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Query: UMLS:C0025202 (melanoma)
 69,561 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mechanism of the cytostatic and cytocidal activities of TNF was studied in human tumour cells. BT-20 breast and ME-180 cervical cancer cells were significantly growth-inhibited by TNF, but other cells were not. When protein synthesis was inhibited by cycloheximide, however, TNF was cytotoxic for all cells except BT-20 cells. This suggests that different mechanisms are responsible for the cytostatic and cytocidal activities of TNF. The sensitivity of different cell lines could not be correlated with the number or affinity of TNF receptors. Some protease inhibitors completely protected human and murine cells from TNF cytotoxicity. Inhibitors of chymotrypsin-like proteases were more effective than inhibitors of trypsin-like proteases. Reversible and irreversible inhibitors (such as alkylating compounds) were both protective. The cells were best protected when pretreated with inhibitors before the addition of TNF. When the protease inhibitors were removed the cells gradually lost their resistance to TNF cytotoxicity. The inhibitors did not interfere with the functioning of TNF-receptor complexes, since SK-MEL-109 melanoma cells treated with a protease inhibitor synthesized TNF-induced proteins. These findings suggest that a protease is involved in the cytocidal activity of TNF.
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PMID:Cytocidal activity of tumour necrosis factor: protection by protease inhibitors. 333 13

The correlation between various types of hormone treatments, especially treatment with combined contraceptive pills and postmenopausal estrogen treatment is complex and interpretation is made difficult by methodological problems. The effects on cancer development vary for different types of cancers, with type and dosage of hormone and probably also, insofar as breast cancer is concerned, with age and age at which treatment was begun. There is clear evidence that the combined contraceptive pills previously used with relatively high doses of estrogen and gestagen protect against both endometrial and ovarian cancer. There is no strong evidence for a generally increased risk of breast cancer and only a few recently published studies indicate that longterm contraceptive pill treatment can increase the risk for premenopausal breast cancer. Longterm treatment has also been reported to increase the risk of cervical cancer, benign and malignant liver tumors, and of melanoma, but available data do not furnish any substantial conclusions on the causal connection. Substitution treatment with estrogens and estrogen-gestagen combinations in the postmenopausal period is probably connected with a moderate and duration-dependent increase in risk of breast cancer. There is convincing evidence that the risk of breast cancer. There is convincing evidence that the risk of endometrial cancer rises with increasing length of treatment but that it can be hindered with cyclic gestagen additives.
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PMID:[Cancer risk in connection with oral contraceptives and postmenopausal hormone treatment]. 341 83

The question of whether the steroidal components in oral contraceptives (OCs) may have an initiating or promotional influence on the development of cancer continues to be raised as a public health issue. It is estimated that since the introduction of OCs nearly 25 years ago, more than 150 million women have used 1 or more types of the formulation and nearly 1 billion woman-years of exposure to the steroids have accumulated. Contraceptive practice in Australia would indicate that about 25% of women of reproductive age are using OCs. The debate about the OC's carcinogenic potential has recently been reopened with 2 reports in "The Lancet" of an association between the incidence of breast and cervical cancer and OC usage. Biologically the relationship between the contraceptive steroids and cancer must continue to be regarded as the most important concern with the longterm use of OCs. The demonstration of receptors to these steriods in these organs, in both normal and malignant tissues, further increases the speculation that the steroid hormones have a biological role in carcinogenesis in these target organs. Theoretical reasons exist for the concern about carcinogenesis and contraceptive steroids. This paper reviews the available evicence. Data can be derived only from large-scale epidemiological research, by means of case-control or cohort studies. No clear evidence exists that OCs cause or increase the chance of developing any cancer in the female genital tract and the breast. In fact, OC offers a significant protection against the development of endometrial and ovarian cancer, especially to those women who have taken OCs for a long time. The association between the risk of breast cancer and OC use is less certain, but factors such as the history of benign breast disease, a close relationship with breast cancer, or nulliparity -- previously considered to be important -- do not appear to contribute significantly to the risk. The weight of evidence indicates that no increased risk of breast cancer exists, even in those younger women aged less than 25 years who decide to use OCs before their 1st full-term pregnancy. There is some evidence that suggests that the risk of cervical neoplasia -- dysplasia, carcinoma-in-situ and invasive carcinoma -- may increase slightly in OC users but the actual part played by the patient's sexual history under these circumstances remains to be defined. There is now strong evidence to implicate multiplicity of sexual partners and wart virus infection in carcinogenesis of the uterine cervix. There does not appear to be an overall relationship between OCs and malignant melanoma. Overall, the evidence is reassuring. The low-dose combined OC can be considered safe, not only in terms of cardiovascular and thromboembolic risks, but also in relation to carcinogenesis.
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PMID:Cancer risks and the contraceptive pill. What is the evidence after nearly 25 years of use? 351 57

Metastasis to the spleen from various neoplasms is very rare. Most of the splenic metastases are found at autopsy, and are part of a widespread disease. Four patients had cervical cancer (1 patient), endometrial cancer (1 patient), lung carcinoma (1 patient), and malignant melanoma (1 patient). All patients had splenic involvement without pathologic evidence of lymph node metastasis, and all underwent splenectomy. Three of the four presented with painful splenomegaly. The time from diagnosis to the development of splenic metastasis varied from 20 to 24 months. Two of the four patients had postoperative radiotherapy, one patient received intraperitoneal chemotherapy, and the patient with the melanoma received adjuvant chemotherapy. The rarity of solitary spleen metastasis from solid tumors and the treatment modalities are discussed.
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PMID:Splenomegaly and solitary spleen metastasis in solid tumors. 358 Oct 23

Preventing death from malignant melanoma is the most pressing issue in preventive dermatology in the United States because the mortality rate has increased markedly. Dermatologists, as the physicians best suited by training to identify early malignant melanoma, need to take the lead in developing a national project of educating physicians, patients, and the public to recognize the clinical features of early malignant melanoma and to appreciate that prompt excision results in a high rate of cure. The immediate challenge is to commit ourselves to examining every new patient and to conducting periodic "skin scans" of every patient at increased risk for melanoma. Just as the Papanicolaou screening test has markedly reduced cervical cancer mortality rates, commitment to early identification and excision of melanomas can mean a comparable triumph for preventive dermatology and will help us meet the challenge of our Australian colleagues to make melanoma a word, not a death sentence.
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PMID:Spotting sinister spots. A challenge to dermatologists to examine every new patient at increased risk for signs of early melanoma. 377 50

We examined the activity reported in phase II trials for all cytotoxic drugs introduced into clinical trial by the National Cancer Institute (NCI) since 1970. For each drug in each tested tumor type we derived a response rate from the pooled data of all trials reported either in the literature or to the NCI. We rated a drug active if the lower 80% confidence bound of the response rate was greater than 10%. Of the 83 drugs developed and introduced by the NCI, there are 47 which we considered evaluable. Of these drugs, 24 were rated active in at least one cancer type, of which ten were analogs of drugs in wide clinical use. Diseases most commonly responsive include lymphoma (74% of the tested drugs rated active), leukemia (35%), urothelial cancer (29%), small cell lung cancer (29%), ovarian cancer (22%), cervical cancer (22%), and breast cancer (18%). For colon cancer and melanoma, only one of 42 and two of 30 tested drugs rated active, respectively. We also examined the completeness of clinical testing: among the 47 drugs there were 20 tested in greater than or equal to 14 patients with leukemia, 23 tested in patients with lymphoma, and 18 tested in patients with small cell lung cancer; whereas 34 drugs for breast cancer, 42 for colon cancer, and 33 for non-small cell lung cancer were more completely evaluated. Considering the "clinical panel" of seven cancer types (breast, non-small cell lung, small cell lung, colon, melanoma, leukemia, and lymphoma), drugs were tested in greater than or equal to 30 patients in a median of four tumor types. Testing in this panel failed to detect activity in only one drug found active in another tumor, although testing in diseases other than this clinical panel was even less complete. Phase II testing should emphasize completion of minimum accrual goals, testing in patient populations with minimum prior therapy, and evaluation in a minimum set of tumor types.
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PMID:Clinical drug development: an analysis of phase II trials, 1970-1985. 379 Dec 70

True annular malignancies of the small bowel with mucosal destruction and shelflike margins are generally thought to be caused by primary adenocarcinoma. At our institution, 18 annular malignancies were diagnosed radiographically in the small bowel by enteroclysis (16 cases) and conventional small bowel follow-through studies (2 cases) between 1977 and 1984. However, pathologic data revealed only 4 primary adenocarcinomas with 10 metastatic lesions (6 colon cancers, 2 malignant melanomas, 1 lung cancer, and 1 cervical cancer), 2 leiomyosarcomas, 1 non-Hodgkin's lymphoma, and 1 malignant carcinoid tumor. While these lesions may be indistinguishable radiographically, annular carcinomas tended to be short, relatively nonobstructing lesions; annular metastases (except those from malignant melanoma) tended to be highly obstructing lesions with significant narrowing and/or angulation of the bowel. Leiomyosarcomas, lymphoma, and metastases from malignant melanoma tended to be longer lesions with extensive ulceration, wider channels, and little or no evidence of obstruction. Nevertheless, surgical resection or biopsy of the lesion is ultimately required for a definitive diagnosis.
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PMID:Annular malignancies of the small bowel. 379 59

Variations in cancer incidence among whites in 1973-77 in 8 geographic areas of the Pacific Basin were compared. Substantial differences were found for the occurrences of lung cancer, cancer of the corpus uteri, and malignant melanoma. White women living in New Zealand and Australia had the lowest risk of developing lung cancer, whereas white men living in the western United States had the highest risk. Cancer of the corpus uteri occurred more commonly in the western United States than elsewhere in the Pacific Basin. Geographic areas located closest to the equator experienced the highest incidence of malignant melanoma. In all areas, the incidence rates of cancers of the lung and corpus uteri and malignant melanoma increased significantly between 1960-66 and 1973-77; after the mid-1970s, rates of cancer of the corpus uteri declined. The incidence of stomach cancer decreased in all areas. Although cervical cancer decreased in incidence over time for most women, it increased noticeably in young women. The incidence of breast cancer also rose during the 17-year period. In at least 1 geographic area, the observed increases in breast cancer incidence were confined to women under age 40.
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PMID:Cancer incidence in Caucasians living in the Pacific Basin. 383 48

The numbers of second cancers among 182,040 women treated for cervical cancer that were reported to 15 cancer registries in 8 countries were compared to the numbers expected had the same risk prevailed as in the general population. A small 9% excess of second cancers (5,146 observed vs. 4,736 expected) occurred 1 or more years after treatment. Large radiation doses experienced by 82,616 women did not dramatically alter their risk of developing a second cancer; at most, about 162 of 3,324 second cancers (approximately equal to 5%) could be attributed to radiation. The relative risk (RR = 1.1) for developing cancer in organs close to the cervix that had received high radiation exposures--most notably, the bladder, rectum, uterine corpus, ovary, small intestine, bone, and connective tissue--and for developing multiple myeloma increased with time since treatment. No similar increase was seen for 99,424 women not treated with radiation. Only a slight excess of acute and non-lymphocytic leukemia was found among irradiated women (RR = 1.3), and substantially fewer cases were observed than expected on the basis of current radiation risk estimates. The small risk of leukemia may be associated with low doses of radiation absorbed by the bone marrow outside the pelvis, inasmuch as the marrow in the pelvis may have been destroyed or rendered inactive by very large radiotherapy exposures. There was little evidence of a radiation effect for cancers of the stomach, colon, liver, and gallbladder, for melanoma and other skin cancers, or for chronic lymphocytic leukemia despite substantial exposures. An excess of thyroid cancer possibly was related to the low dose received by this organ. Ovarian damage caused by radiation may have been responsible for a low breast cancer risk (RR = 0.7), which was evident even among postmenopausal women. A substantial excess of lung cancer (RR = 3.7) largely may be due to misclassification of metastases and the confounding influence of cigarette smoking. Women who were under 30 or over 50 years of age when irradiated were at greatest absolute risk for developing a second cancer. The RR, however, was higher among those under age 30 years at exposure (RR = 3.9) than among older women. The expression period for radiation-induced solid tumors appeared to continue to the end of life.
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PMID:Second cancers following radiation treatment for cervical cancer. An international collaboration among cancer registries. 385 84

Eleven patients with spinal cord compression due to metastatic epidural tumors were analyzed. Primary tumors were Hodgkin's disease, non-Hodgkin's lymphoma, multiple myeloma (two patients each), cervical cancer, malignant melanoma, gastric cancer, lung cancer, and neuroblastoma (one patient each). It was felt that myelography is the most important diagnostic test, although CT scan and bone scan may give further diagnostic information in some patients. Six patients were treated with decompressive laminectomy and postoperative radiotherapy, and five with radiotherapy alone. Regardless of the pretreatment neurological status and the type of treatment given, the functional prognosis in our small series of patients appeared to be favorable for radiosensitive tumors such as malignant lymphoma and multiple myeloma.
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PMID:[Clinical study of spinal cord compression due to metastatic epidural tumors]. 395 Nov 27


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