Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0596263 (carcinogenesis)
 64,820 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report about two cases of cancer of the testis occurring 2 and 7 years after Hodgkin's disease treated with combined chemotherapy and radiation therapy. From an etiopathogenic point of view, this association may, of course, be accidental, but it may also have an iatrogenic origin or be caused by contiguous carcinogenesis, or even by an immune deficiency. In addition to orchidectomy, the therapeutic history of these patients requires an adaptation of the treatment of their tumors of the testes.
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PMID:[Cancer of the testis after Hodgkin's disease. Apropos of 2 cases]. 128 22

To clarify the mechanism by which Cd initiates rat testicular cancer, the ability of Cd or H2O2 to induce DNA single strand breakage was evaluated in testicular Leydig cells using a simple and rapid DNA precipitation method. Effects of Cd, Fe, Zn and Ca on the oxidant-induced DNA damage and effects of reduced glutathione (GSH) on the genotoxicity caused by the peroxide and/or Fe were also assessed. H2O2 induced strong DNA single strand breakage. Cd alone did not exhibit such a genotoxicity nor did it enhance the peroxide-induced DNA damage. Ca and Fe(II) potentiated the oxidant-induced DNA single strand breakage, while Zn partially protected cells from the oxidative damage of DNA caused by the peroxide. GSH attenuated single strand breaks of DNA brought about by H2O2 and/or Fe. These results suggest that the initiation of carcinogenesis in the rat testis by Cd is triggered by active oxygen species such as H2O2, which is generated by the metal exposure, rather than by a direct genotoxicity of Cd. The oxidant-mediated initiation is clearly a complicated event accomplished by multiple factors.
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PMID:DNA damaging activity of cadmium in Leydig cells, a target cell population for cadmium carcinogenesis in the rat testis. 145 53

As part of a search for an effective and safe antiestrogen to be used as adjunct therapy in the treatment of breast cancer, we examined the potential of RU 39,411 and keoxifene to inhibit the incidence of estradiol-induced kidney tumors in Syrian hamsters. Groups of 10 hamsters were chronically treated with implants of either keoxifene, RU 39,411, estradiol plus keoxifene, or estradiol plus RU 39,411 for 8 months. Five hamsters received only estradiol and 5 control animals remained untreated. There was a 100% kidney tumor incidence in estradiol-treated hamsters, which was not statistically different from that in animals co-treated with estradiol plus keoxifene (3 of 4 hamsters with tumors) or estradiol plus RU 39,411 (7 of 8 hamsters with tumors). Rodents treated only with antiestrogen remained tumor free. In addition to kidney tumors, testicular cancer was also found in animals cotreated with either estradiol plus keoxifene (2 of 4 hamsters with tumors) or estradiol plus RU 39,411 (3 of 8 hamsters with tumors). Two animals of this latter group also developed liver tumors. Testicular or liver neoplasms were not observed in hamsters implanted only with estradiol or only with antiestrogen. The lack of inhibition of estrogen-induced carcinogenesis in hamsters by RU 39,411 or keoxifene suggests that these two antiestrogens are not as effective as previously tested substances in inhibiting the appearance of this cancer. However, their concentrations were sufficient to induce, in combination with estradiol, the development of testicular tumors in these hamsters.
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PMID:Lack of effectiveness of antiestrogens RU 39,411 or keoxifene in the prevention of estrogen-induced tumors in Syrian hamsters. 159 73

Simultaneous tumors are rarely encountered during the course of acute leukemias. We report on a case of seminoma of the testis that occurred during the evolution of acute myelogenous leukemia. To our knowledge, this simultaneous association has not previously been described, but a causal relationship was not apparent in the present case. The likelihood of a common carcinogenesis existed, but direct exposure to carcinogens could not be established. Although the results of a physical examination and echography were normal at the time of diagnosis, we cannot exclude the presence of microscopic cancer of the testis. Since the dissemination pattern of seminoma is usually slower than that observed in this case and the disease remains limited to the lymph nodes for long periods following dissemination, the rapid development of the present case might have been attributable to the immunosuppression and the scrotal sepsis that occurred during the induction therapy. Immunosuppression might have stimulated the progression of a primary microscopic seminoma and the development of metastasis, whereas the scrotal sepsis and inflammation might have favored the occurrence of metastasis through bypass of the lymphatic barrier.
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PMID:Simultaneous occurrence of acute myelogenous leukemia and seminoma of the testis. 162 74

Previous studies have shown that platinum-DNA adduct level in leukocyte DNA (measured by antibody methodology) is directly related to disease response in ovarian cancer and testicular cancer. To determine if this principle could be more broadly applied, platinum-DNA damage was studied in a blinded fashion in leukocyte DNA of 21 cancer patients who received carboplatin (day 1) and cisplatin (day 3) in a phase 1 clinical trial. Fifteen different tumor types were included in this cohort. Using atomic absorption spectrometry with Zeeman background correction, DNA-bound platinum was measured during cycles 1 (C1) and 2 (C2) of therapy for most patients. For each of two cycles of therapy, most patients developed measurable levels of adduct after carboplatin, and in most patients adduct levels increased further after cisplatin, often in a supra-additive fashion. Total mg dose levels varied by less than 2-fold, whereas individual patients differed by as much as 10(3) in their adduct measurements after C1 and after C2, and by 29-fold after the very first carboplatin dose. All patients had refractory disease at the initiation of therapy, and 19 patients were evaluable for disease response. Adduct determinations were made 24 h after the first dose of platinum therapy in 17 of these individuals. Mean adduct levels after the first dose of carboplatin were higher in six responders (50 fmol/micrograms DNA +/- 26) than in 11 non-responders (14 fmol/micrograms DNA +/- 10); Wilcoxon two sample test two-sided P = 0.0071. The six responders were patients with pleural mesothelioma (2), breast cancer, buccal mucosa cancer, esophageal cancer and ovarian cancer. Adduct levels were consistently higher in the group of responders on each day that adduct was measured, with a summary two-sided P value of 0.00011. We conclude that analysis of platinum-DNA adduct formation may help determine whether pharmacogenetics are important in cancer drug resistance; and may help to determine the relationship between DNA damage in the peripheral blood compartment and internal organ response to in vivo exposures to DNA-damaging agents.
Carcinogenesis 1991 Jul
PMID:Platinum-DNA damage in leukocyte DNA of patients receiving carboplatin and cisplatin chemotherapy, measured by atomic absorption spectrometry. 207 Apr 90

Seventeen patients with 'poor prognosis' non-seminomatous testicular cancer were monitored for formation of intrastrand bidentate N7-d(ApG)- and N7-d(GpG)-diammineplatinum adducts in peripheral blood cell DNA during the course of cisplatin-based chemotherapy. Adduct values from blood cell DNA samples were compared with disease response data from the same individuals. Patients who received a dose of 40 mg/m2 cisplatin for 5 days generally formed more adducts than patients receiving 20 mg/m2 for 5 days, and adduct levels ranged from 0 to approximately 300 amol/micrograms DNA. Among the individuals who achieved a complete response, the median adduct level was 170 amol/micrograms DNA and the mean was 162. Among the individuals who achieved a partial response, the median adduct level was 78 amol/micrograms DNA and the mean was 83. Comparison of adduct levels between response groups using the Mann-Whitney test gave a two-sided P value of 0.072 (one-sided P value 0.036). Of 11 patients forming high levels of adduct (greater than 140 amol/micrograms DNA), 10 achieved a complete response; this compares with two complete responders in the group of six patients forming low levels (less than 100 amol/micrograms DNA) of adduct (P = 0.055, two-sided Fisher exact test). We conclude that cisplatin-DNA adduct formation in peripheral blood cell DNA correlates with the occurrence of complete response in patients with poor prognosis testicular cancer.
Carcinogenesis 1988 Oct
PMID:The measurement of cisplatin-DNA adduct levels in testicular cancer patients. 245 57

Herbst and his colleagues first showed in 1971 that girls born to mothers who had taken diethylstilboestrol (DES) during pregnancy were at an increased risk of clear-cell adenocarcinoma of the vagina and cervix. At first it was feared that these girls would have a high probability of developing clear-cell carcinomas, but the latest report from the Registry for Research on Hormonal Transplacental Carcinogenesis of the University of Chicago puts the risk at only 1 per 1000 of those exposed, from birth through to age 34. On this basis, Herbst and his colleagues have suggested that DES is not a complete carcinogen, but that some other factor is involved in the pathogenesis of clear-cell carcinoma of the vagina and cervix. Women exposed in utero to DES have a high prevalence of vaginal adenosis and tend, therefore, to have an extensive transformation zone on the cervix and in the vagina. There is considerable controversy as to whether or not such women are at increased risk for vaginal and cervical intraepithelial neoplasia. The latest findings from the Study of the Incidence and Natural History of Genital Tract Anomalies and Cancer in Offspring Exposed in Utero to Synthetic Estrogens (the DESAD project) are, however, worrying; during follow-up, vaginal and cervical intraepithelial neoplasia occurred at a rate of 15.7/1000 woman-years in the exposed and at a rate of 7.9/1000 woman-years in the controls (p = 0.01). There is some evidence that exposure in utero to exogenous oestrogens increases the risk of testicular cancer in males. The findings, however, are not conclusive, and the effect does not seem to be specific to DES and related nonsteroidal oestrogens.
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PMID:Epidemiological studies of the effects of diethylstilboestrol. 268 Sep 51

Several large studies have established the usefulness of alpha fetoprotein (AFP) detection as a diagnostic test in patients suspected of having primary hepatoma. in the current study, 65% of patients from Hong Kong and 50% of eastern U.S. patients with hepatocellular carcinoma had AFP in their sera. AFP was not found in normal adult sera in any of the reported series. In this series, AFP was not detected in sera of patients with other hepatic diseases, often associated with AFP occurrence, or in sera of 6 patients with embryonal cell carcinoma of the testis though that disease has also been associated with AFP detection in sera. However, the occurrence of AFP in various tissue extracts was detected in 1/2 extracts of primary hepatoma and in 2/6 extracts of embryonal cell carcinoma of the testis, but not in other tumors. The hepatoma extract containing AFP was from a patient with AFP in serum; the serum from the other patients with hepatoma was negative. Sera from the patients with testicular cancer were not available for testing. Theories on the function of AFP and its relationship to carcinogenesis are also discussed.
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PMID:Alpha-fetoprotein: occurrence in certain malignant diseases and review of clinical applications. 419 53

One-hundred thirty-seven patients with a history or clinical evidence of cryptorchidism and testicular germinal tumor were treated at our hospital from 1934 to 1976. Cryptorchidism was corrected ipsilaterally or contralaterally in 93 patients with intrascrotal testis cancer when they were from 2 to 42 years old, either spontaneously (24 patients), by orchiopexy (58 patients), or by hormonal therapy (11 patients). Forty-four cryptorchid patients (uncorrected cases) had either ipsilateral inguinal (24 patients), or abdominal (14 patients), or contralateral intrascrotal tumors (six patients). Tumor histologic types on orchiectomy were pure seminoma in 56 patients, embryonal carcinoma in 41, teratocarcinoma in 37, and pure choriocarcinoma in 3. The five-year survival rates were similar in the corrected (61%) and uncorrected (63%) cases, and they were higher in patients with pure seminoma (79%) than in patients with germinal carcinomas (50%). The majority (64 of 80) of five-year survivors received regional lymphatic irradiation in 41 patients with pure seminoma and/or systemic chemotherapy in 23 patients with other germinomas. Since the testicular tumors that developed despite correction of the cryptorchid state were predominantly (72%) germinal carcinomas, unilateral cryptorchidism, which usually is associated with testicular atrophy, should be treated by orchiectomy instead of orchiopexy to prevent ipsilateral carcinogenesis. Cryptorchid patients with testicles that descended late should be observed periodically, especially after the 20-year latent period, for early detection of cancer.
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PMID:Testicular cancer in cryptorchids. 612 Jul 55

A spectrum of genitourinary abnormalities occur in patients with cryptorchidism; the most important is the enhanced susceptibility to developing testis cancer. While the etiologic basis for developing testis cancer in cryptorchid patients remains controversial, failure of normal testicular development--testicular dysgenesis--may underlie carcinogenesis in the cryptorchid testis. This report reviews these associations as well as the characteristics of testis cancer in the cryptorchid testis and the evidence supporting early orchiopexy.
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PMID:The spectrum of genitourinary abnormalities in patients with cryptorchidism, with emphasis on testicular carcinoma. 612 55


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