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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prostate cancer is the most frequently occurring non-skin cancer in men in the U.S.A. and other Western countries, but its etiology is poorly understood. Human prostate carcinogenesis has been viewed as a multi-step process involving progression from low histologic grade, small latent carcinoma, to large, higher grade, metastasizing carcinoma. However, recent data suggest that a variety of pathogenetic pathways exist. The precise role of hormones in the genesis of human prostate cancer remains largely undefined. It is difficult to investigate stages in the development of human prostate cancer, but some animal models provide opportunities in this regard. Short-term treatment of rats with chemical carcinogens will produce a low incidence (5-15%) of prostate cancer, provided that prostatic cell proliferation is enhanced during carcinogen exposure. A high carcinoma incidence can only be produced by chronic treatment with testosterone following administration of carcinogens such as N-methyl-N-nitrosourea (MNU). Testosterone markedly enhances prostate carcinogenesis even at doses that do not measurably increase circulating testosterone. Thus, testosterone is a strong tumor promoter for the rat prostate. All such MNU-initiated, testosterone-promoted tumors are adenocarcinomas mostly originating from the dorsolateral and anterior, but not ventral, prostate lobes. A high frequency (70%) of activation of the K-ras gene by a G35 to A mutation occurs in these carcinomas. A variable frequency of activation of H-ras and K-ras genes occurs in human prostate carcinomas. Another rat model, representing a different pathogenetic pathway, involves chronic administration of estradiol-17 beta in combination with low-dose testosterone. The resulting carcinomas are low-grade and originate exclusively from periurethral ducts of the dorsolateral and anterior prostate. We recently found a major adduct by 32P postlabeling analysis in the tissue region that includes these ducts, but not in, e.g., the ventral prostate, of rats treated for 16-24 weeks. While it is unknown whether testosterone is a tumor promoter in this system, the presence of a DNA adduct suggests that estradiol-17 beta acts as a tumor-initiating agent in this system.
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PMID:Multistage prostate carcinogenesis: the role of hormones. 184 35

A rare case of bilateral renal tumor with benign clinical evolution, associated with staghorn calculosis and skin cancer, is reported. Delayed operative treatment was due to difficulties in establishing the diagnosis, controversial results of the sonographic and X-ray examination and lack of cooperation by the patients. The right kidney and regional lymph nodes were removed; metastases were verified on histologic examination of the lymph nodes. After the operation the patient received complex radio-, chemo- and hormonal therapy. Basocellular skin cancer which later developed was cured by contact radiotherapy.
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PMID:[A case of bilateral kidney tumor combined with staghorn calculi and skin cancer]. 189 92

Facial defects created by removal of various types of skin cancer are usually closed primarily. There are some areas of the face where primary closure produces less than optimal results. We have utilized a non-reactive collagen sponge (Collagen Matrix) to enhance closure by secondary intention following removal of skin cancers. This presentation describes the properties of Collagen Matrix as well as the technique we utilized for closure of facial defects following tumor removal.
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PMID:The use of Collagen Matrix to enhance closure of facial defects. 193 21

Incidence of various cancers was evaluated in a cohort of 5359 multiple sclerosis (MS) patients, identified through hospital discharge records between 1977 and 1987 and followed for an average of 5.2 years. Computerized linkage with the Danish Cancer Registry uncovered 210 cancer cases which was significantly more than expected based on national rates (relative risk (RR) = 1.29). Over half of the excess, however, was observed for non-melanoma skin cancer and tumors of the urinary tract, which may be related to increased medical surveillance among MS patients compared to the Danish population as a whole. There was a significant excess of nasopharyngeal carcinomas in the cohort (RR = 17.3), but based on only 3 cases and seen only among women. Hematologic and lymphatic malignancies were not increased, adding little support to previous suggestions of a possible association of these malignancies with MS. An excess of brain tumors, seen only in women, may represent situations where the tumor caused symptoms which were interpreted as MS. Overall, the data suggest that a patient with MS is not at unusual risk for subsequent cancer development, but the relatively short follow-up of the population is a limitation of the investigation.
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PMID:Cancer incidence following hospitalization for multiple sclerosis in Denmark. 195 Apr 64

Eighty-five squamous cell skin cancers treated with radiation therapy were reviewed, including 23 untreated primary tumors, 6 recurrent tumors, 16 synchronous or metachronous nodal metastases including 3 patients from the previous two groups, and 38 sites irradiated for microscopic residual cancer after surgery. The 5-year actuarial local controls were 0.54, 0.0, 0.42, and 0.79, respectively. No relationship between local control and either tumor size or radiation dose could be shown. Salvage treatment was attempted in 7 of 32 local failures, and has been successful in 4. Cancers arising in the settings of prior irradiation, renal transplant, hematopoietic malignancies, or chronic inflammation did not fare worse, and patients with parotid node metastases generally fared better with combined irradiation and surgery. Surgery followed by adjuvant irradiation confers a 5-year disease control probability of 0.79. Irradiation alone for untreated primary lesions, for recurrent primary lesions, or for untreated nodal metastases confers a disease control probability of approximately 0.50. Local or systemic predisposing factors do not confer an appreciably different prognosis. Parotid lymph node metastases are best served by combined modality treatment.
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PMID:Radiation therapy for squamous cell carcinoma of the skin. 195 Nov 74

Radiotherapy is one of the main therapeutic methods for malignant tumors, but on the other hand it can also induce new malignant tumors. Recently, we experienced a case of a 22-year-old woman with triple cancers (Wilms' tumor, thyroid cancer and mucoepidermoid carcinoma of the lung). She had been treated repeatedly for right-sided pulmonary metastases from the Wilms' tumor. The last cancer arose from a different organ in the field irradiated to treat the first cancer, after a latent period of about 20 years. Therefore, this case is classified as highly probable radiation-induced cancer (A-1 group) by the diagnostic criteria for radiation-induced cancer proposed by Sakai et al. Second cancers (radiation-induced cancers) mainly consist of soft tissue sarcomas, leukemias, skin cancers, urinary bladder cancers, large bowel cancers and other tumors. The occurrence of mucoepidermoid carcinoma of the lung as a radiation-induced tumor had not been reported. This patient also showed poor growth of the right breast and marked deformity of the right side of the thorax as late damage from irradiation. We must make efforts to decrease late damage from radiotherapy for pediatric cancers.
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PMID:[A case of radiation-induced mucoepidermoid carcinoma of the lung following radiotherapy for pulmonary metastasis of Wilms' tumor]. 196 24

The development of skin tumors (mainly squamous cell carcinomas) in hairless Skh-HR1 mice after discontinuation of a course of daily UV irradiations (wavelengths, 280-370 nm) is compared to that when the daily irradiations are continued. Under conditions of continued daily exposures 50% of 22 animals contracted tumors with diameters of at least 4 mm in 135 days. With exposures stopped after 35 or 19 days (2 groups with 24 and 23 mice) this time interval increased to 280 and 645 days, respectively; the rate at which multiple tumors developed on the mice was correspondingly lower. A mathematical model, derived from a larger experiment (223 mice) with different levels of chronic UV exposure, successfully predicts the tumor development after discontinuation of UV exposure. This model is similar to those used in risk assessments for skin cancers in human populations, e.g., in relation to stratospheric ozone depletion, sunbeds, etc. The model separates UV-driven processes from purely time-dependent processes. These stochastic processes, described by Weibull statistics, form stages in the tumorigenesis. This interpretation of the data indicates that a late, UV-independent stage occurs between the smallest observable tumors and larger ones with diameters of over 4 mm. This could be a simple growth stage, but histopathology suggests that it may also entail a transition from actinic keratosis to squamous cell carcinoma.
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PMID:Development of skin tumors in hairless mice after discontinuation of ultraviolet irradiation. 198 42

We examined data from San Francisco and other areas participating in the Surveillance, Epidemiology, and End Results (SEER) Program to determine the effect of the human immunodeficiency virus (HIV) epidemic on cancer incidence between 1973 and 1987. In this period, non-Hodgkin's lymphoma incidence has increased over 10-fold and Kaposi's sarcoma incidence has increased over 5000-fold in single San Francisco men 20 to 49 years of age. Increases in non-Hodgkin's lymphoma have been restricted to high-grade and diffuse large-cell (intermediate-grade) histological types. With the exceptions of non-Hodgkin's lymphoma and Kaposi's sarcoma, no other tumor has significantly increased in incidence. During 1987, we estimate that HIV-seropositive men in San Francisco had a 0.47% risk of developing non-Hodgkin's lymphoma and a 1.6% risk of developing Kaposi's sarcoma. The relative risks for non-Hodgkin's lymphoma and Kaposi's sarcoma associated with HIV infection were 104 and 40,000, respectively. For 1987, HIV was associated with 14% of all reported cancers (except non-melanoma skin cancer) in men aged 20 to 49. We expect that 1,890 to 2,730 excess cases of non-Hodgkin's lymphoma and 6,490 to 8,320 excess cases of Kaposi's sarcoma will occur in the United States in 1990.
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PMID:Increasing incidence of cancers associated with the human immunodeficiency virus epidemic. 200 49

Merkel cell carcinoma is a skin cancer that bears histologic, ultrastructural, and immunohistochemical resemblance to small cell lung cancer. Although this tumor is often localized and may be treated with wide excision, metastatic Merkel cell carcinoma does appear in 18%-28% of patients and may be aggressive and lethal. We report a case of metastatic Merkel cell carcinoma who responded to treatment with cisplatin/etoposide. Review of the literature reveals that doxorubicin/cyclophosphamide-based regimens and cisplatin-based regimens have been most commonly studied. Complete and partial responses are often achieved although the duration of response tends to be short. Further investigation of chemotherapeutic regimens similar to those used in small cell lung cancer should be undertaken.
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PMID:Chemotherapy of metastatic Merkel cell carcinoma: case report and review of the literature. 202 25

Ultraviolet (UV) irradiation of C3H/HeN mice induces skin cancer and an immunosuppression that prevents the host from rejecting antigenic UV-induced tumors. The capacity of topical vitamin E (dl-alpha-tocopherol) to prevent photocarcinogenesis or the immunosuppression induced by UV irradiation were assessed. Skin cancer incidence in UV-irradiated mice was 81% at 33 weeks after the first UV exposure; application to mice of 25 mg vitamin E three times per week for three weeks before UV irradiation, and throughout the experiment, reduced this incidence to 42% (p = 0.0065, log rank test). Immunoenhancement by vitamin E was assessed by comparing levels of immunosuppression by splenocytes from normal or UV-irradiated mice, with and without topical vitamin E treatment. Transfer of splenocytes from UV-irradiated mice to naive mice prevented the recipients from rejecting a UV-induced tumor challenge, whereas splenocytes from UV-irradiated mice treated with vitamin E did not prevent recipients from rejecting a similar tumor challenge. Phenotypic analysis of splenocytes used in the passive transfer assay, conducted with a biotin-avidin-immunoperoxidase technique, revealed that vitamin E treatment of mice undergoing UV irradiation prevented the UV-induced down regulation of Ia expression in splenocytes and increased the proportion of Lyt-2+ and L3T4+ splenocytes. Therefore, chronically applied vitamin E can effectively reduce cancer formation and immunosuppression induced by UV irradiation. Prevention of UV-induced down regulation of Ia expression may have contributed to this immunomodulation.
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PMID:Topical vitamin E inhibition of immunosuppression and tumorigenesis induced by ultraviolet irradiation. 203 69


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