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 28,837 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Efforts to diminish the overall morbidity and mortality of malignancy have required a variety of strategies and a balanced national research agenda. The design of curative regimens against leukemia, lymphomas, testis cancer, and childhood malignancies is a tribute to the interactions between laboratory and clinical scientists. Laboratory models illustrated the importance of dose and the need for combinations to avoid the emergence of drug resistance in heterogeneous tumors. In addressing the incurability of common epithelial cancers in adults once disseminated, again laboratory models suggested that regimens which produced responses in advanced disease might be curative in patients with micro-metastases. Such proved to be the case in adjuvant therapy for breast cancer involving lymph nodes and for osteogenic sarcoma. Recent studies have extended this strategy to less advanced breast cancer and to locally advanced colon cancer. Lung cancer has required a different strategy. A coalition has developed to support the strongest possible public position against smoking. For the first time lung cancer incidence has leveled off in white males. Women and minorities continue to be a major target for smoking cessation programs. While large randomized trials are expensive (and to some scientists, unexciting), they are our most reliable means of detecting treatment differences of 10 to 15%. Because lung, breast, and colon cancer kill almost 250,000 Americans each year, such "small" differences represent thousands of Americans. There are also a number of interesting current studies that may impact in the longer term on the care of patients with cancer. Research of three different groups of investigators has recently converged. Over the past 3 decades several groups of basic laboratory investigators had been studying and cloning hematopoietic growth factors. Large randomized trials now confirm that myelosuppression after intensive chemotherapy can be substantially ameliorated, reducing infections and decreasing hospital days, risks, and costs. Another cohort of clinical pharmacologists and clinicians were studying bone marrow transplantation, developing combinations of agents that can be given at high dose to overcome resistance, albeit with considerable toxicity. Other groups in blood banks and those interested in the regulation of hematopoiesis recognized that early hematopoietic progenitor cells circulate in the peripheral blood. Their number were increased after certain chemotherapy regimens, by growth factors and most remarkably, with growth factors given after chemotherapy. Patients supported with peripheral blood progenitor cells reengraft both platelets and granulocytes more rapidly than those given marrow, in the time frame of recovery after standard doses of chemotherapy (i.e., 21 days).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:New developments in clinical oncology: the interdependence of bench and bedside. 167 75

A Phase I clinical trial of 1-beta-D-arabinofuranosyl-5-azacytosine (ara-AC or fazarabine) given as a 72-h continuous infusion on a 21-day cycle was conducted in 27 adult patients with refractory cancer. The major toxicity was reversible granulocytopenia and thrombocytopenia. Dose-limiting toxicity was observed at a dose rate of 1.96 mg/m2/h in which Grade IV leukopenia (WBC less than 1,000/mm3) occurred in 4 of 11 patients and Grade IV thrombocytopenia (platelets less than 25,000/mm3) occurred in 3 of 11 patients. Plasma steady-state levels ranged from 0.13 to 0.6 microM for doses of 1.25 to 5.94 mg/m2/h. Mean total body clearance was 647 ml/min/m2. Minor clinical responses were seen in one patient with testicular cancer, one patient with colon cancer, one patient with breast cancer, and one patient with acute nonlymphocytic leukemia. Another patient with adenocarcinoma of unknown primary had stable disease during 13 cycles of therapy. Based on the results of this study, the recommended dose for Phase II studies of 1-beta-D-arabinofuranosyl-5-azacytosine administered as a 72-h continuous infusion is 2.0 mg/m2/h (48 mg/m2/day).
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PMID:Phase I and pharmacokinetic study of arabinofuranosyl-5-azacytosine (fazarabine, NSC 281272). 168 36

We conducted a series of case-control studies to investigate the risks of 16 cancer types in relation to occupational physical activity. These studies were based on Missouri Cancer Registry data for 17,147 White male cancer patients registered between 1984 and 1989. Colon cancer risk was increased for both the moderate (odds ratio (OR) = 1.1; 95% confidence interval (CI) = 1.0, 1.3) and low (OR = 1.2; 95% CI = 1.0, 1.5) activity levels. Similar elevations were observed for prostate cancer at the moderate (OR = 1.1; 95% CI = 1.0, 1.3) and low (OR = 1.5; 95% CI = 1.2, 1.8) levels of activity, and for cancer of the testis at the low activity level (OR = 2.2; 95% CI = 1.3, 3.7). An opposite trend (p less than 0.01) was noted for lung cancer, which showed decreased risk at the moderate (OR = 0.9; 95% CI = 0.8, 1.0) and low (OR = 0.8; 95% CI = 0.6, 0.9) activity levels. These associations suggest that further study of the relationship between physical activity and site-specific cancer risk is warranted.
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PMID:Physical activity on the job and cancer in Missouri. 201 69

The effective treatment of systemic cancer began in the 1950s on two fronts, i.e., childhood leukemia and choriocarcinoma. These two diseases were successfully treated as a direct result of the use of antifolate methotrexate. The demonstration of complete durable remissions in these diseases quickly led to development of other anticancer drugs, tested using the prospective clinical trials. In the 1960s as the number of active drugs increased, combination chemotherapy was introduced. Other systemic cancers, such as Hodgkin's, large cell lymphoma, and testicular cancer, became curable in the 1970s. For the common low-growth fraction solid tumors, the curability of systemic disease remained elusive until the introduction of adjuvant therapy to treat micrometastases. The past decade of the 1980s has seen improvement in the outcomes for breast cancer, osteosarcoma, and possible colon cancer utilizing adjunctive chemotherapy. The 1980s also saw the introduction of biologic therapies that have further improved the outcomes of several leukemias and produced consistent responses in patients with renal cell and melanoma. The 1990s will undoubtedly see more improvements as the effects of current drugs will be enhanced not only by improved integration of systemic and local therapies but also by utilizing cytokines and biologic response modifiers in concert with cytotoxics. Moreover, as we understand more about the process of cancer induction, promotion, and progression, more specific anti-cancer approaches will be developed to control cancer even before clinical cancer is diagnosed. Underlying and facilitating the improvement in cancer therapy have been not only the experimental results of many laboratory scientists but also the outcomes from many controlled clinical trials, the laboratory of clinical scientists.
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PMID:Progress in the systemic treatment of cancer. Concepts, trials, drugs, and biologics. 230 52

Physicians are increasingly aware of their complex responsibilities in finding the difficult compromise necessary to achieve cost-effective follow-up care of cancer patients. They must consider not only the best interests of their patients but also the interests of a cost-conscious society. To meet their new societal obligations, physicians trained solely to serve the patient's best interest must now learn how to do so at the least expense. This implies knowing both the costs and the performance characteristics of the diagnostic tests ordered in follow-up. The authors analyze this dilemma as it applies to follow-up of patients following primary treatment for colon cancer or nonseminomatous testicular cancer. Principles of cost-effective patient management are reviewed.
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PMID:Cost-effective follow-up of the cancer patient. Time for a new look. 312 91

Clinical studies have demonstrated an altered pineal function in cancer patients. Owing to the documented antineoplastic activity of the pineal gland, these anomalies could have a prognostic significance. This study was carried out to monitor changes in blood levels of melatonin, the most important pineal hormone, in relation to the clinical response to chemotherapy in human neoplasms. The study included 42 cancer patients of both sexes (breast cancer, 10; lung cancer, 13; colon cancer, 11; soft tissue sarcoma, 4; testicular cancer, 1; Hodgkin's disease, 1; peritoneal mesothelioma, 2). Melatonin serum levels were measured by radioimmunoassay before and 28 days after each cycle of chemotherapy. The results showed that, irrespectively of the type of tumor and chemotherapeutic regimen, 12/16 patients (75%) whose melatonin markedly enhanced after chemotherapy had an objective regression. In contrast, 2/26 patients only (8%) whose melatonin did not enhance after chemotherapy had a clinical response. The percentage of objective responses was statistically significantly higher in patients with a chemotherapy-induced melatonin increase than in those with no melatonin increase (p less than 0.001). This study seems to demonstrate that melatonin determination can be used as a predictor of the objective response to chemotherapy in cancer patients. Moreover, it suggests that the antineoplastic effect of cytotoxic drugs may require participation of the pineal gland.
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PMID:Melatonin increase as predictor for tumor objective response to chemotherapy in advanced cancer patients. 340 Jan 24

The risk of a second primary cancer developing was evaluated in nearly 20,000 men with cancers of the prostate or testis in Connecticut, 1935-82. Among 18,135 men with prostate cancer, a significant 15% deficit of all second cancers was observed [1,053 vs. 1,241; relative risk (RR) = 0.85; 95% CI = 0.80-0.90], most notably for respiratory (RR = 0.7) and digestive cancers (RR = 0.8). The absence of a colon cancer risk lends little support to the idea of common risk factors such as dietary fat consumption. Only the risk for salivary gland cancer was significantly increased, possibly due to chance. Leukemia was significantly elevated among men observed for 10 and more years (RR = 2.2). In contrast to most other index tumors, the prostate stands out as being associated with an overall low risk of second cancer development. The reasons for these deficiencies have not been explained. Among 1,446 men with testis cancer, a significant twofold risk of second cancers was seen (104 vs. 50.1). A fivefold risk of leukemia (8 vs. 1.5) was not related to treatment or age. Contralateral testis cancer (6 vs. 0.5) was elevated in men treated with and without radiation. Risks for kidney cancer (5 vs. 1.5), bladder cancer (9 vs. 3.4), pancreatic cancer (6 vs. 1.5), non-Hodgkin's lymphoma (6 vs. 1.5), and prostate cancer (12 vs. 5.9) were significantly increased. No trends over time were noted for any cancer. Overall risk of second cancer development tended to be higher in younger men with testis cancer. The relationship of leukemia to testis and prostate cancers should be investigated in future research.
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PMID:Second cancer following cancer of the male genital system in Connecticut, 1935-82. 408 95

Phase III randomized clinical trials have greatly contributed to our understanding of the pathobiology of neoplastic disease and, particularly, to therapeutic progress. However, randomized Phase III studies are no better than or are critically dependent on Phase I and Phase II studies for positive therapeutic leads that are compelling enough to test in the Phase III arena. The variables involved in the series of randomized trials that led to the curative treatment of acute lymphocytic leukemia also resulted in an understanding of the principles of cancer therapy in therapeutic research. These principles, when applied to Hodgkin's disease in non-Hodgkin's lymphoma, testis cancer, childhood solid tumors, and others, resulted in a substantial cure rate for those diseases. However, for the adult epithelial common solid tumors, a second strategy, adjuvant chemotherapy, was required This has resulted in a 20% reduction in mortality in patients with node positive and node negative breast cancer. Tamoxifen has been similarly effective in patients with postmenopausal breast cancer. In colon cancer, adjuvant chemotherapy with fluorouracil plus levamisole has decreased mortality to a comparable degree. New agents, modulations, combination chemotherapy, and biotherapeutics are being addressed to the adjuvant situation which has proven effective in a variety of neoplastic diseases. A third strategy is neoadjuvant chemotherapy. This involves the use of chemotherapy first for patients with solid tumors, designed to down-stage the primary tumor thus making it more susceptible to less radical surgery and to organ- or limb-sparing procedures in osteogenetic sarcoma and in head and neck cancer. For example, neoadjuvant chemotherapy has not resulted in an increased survival as compared with the appropriate control but has allowed for important quality-of-life contributions, such as limb-sparing and radical surgery-sparing procedures. In addition to new agents and combination chemotherapy, dose is a critical variable. This is most evident clinically in the transplantation arena. Comparative studies recently completed, for example, in patients with adjuvant breast cancer and with acute leukemia indicate that dose is a significant factor in tumor control.
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PMID:Randomized clinical trials and other approaches in clinical research. 795 73

The incidence of cancer at sites other than the testis has been investigated in the families of 797 Norwegian and 178 Swedish patients diagnosed with testicular cancer during 1981-91. In the families of the Norwegian patients, the total number of cancers in the relatives was significantly lower than the expected number derived from national incidence rates [observed number of cancers 250, expected number of cancers 281.92, standardised incidence ratio (SIR) 0.89, 95% confidence interval (CI) 0.78-1.00]. This finding can be accounted for almost entirely by the finding of fewer than expected prostate and gastrointestinal cancers in the parents of cases. The other common cancers were found at slightly lower than or near the expected levels in the relatives. In the Swedish cohort, which accounts for less than 20% of cases, the observed number of cancers was very close to the expected number. Fourteen fathers of cases had prostate cancer compared with 27.57 prostate cancers expected, giving a SIR of 0.51 (P=0.006). Mothers had more lung cancers (ten cases observed, SIR=2.11, P=0.04) and cancers of the endometrium than expected (13 cases observed, SIR=1.73, P=0.09). These findings may be interpreted as support for theories proposing hormonal dysfunction as causing testicular cancer. Fifty-four gastrointestinal cancers were observed in the parents compared with 68.48 expected (SIR=0.78, P=0.082). Furthermore, testicular cancer was not found to be associated with the known dominantly inherited cancer syndromes [Familial breast (-ovarian) cancer, hereditary no-polyposis colon cancer]. However, one patient belonged to a Li-Fraumeni family, raising the possibility that testicular cancer may be an infrequent component of this rare cancer syndrome. This study supports the hypothesis that families of testicular cancer patients are not prone to cancer.
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PMID:Risk of cancer in relatives of testicular cancer patients. 861 17

The expression of HLA class I antigens was studied by immunohistochemistry in various tumors in correlation with clinicopathologic characteristics. Reduced expression was observed in germ cell testicular cancer, kidney, prostate, gastric and colon cancer, and was associated with tumor aggressiveness, grade and penetration of the tumor through the organ wall. In bladder cancer reduced expression was associated with poor survival. Irradiation of brain tumors resulted in an increase in class I expression. Soluble class I levels were studied in breast and colon cancer patients and were found to be high in those with metastatic disease. The clinical relevance of reduced class I levels are discussed.
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PMID:HLA class I antigen expression in human solid tumors. 900 63


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