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PubMed1998

Lung and kidney cancer mortality associated with arsenic in drinking water in Córdoba, Argentina.

BACKGROUND: Studies in Taiwan have found dose-response relations between arsenic ingestion from drinking water and cancers of the skin, bladder, lung, kidney and liver. To investigate these associations in another population, we conducted a study in Córdoba, Argentina, which has a well-documented history of arsenic exposure from drinking water. METHODS: Mortality from lung, kidney, liver and skin cancers during the period 1986-1991 in Córdoba's 26 counties was investigated, expanding the authors' previous analysis of bladder cancer in the province. Counties were grouped a priori into low, medium and high arsenic exposure categories based on available data. Standardized mortality ratios (SMR) were calculated using all of Argentina as the reference population. RESULTS: We found increasing trends for kidney and lung cancer mortality with arsenic exposure, with the following SMR, for men and women respectively: kidney cancer, 0.87, 1.33, 1.57 and 1.00, 1.36, 1.81; lung cancer, 0.92, 1.54, 1.77 and 1.24, 1.34, 2.16 (in all cases, P < 0.001 in trend test), similar to the previously reported bladder cancer results (0.80, 1.28, 2.14 for men, 1.22, 1.39, 1.81 for women). There was a small positive trend for liver cancer but mortality was increased in all three exposure groups. Skin cancer mortality was elevated for women only in the high exposure group, while men showed a puzzling increase in mortality in the low exposure group. CONCLUSIONS: The results add to the evidence that arsenic ingestion increases the risk of lung and kidney cancers. In this study, the association between arsenic and mortality from liver and skin cancers was not clear.

Argentina↗
PubMed2005

Continuous infusion interleukin-2 and antihistamines in metastatic kidney cancer.

A prior randomized trial suggested a possible survival advantage favoring the combination of histamine and subcutaneous interleukin-2 (IL-2), compared to IL-2 alone in patients with metastatic melanoma. It has been postulated previously that antihistamines may, therefore, actually be antagonistic to IL-2 and thus interfere with its antitumor activity. We have previously shown no such antagonistic effect in patients with melanoma receiving IL-2 and antihistamines when reviewing the known literature. We sought to determine whether there was any negative effect of the combination in patients with metastatic kidney cancer. A PubMed literature search between 1985 and 2005 was done. High-dose continuous (or constant) infusion (CIV) interleukin-2 was used as the reference therapy because of the relatively constant IL-2 levels generated by this approach. Studies in which cimetidine, ranitidine, or famotidine were regularly scheduled and administered concurrently with IL-2 were included. Thirteen studies were identified. A total of 47 patients responded to therapy. Total response rate = 22%; 95%; Confidence Interval: 17%-28%. Eleven complete responses were noted. Complete response rate = 5%; 95% Confidence Interval: 3%-9%. These response rates are consistent with previously noted IL-2 response rates. In this study of CIV IL-2 and antihistamines, this combination appears to be active in metastatic kidney cancer. There appears to be no negative effect of antihistamine on the CIV IL-2 response rate in this disease.

Adjuvants, Immunologic↗
PubMed2005

Correlation between development of pulmonary edema and response of pulmonary metastases of metastatic melanoma and kidney cancer to high-dose continuous-infusion interleukin-2.

The administration of high-dose continuous intravenous infusion interleukin-2 (IL-2) is able to induce the presence of lymphokine-activated killer (LAK) cells. LAK are able to nonspecifically lyse tumor cells. They are also able to lyse endothelial cells, which accounts for, at least in part, the capillary leak syndrome seen as one of the toxicities with this therapy. A pulmonary manifestation of capillary leak syndrome is the presence of pulmonary edema. We postulated that capillary leak may also be a mechanism by which LAK could conceivably reach pulmonary metastases or could be a reflection of damage of endothelial cells in vasculature supplying metastases and that capillary leak syndrome may actually correlate with the response of pulmonary metastases. We examined our database of patients with lung metastases treated with high-dose continuous infusion IL-2 (18 MIU/m(2)/day for 3 days) regimens. Eighteen patients had the following characteristics: melanoma (11), renal cancer (7), median age of 67 years (range, 28-79 years), and males (15). All patients were treated by oncology nurses on either the stem cell transplant unit or oncology ward. Pulmonary edema was defined as the presence of pleural fluid on a chest X-ray, computed tomography (CT) scan, and/or as noted on a physical examination by at least 2 observers. No patients required endotracheal intubation, mechanical ventilation, or an intensive care unit transfer. The median number of cycles received was 6 (range, 1-13). All 8 responding patients (6 patients with melanoma, 2 patients with kidney cancer) manifested pulmonary edema during interleukin-2 therapy. Four patients with pulmonary edema were nonresponders. The presence of pulmonary edema correlated with the response to therapy (p = 0.01). The median duration of response of pulmonary nodules was 5 months (range, 1-16 months). There is a correlation between the development of pulmonary edema and the response of pulmonary metastases in patients with melanoma and kidney cancer treated with high-dose continuous infusion interleukin-2.

Adult↗
PubMed2003

Gemcitabine, paclitaxel, pemetrexed and other newer agents in urothelial and kidney cancers.

Significant progress has been made in understanding the biology of urothelial and kidney cancers. Approaches to advanced urothelial cancer include dose intensification, reducing toxicity in unfit or elderly patients, doublet and triplet combination chemotherapy and sequential regimens. Promising new chemotherapeutic agents such as the epothilones, pemetrexed (Alimta), topoisomerase inhibitors and vinflunine act at different phases of the cell cycle and on folate metabolism. New agents that are combined with chemotherapy in urothelial cancer include the farnesyl transferase inhibitors and growth factors receptor inhibitors. Renal cell carcinoma (RCC) is particularly resistant to cytotoxic agents, although a gemcitabine/fluorinated pyrimidine combination may have modest but real clinical benefit. In metastatic RCC, new biologic and targeted therapies include anti-angiogenesis agents such as anti-vascular endothelial growth factor (VEGF) antibody and thalidomide, as well as toremifene, CCI-779 and allogeneic stem cell transplantation. Metastatic urothelial and renal cell cancers continue to be the clinical trial focus of many novel agents. The molecular biology of these diseases is being unravelled and as knowledge accumulates, our ability to target these cancers will continue to increase.

Angiogenesis Inhibitors↗
PubMed1995

Somatic mutations of von Hippel-Lindau (VHL) tumor-suppressor gene in European kidney cancers.

Somatic mutations of von Hippel Lindau (VHL) tumor-suppressor gene have been identified in kidney cancers from North America and Japan. We studied VHL gene mutation in 31 kidney tumors from France. Of these tumors, 45% (14/31) displayed mutations, 60% of which occurred at A:T base pairs. The frequency and the spectrum of mutations identified in kidney tumors from Europe were similar to those reported for tumors from other geographical locations.

Adult↗
PubMed2000

Short-term tumor cell lines from renal cell carcinoma for use as autologous tumor cell vaccines in the treatment of kidney cancer.

OBJECTIVE: We have tried to establish short-term cultures of autologous tumors from patients with renal cell carcinoma that could be used as active specific immunotherapy (i.e., autologous vaccine) in such patients after resection of primary kidney cancer, and/or for the treatment of metastatic cancer. METHODS: Between 10/90 and 9/99 the cell biology laboratory of the Hoag Cancer Center received 69 kidney tumor samples that had been surgically excised, including 43 primary tumors and 26 metastatic lesions. Efforts were made to establish short-term tumor cell cultures, as defined by the growth of 10(8) cells; malignant nature and renal cell origin were confirmed by morphology and antigenic phenotyping. Variables associated with successful growth of short-term cell lines were examined. RESULTS: Short-term cell lines were successfully established from 55/69 samples [80%] including 36/43 (84%) from primary tumors and 19/26 (73%) from metastatic lesions. The success rate for tumors harvested at Hoag Hospital was 40/50 (80%); the success rate for tumors obtained from other geographic areas was 15/19 (79%). Tumor cell lines were successfully established from metastatic lesions ranging in size from a 0.5 g vertebral lesion to a 22 g rib/lung chest wall metastasis, and from primary renal cell lesions ranging in size from 1.5 g to 39.7 g. CONCLUSIONS: Short-term cell lines can be established for most patients with primary or metastatic renal cell carcinoma making a pure autologous tumor-cell vaccine approach feasible. Vaccines have been prepared for 41 patients and a vaccine therapy trial is in progress.

Bone Neoplasms↗
PubMedDate not supplied

Urinary tract cancers: kidney and urinary bladder.

The present paper analyses temporal trends for cancers of the kidney including urinary tract and of the urinary bladder, in the Italian Network of Cancer Registries (pool AIRT), for the period 1986-1997. As regards kidney cancer (14,915 cases and 5,857 deaths analysed) a statistically significant increase has been observed in incidence rates. Such increase was present from 1986 to 1991 among males, +5.4%/year, afterwards it became rather stable; among females, the incidence increased along the whole period, +2. 7%/year. Mortality rates were stable along the analysed time period. Bladder cancer incidence (33,283 cases) showed a significant increase in both sexes, + 1. 6%/year among males and +2.5% among females, whereas mortality (9,348 deaths) showed a significant decreasing trend in both males, -2.7%/year, and females, -3.5%/year.

Adolescent↗
PubMed1991

The association of oral contraception with kidney cancer, colon cancer, gallbladder cancer (including extrahepatic bile duct cancer) and pituitary tumours.

This paper reviews the evidence for a relationship between oral contraceptive use and certain neoplasms: cancers of the kidney, colon and gallbladder (including the extrahepatic bile ducts) and tumours (benign or malignant) of the pituitary. Special reference is made to controlled epidemiological studies, both case-control and cohort. There is no convincing evidence that oral contraceptive use is causally related, either negatively or positively, to any of the tumours studied.

Bile Duct Neoplasms↗
PubMed2003

Von Hippel-Lindau tumor suppressor protein and hypoxia-inducible factor in kidney cancer.

The development of hereditary von Hippel-Lindau (VHL) disease and the majority of sporadic kidney cancers are due to the functional inactivation of the VHL gene. The product of the VHL gene, pVHL, in association with elongins B and C, cullin 2, and Rbx1 form an E3 ubiquitin-ligase complex VEC that targets the alpha subunits of hypoxia-inducible factor (HIF) for ubiquitination. Ubiquitin-tagged HIF-alpha proteins are subsequently degraded by the common 26S proteasome. pVHL functions as the substrate-docking interface that specifically recognizes prolyl-hydroxylated HIF-alpha. This hydroxylation occurs only in the presence of oxygen or normoxia. Thus, under hypoxia, HIF-alpha subunits are no longer subjected to degradation and are thereby able to dimerize with the common and constitutively stable beta subunits. The heterodimeric HIFs upregulate a myriad of hypoxia-inducible genes, triggering our physiologic response to hypoxia. Inappropriate accumulations of HIF-alpha in VHL disease are believed to contribute to the pathogenesis via the upregulation of several of these HIF target genes. Our current molecular understanding of the roles of HIF and pVHL in the development of VHL-associated clear-cell renal cell carcinoma (CC-RCC) is the focus of this review.

Adenocarcinoma, Clear Cell↗
PubMedDate not supplied

Kidney cancer, leukemia, and liver cancer. Part 3.

This is the third of a six-part series on metastatic spread and natural history of 18 common tumors. Part one summarized symptom/problem anticipation, cancer metastasis, and the 18 tumors that each cause more than 6,000 deaths per year in the United States. Bladder and brain cancers were discussed, with information given on tumor types, metastatic spread and invasion, and common symptoms. Part two charted the natural histories, problems, and assessment parameters of advanced breast, colon and rectum (colorectal), and esophageal cancers. Part three presents the natural histories, problems, and assessment parameters of advanced kidney cancer, leukemia, and liver cancer. Each of these cancers is presented separately, with information given on mortality rates, the most common tumor types, sites of metastases, common problems, and common oncologic emergencies. Sites of spread, resulting problems (including site-specific symptoms), and assessment parameters are presented as tables. Material is presented so that clinicians will be able to anticipate the spread of these cancers and can thus identify problems early in their development so that that they are more easily managed.

Humans↗
PubMedDate not supplied

[The late results of organ-saving operations in T1,2 N0M0 kidney cancer].

The analysis of organ-saving operations for renal cancer T1,2 N0M0 demonstrates that in cancer of the kidney up to 5 cm in size organ-saving operations are not inferior to routine nephrectomy by 5-year survival (95.4 +/- 4.5% versus 84.0 +/- 8.1%, respectively). The operated kidney functions well in 89.2 +/- 5.1% of cases.

Adult↗
PubMed2006

Obesity, high energy intake, lack of physical activity, and the risk of kidney cancer.

The authors conducted a population-based case-control study of 810 cases with histologically confirmed incident kidney cancer and 3,106 controls to assess the effect of obesity, energy intake, and recreational physical activity on renal cell and non-renal cell cancer risk in Canada from 1994 to 1997. Compared with normal body mass index (BMI; 18.5 to <25.0 kg/m2), obesity (BMI, >or=30.0 kg/m2) was associated with multivariable-adjusted odds ratios (OR) and 95% confidence intervals (95% CI) of 2.57 (2.02-3.28) for renal cell cancer and 2.79 (1.70-4.60) for non-renal cell cancer. The OR (95% CI) associated with the highest quartiles of calorie intake was 1.30 (1.02-1.66) for renal cell cancer and 1.53 (0.92-2.53) for non-renal cell cancer. Compared with the lowest quartile of total recreational physical activity, the highest quartile of total activity was associated with an OR (95% CI) of 1.00 (0.78-1.28) and 0.79 (0.46-1.36) for the two subtypes. There were no apparent differences between men and women about these associations. The influence of obesity and physical activity on the risk of renal cell and non-renal cell cancer did not change by age, whereas the effect of excess energy intake was stronger among older people. No significant effect modifications of physical activity on BMI among both genders and of energy intake on BMI among men were observed, with a synergic effect of obesity and high energy intake on renal cell cancer risk found among women. This study suggests that obesity and excess energy intake are important etiologic risk factors for renal cell and non-renal cell cancer. The role of physical activity needs further investigation.

Adult↗
PubMed1987

The enhanced 32P labeling of CDP-diacylglycerol in c-myc gene expressed human kidney cancer cells.

Correlation between c-myc gene expression and phosphatidylinositol (PI) metabolism was studied using seven human kidney cancer cell lines. We found that the exceptional incorporation of 32P into CDP-diacylglycerol (CDP-DG) was observed in only two cell lines, in which c-myc expression was increased among seven cell lines tested. In these two cell lines, PI was also labeled. The other five cell lines indicated the accumulation of radioactive PI, whereas CDP-DG was unlabeled.

Cell Division↗
PubMed1992

Risk factors for kidney cancer in New South Wales--I. Cigarette smoking.

In a population-based case-control study of kidney cancer in New South Wales, data from structured interviews with 489 cases of renal cell cancer (RCC), 147 cases of renal pelvic cancer (CaRP) diagnosed in 1989 and 1990, and 523 controls from the electoral rolls confirmed an increased risk associated with cigarette smoking in both types of cancer. The risk among current smokers was consistently higher than among ex-smokers, and was nearly twice as great for CaRP than for RCC. Additional information provided by this study includes reduced risks following cessation of smoking within 12 years for CaRP, but only after 25 years for RCC. Starting to smoke before, rather than after, the age of 18 years is linked independently with almost twice the risk for CaRP, but does not affect the risk for RCC. No independent trend was found with number of cigarettes smoked per day.

Adult↗
PubMed1995

[Diagnosis of kidney cancer using modern imaging techniques].

Basing on own material comprising 88 patients with diagnosed and operatively and microscopically verified kidney cancer the authors retrospectively assessed diagnostic value of urozonography, USG and CT imaging. Zonography was found to have the smallest diagnostic value (62.5%). USG had 84.1% and CT 92% diagnostic value.

Adult↗
PubMed1999

Localization of hydroxynonenal protein adducts in normal human kidney and selected human kidney cancers.

Both polyclonal and monoclonal antibodies to 4-hydroxy-2-nonenal (HNE) protein adducts were used to identify lipid peroxidation products in normal human kidney and in selected human kidney cancers using immunoperoxidase techniques at the light microscopic level and immunogold techniques at the ultrastructural level. HNE protein adducts were detected in most cell types in normal kidney, although in highly variable amounts. All six morphologic types of renal tumors examined showed some staining with antibodies to HNE protein adducts, although the intensity of staining varied considerably depending on tumor type. Renal oncocytoma and the granular cell variant of renal adenocarcinoma both showed greater cytoplasmic staining for HNE protein adducts than the other tumors examined; these tumors both contain high numbers of mitochondria and suggest that mitochondria are a major source of lipid peroxidation products. To test this possibility, immunogold ultrastructural analysis was performed. HNE protein adducts were identified in nuclei and mitochondria in both normal proximal tubule and three types of renal carcinoma examined; these results localize oxidative damage at the subcellular level in both benign and malignant epithelium to nuclei and mitochondria. In conclusion, HNE protein adducts occur in kidneys in both normal and tumor cells, although immunomorphologic analyses suggest less HNE protein adducts in tumor cells.

Aldehydes↗