiltrating tumours have been successfully employed, alone or in combination with chemotherapy. The use of radical surgery can therefore be restricted to cases which are unsuitable for conservative treatment or to relapses. Survival mainly depends on nodal metastases, but management of regional lymph nodes is controversial. Radical inguinal or ileoinguinal lymphadenectomy can cure approximately 40-50% of patients with positive nodes, but nearly half of the patients with clinically enlarged nodes actually have no metastases. Invalidating oedema is a frequent complication of inguinal lymphadenectomy. The point is to restrict the operation to patients with positive nodes. Expectant policy can be dangerous because results of delayed lymphadenectomy are usually poor. Fine needle aspiration biopsy and imaging may be of help in diagnosing nodal metastases. Modified surgical procedures have been advocated in order to obtain a pathological staging of the inguinal nodes avoiding invalidating sequelae, but results are controversial. Depth of invasion, tumour grade and growth pattern are of help in identifying patients at a very high risk of harbouring nodal metastases. Squamous cell carcinoma of the penis is relatively responsive to chemotherapy. Limited experiences suggest that adjuvant chemotherapy can improve the long-term survival of patients with radically resected positive nodes, and primary chemotherapy can make resectable approximately 50% of cases with fixed inguinal metastases. However, chemotherapy alone is not curative for metastatic disease.
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PMID:Up-to-date management of carcinoma of the penis. 926 25

Consideration of cost-effectiveness has guided public and insurers' decisions about preventive services for almost 20 years. Legislative decisions on coverage of specific cancer screening tests under Medicare and Medicaid have traditionally followed studies of their cost-effectiveness. This paper reviews the principles of cost-effectiveness analysis in health care. Cost-effectiveness analysis is a stylized form of investment analysis, where the returns on the investment are measured in improvements in health rather than in dollars and consider society as a whole as the relevant investor. Cost-effectiveness studies of screening for two common cancers, cervical and colorectal, illustrate the strengths and weaknesses of cost-effectiveness analysis. Dependence on models of the disease process, which may be sketchy, and uncertainty about costs and benefits of screening are inherent in the methodology. Although economic evaluations of both cervical and colorectal cancer screening have found them to be relatively cost-effective compared with doing nothing, such studies have not resolved the uncertainty about the best screening strategy for either disease. With cervical cancer, new evidence about the relationship between human papilloma virus and high-grade neoplasia suggests the need for new models of the disease process that can support additional cost-effectiveness analyses. Colorectal cancer screening models must be validated against new information from recent randomized clinical trials. Despite uncertainty and contradictions in existing studies of screening for both diseases, investment models force clinicians and decision-makers to consider all important consequences for health care costs and outcomes.
Cancer Metastasis Rev
PMID:Cost-effectiveness of screening for common cancers. 943 40

Patients without any evidence of lymph node metastases are supposed to have a fair prognosis, but some of these patients develop recurrent disease unexpectedly after surgery. The object of this study is to examine whether the detection of human papilloma virus (HPV) DNA could be used as a diagnostic marker to predict such recurrences. Two hundred and thirty-six patients undergoing radical hysterectomy and pelvic lymphadenectomy for stage Ib and II cervical cancer at Okayama University Hospital (Japan) from 1988-1994 were reviewed, and only those cases positive for HPV-16 or HPV-18 in primary sites were included in this survey. The E6-E7 region of the HPV genome was amplified by a sensitive nested PCR from archival pelvic lymph node specimens. HPV sequences identical to those of the primary sites were detected in histologically confirmed negative lymph nodes, regardless of histological type or HPV type of the primary lesion, in 9 of 10 patients who recurred within 4 years of surgery. In contrast, histologically confirmed negative lymph nodes from 12 patients with stage IIb disease without evidence of recurrent disease were all negative for the presence of HPV, except for 1 lymph node. The presence of HPV DNA in histologically negative nodes implies the possibility of early nodal involvement or coexistence of undetectable hematogenic dissemination and could therefore be used as a diagnostic marker to predict the unexpected recurrence of these patients.
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PMID:Presence of human papilloma virus DNA in pelvic lymph nodes can predict unexpected recurrence of cervical cancer in patients with histologically negative lymph nodes. 956 93


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