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Showing papers in "Journal of the National Cancer Institute in 1969"




Journal ArticleDOI
TL;DR: While suggesting the role of inheritance, the familial patterns seen with rhabdomyosarcoma may result from an interaction of genetic and environmental (?viral) fadors.
Abstract: To study the origins of childhood rhabdomyosarcoma, an examination was made of the 418 death certificates of U.S. children who died of this neoplasm, 1960-64, and of 280 medical charts from 17 hospital centers. Of exceptional interest was the presence in 5 Families of a second child with a soft-tissue sarcoma, 3 sibs (vs. 0.06 expeded by chance), and 2 cousins. The parents, grandparents, and other relatives of children in these families had a high Frequency of carcinoma ofthe breastand diverse neoplasms (e.g., acute leukemia and carcinomas of the lung, pancreas, and skin) at relatively young ages, suggesting a new Familial syndrome of multiple primary cancers. Additional components of the syndrome were implicated by the occurrence of adrenocortical carcinoma and brain tumor in the ~rst­ degree relatives of 2 other children with rhabdomyosarcoma. While suggesting the role of inheritance, the familial patterns seen with rhabdomyosarcoma may result from an interaction of genetic and environmental (?viral) fadors. The oncogenic agents and mechanisms in human cancer may be identified by the use of such family aggregations For laboratory studies and Further epidemiologic studies. Like most childhood neoplasms, rhabdomyosarcoma showed a peak mortality beFore 4 years of age and occurred slightly more often in males. This neoplasm was diagnosed in 29 children in the hospital series beFore 1 year of age and in 9 within 1 month of birth; this indicates that rhabdomyosarcoma may arise in utero. Unlike most neoplasms of

435 citations







Journal ArticleDOI
TL;DR: The hypothesis that inhaled arsenic is a respiratory carcinogen in man, but an inRuence of sulfur dioxide or unidentified chemicals, varying concomitantly with arsenic exposure, cannot be discounted is supported.
Abstract: To clarify the role of arsenic in human carcinogenesis, the mortality experience of 8,047 white male smelter workers exposed to arsenic trioxide during 1938-63 was studied and compared with that of the white male population of the same States. Smelter workers had an excess total mortality, due mainly to malignant neoplasms of the respiratory system and diseases of the heart. The threefold increase in respiratory cancer was analyzed in relation to the length of employment and degree of exposure to arsenic, sulfur dioxide, and other elements in the smelter. The excess of respiratory cancer was as high as eightfold among employees who worked more than 15 years and who were heavily exposed to arsenicj it showed a gradient in proportion to the degree of exposure to arsenic and sulfur dioxide. The findings support the hypothesis that inhaled arsenic is a respiratory carcinogen in man, but an inRuence of sulfur dioxide or unidentified chemicals, varying concomitantly with arsenic exposure, cannot be discounted.-J Nat Cancer Inst 42: 1045-1052,1969.

243 citations


Journal ArticleDOI
TL;DR: The increased risk of breast cancer and cancers of the corpus uteri and ovary would seem to reflect an established link with infertility, and combination of these factors with the excess incidence of cancer of the large intestine among postmenopausal nuns suggests a common pathogenic mechanism of a hormonal nature operating in some women.
Abstract: To clarify the role of marital status in human carcinogenesis a 1968 Cancer Institute study analyzed the cancer mortality experience of 31658 white Catholic nuns from 41 religious orders in the U.S. from 1900-1954. The national white female population was used for cause-specific comparison and both groups were assigned cohorts depending upon the year of birth. When examined by 10-year age groups rates for cancer at all sites was generally lower for nuns than for controls aged 59 or 69 but were substantially higher at older ages. Postmenopausal nuns (aged 69 and over) displayed a higher rate (38.6%) of cancer of the large intestine than did controls (22.6%) but had a lower proportion of deaths from cancer of the biliary passages and liver (13.0% vs. 22.6%). Nuns displayed a striking excess in breast cancer mortality over the age span of 40-74 years and had consistently higher rates than controls for each age group above 39 years. Lower cervical cancer rates for nuns (10.8%) than for controls (56.6%) seemed related to coital factors. Cancer of the uterus accounted for 63% of the genital cancer deaths among sisters. Overall the genital cancer mortality rates for nuns were consistent with high mortality rates for the single white female population of the U.S. The increased risk of breast cancer and cancers of the corpus uteri and ovary would seem to reflect an established link with infertility. Combination of these factors with the excess incidence of cancer of the large intestine among postmenopausal nuns suggests a common pathogenic mechanism of a hormonal nature operating in some women.

216 citations










Journal ArticleDOI
TL;DR: Tumor cells (L1210 and Ehrlich ascites) were labeled with 1261-iododeoxyuridine and inoculated into nonradioactive hosts and their fate was monitored at daily intervals by measuring the retention of individual live mice in a well-type crystal scintillation counter.
Abstract: Tumor cells (L1210 and Ehrlich ascites) were labeled with 1261-iododeoxyuridine and inoculated into nonradioactive hosts. The fate of the labeled cells and their progeny was monitored at daily intervals by measuring the 1retention of individual live mice in a well-type crystal scintillation counter. The excretion of 1from the testanimals was linked to in vivo death and breakdown of tumor cells. The fractional rate of tumor cell death depended on the route of implantation, i.e., on the location of tumor cells within the host. After intraperitoneal inoculation of labeled tumorcells, the rate of cell death wasabout 15% perday. Subcutaneous and intramuscular implantation produced much higherdeath rates (20-40%/day), and up to 55% of the cells died each day aFter intravenous inoculation. When prekilled tumor cells were inoculated into mice, 1 was rapidly excreted From the test animals. The anatomical distribution of tumor cells also varied with the route of their administration. After intraperitoneal implantation, large numbers of tumor cells migrated from the peritoneal cavity. Tumor cells inoculated at extra peritoneal sites did not invade the peritoneal cavity. Liver and spleen were major recipients of migrating tumor cells, especially after intravenous inoculation.-J Nat Cancer Inst 43: 763-773,1969.











Journal ArticleDOI
Hitoshi Kobayashi1, F Sendo1, T Shirai1, H Kaji1, Takao Kodama1 
TL;DR: Three transplantable tumor cell lines exposed to Friend virus had a low success rate of transplantation into susceptible rats, and even when transplantation was accomplished, the tumor cells regressed spontaneously.
Abstract: Three transplantable tumor cell lines (WST-5 sarcoma, Takeda sarcoma, and DLT I ung carcinoma) exposed to Friend virus had a low success rate of transplantation into susceptible rats, and even when transplantation was accomplished, the tumor cells regressed spontaneously. Of the 3 lines, the rapid growth rate of the Takeda sarcoma resulted in early death of the host, and the effect of infection with Friend virus could not always be discerned. When the host was previously immunized with Friend virus, however, the effect became as clearly discernible as in the two other lines. This was not because the rat tumor cell showed the cytopathic effect of Friend virus nor because of the environmental change of the host brought about by Friend virus inoculation, but was probably because of the production of Friend virus-related antigen on the surface of the tumor cell resulting from Friend virus infection. The significance of using a noncytopathic virus, which altered the surface of tumor cells and which was too weakly infectious to the host to modify the growth of tumor, is discussed.-J Nat Cancer Inst 42: 413-419,1969.