Guy R Newell, Margaret R Spitz, Joanne G Sider, Earl S Pollack
Analyses were made of the marital status of 3,346 patients with the diagnosis of testicular cancer. Among whites, blacks, and Puerto Rico Hispanics, the risk was greater among single than married men. Among whites and both Puerto Rico and New Mexico Hispanic groups, the elevated risk was apparent for histologic types other than seminoma. Among single white men, this excess risk began after 25-29 years of age. During the 10 years 1973 through 1982, incidence increased among single men under age 45, but little increase in incidence was found for married men. There was a striking increase among single men ages 30-44. These data confirm that single men are more susceptible to nonseminoma testicular cancer than are married men after the age of 30. Testicular cancer is increasing fastest among single men of ages 30-44.—JNCI 1987; 78:881-885.
{"title":"Incidence of Testicular Cancer in the United States Related to Marital Status, Histology, and Ethnicity","authors":"Guy R Newell, Margaret R Spitz, Joanne G Sider, Earl S Pollack","doi":"10.1093/jnci/78.5.881","DOIUrl":"https://doi.org/10.1093/jnci/78.5.881","url":null,"abstract":"Analyses were made of the marital status of 3,346 patients with the diagnosis of testicular cancer. Among whites, blacks, and Puerto Rico Hispanics, the risk was greater among single than married men. Among whites and both Puerto Rico and New Mexico Hispanic groups, the elevated risk was apparent for histologic types other than seminoma. Among single white men, this excess risk began after 25-29 years of age. During the 10 years 1973 through 1982, incidence increased among single men under age 45, but little increase in incidence was found for married men. There was a striking increase among single men ages 30-44. These data confirm that single men are more susceptible to nonseminoma testicular cancer than are married men after the age of 30. Testicular cancer is increasing fastest among single men of ages 30-44.—JNCI 1987; 78:881-885.","PeriodicalId":501635,"journal":{"name":"Journal of the National Cancer Institute","volume":"8 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147462067","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kenneth P Cantor, Robert Hoover, Patricia Hartge, Thomas J Mason, Debra T Silverman, Ronald Altman, Donald F Austin, Margaret A Child, Charles R Key, Loraine D Marrett, Max H Myers, Ambati S Narayana, Lynn I Levin, J W Sullivan, G Marie Swanson, David B Thomas, Dee W West
Data from a population-based case-control interview study of incident bladder cancer in 10 areas of the United States were used to estimate relative risks among white men (2,116 cases, 3,892 controls) and women (689 cases, 1,366 controls) according to beverage intake level and type of water source. Individual year-by-year profiles of water source and treatment were developed by linking lifetime residential information with historical water utility data from an ancillary survey. Risk of bladder cancer increased with intake level of beverages made with tap water. The odds ratio (OR) for the highest vs. lowest quintile of tap water consumption was 1.43 [95% confidence interval (CI) = 1.23, 1.67; χ2 for trend = 26.3, P < .001]. The risk gradient with intake was restricted to persons with at least a 40-year exposure to chlorinated surface water and was not found among long-term users of non-chlorinated ground water. The ORs for the highest vs. lowest quintiles of tap water intake were 1.7 and 2.0, respectively, among subjects with 40–59 and ≥60 years exposure. Duration of exposure to chlorinated surface water was associated with bladder cancer risk among women and non-smokers of both sexes. Among non-smoking respondents with tap water consumption above the population median, the OR increased with exposure duration to a level of 3.1 (CI = 1.3, 7.3; χ2 for trend = 6.3, P =.01) for ≥60 years of residence at places served by chlorinated surface water (vs. non-chlorinated ground water users). These results extend findings of earlier epidemiologic studies and are consistent with environmental chemistry and toxicologic data demonstrating the presence of genotoxic by-products of chlorine disinfection in treated surface waters.—JNCI 1987; 79:1269-1279.
{"title":"Bladder Cancer, Drinking Water Source, and Tap Water Consumption: A Case-Control Study","authors":"Kenneth P Cantor, Robert Hoover, Patricia Hartge, Thomas J Mason, Debra T Silverman, Ronald Altman, Donald F Austin, Margaret A Child, Charles R Key, Loraine D Marrett, Max H Myers, Ambati S Narayana, Lynn I Levin, J W Sullivan, G Marie Swanson, David B Thomas, Dee W West","doi":"10.1093/jnci/79.6.1269","DOIUrl":"https://doi.org/10.1093/jnci/79.6.1269","url":null,"abstract":"Data from a population-based case-control interview study of incident bladder cancer in 10 areas of the United States were used to estimate relative risks among white men (2,116 cases, 3,892 controls) and women (689 cases, 1,366 controls) according to beverage intake level and type of water source. Individual year-by-year profiles of water source and treatment were developed by linking lifetime residential information with historical water utility data from an ancillary survey. Risk of bladder cancer increased with intake level of beverages made with tap water. The odds ratio (OR) for the highest vs. lowest quintile of tap water consumption was 1.43 [95% confidence interval (CI) = 1.23, 1.67; χ2 for trend = 26.3, P &lt; .001]. The risk gradient with intake was restricted to persons with at least a 40-year exposure to chlorinated surface water and was not found among long-term users of non-chlorinated ground water. The ORs for the highest vs. lowest quintiles of tap water intake were 1.7 and 2.0, respectively, among subjects with 40–59 and ≥60 years exposure. Duration of exposure to chlorinated surface water was associated with bladder cancer risk among women and non-smokers of both sexes. Among non-smoking respondents with tap water consumption above the population median, the OR increased with exposure duration to a level of 3.1 (CI = 1.3, 7.3; χ2 for trend = 6.3, P =.01) for ≥60 years of residence at places served by chlorinated surface water (vs. non-chlorinated ground water users). These results extend findings of earlier epidemiologic studies and are consistent with environmental chemistry and toxicologic data demonstrating the presence of genotoxic by-products of chlorine disinfection in treated surface waters.—JNCI 1987; 79:1269-1279.","PeriodicalId":501635,"journal":{"name":"Journal of the National Cancer Institute","volume":"9 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147462073","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Engikolai C Krishnan, Leela Krishnan, Brian Jewell, Paramiit Bhatia, William R Jewell
It has been postulated that the damage to microvasculature may be a major factor in the manifestation of late radiation damage to organized tissue. In this study, the radiation damage to microvasculature was investigated in a rabbit model during the early phases of irradiation with the use of vascular permeability as a marker. By means of a triple isotopic technique, the vascular, extravascular, and intracellular spaces could be defined. A forelimb and hindlimb of New Zealand White rabbits were irradiated with single doses of 2-30 Gy. 125I- and 131I-labeled bio-screened albumin were used to determine the changes in vascular permeability due to irradiation. The rabbits were sacrificed at various intervals post irradiation. Vascular and extravascular spaces and the respective albumin concentrations in tissue samples from irradiated limbs were compared with control values from the unirradiated contralateral limbs in each animal. The results indicated a definite increase in the vascular permeability of albumin secondary to irradiation. The increase in vascular permeability was apparent instantaneously with irradiation, even at 2 Gy. The microvascular compromise appeared to be dose related. When examined at 16-24 hours post irradiation, the excess extravasation of albumin was significant at and beyond 8 Gy. At 10-30 days post irradiation, injury was not apparent up to 15 Gy. Thus there appeared to be an instantaneous injury at the capillary level due to irradiation, which appeared to be dose related. A repair process became evident as early as 16-24 hours and appeared to be dose related as well as related to elapsed time post irradiation.—JNCI 1987; 79:1321-1325.
{"title":"Dose-Dependent Radiation Effect on Microvasculature and Repair","authors":"Engikolai C Krishnan, Leela Krishnan, Brian Jewell, Paramiit Bhatia, William R Jewell","doi":"10.1093/jnci/79.6.1321","DOIUrl":"https://doi.org/10.1093/jnci/79.6.1321","url":null,"abstract":"It has been postulated that the damage to microvasculature may be a major factor in the manifestation of late radiation damage to organized tissue. In this study, the radiation damage to microvasculature was investigated in a rabbit model during the early phases of irradiation with the use of vascular permeability as a marker. By means of a triple isotopic technique, the vascular, extravascular, and intracellular spaces could be defined. A forelimb and hindlimb of New Zealand White rabbits were irradiated with single doses of 2-30 Gy. 125I- and 131I-labeled bio-screened albumin were used to determine the changes in vascular permeability due to irradiation. The rabbits were sacrificed at various intervals post irradiation. Vascular and extravascular spaces and the respective albumin concentrations in tissue samples from irradiated limbs were compared with control values from the unirradiated contralateral limbs in each animal. The results indicated a definite increase in the vascular permeability of albumin secondary to irradiation. The increase in vascular permeability was apparent instantaneously with irradiation, even at 2 Gy. The microvascular compromise appeared to be dose related. When examined at 16-24 hours post irradiation, the excess extravasation of albumin was significant at and beyond 8 Gy. At 10-30 days post irradiation, injury was not apparent up to 15 Gy. Thus there appeared to be an instantaneous injury at the capillary level due to irradiation, which appeared to be dose related. A repair process became evident as early as 16-24 hours and appeared to be dose related as well as related to elapsed time post irradiation.—JNCI 1987; 79:1321-1325.","PeriodicalId":501635,"journal":{"name":"Journal of the National Cancer Institute","volume":"20 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147462112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Dietrich Hoffmann, John D Adams, Donald Lisk, Isabel Fisenne, Klaus D Brunnemann
The oral use of snuff is causatively associated with cancer of the oral cavity. Since most epidemiologic studies to date relate to the long-term use of dry snuff, which has dominated the U.S. smokeless tobacco market in the past, the concentrations of several toxic and carcinogenic agents in the three most popular dry snuff brands have been compared with those in the five most popular moist snuff brands sold in the United States. All eight samples were analyzed for nitrate, alkaloids, polyphenols, volatile carbonyl compounds, lead, cadmium, selenium, and the carcinogenic compounds benzo[a]pyrene (CAS: 50-32-8), polonium-210 (CAS: 13981-52-7), volatile N-nitrosamines (VNAs), N-nitrosodiethanolamine (CAS: 1116-54-7), and the tobacco-specific N-nitrosamines (TSNAs). Most of the snuff brands were rich in nitrate (≥1.5%), total polyphenols (>2%), and in nicotine (≥1.5%), which is the habituating factor in tobacco use. Concentrations of the VNAs were significantly above the permissible limits set for some food products; the concentrations of the TSNAs in both snuff types exceeded the levels of nitrosamines in other consumer products by at least two to three orders of magnitude. The extremely high levels of the TSNAs in snuff have remained unchanged during the last decade and present the major carcinogenic risk factor for the oral use of snuff. Polonium-210 contributes further to the carcinogenic risk associated with snuff. The chemical-analytical data presented in this study do not indicate marked differences in the carcinogenic potential of moist snuff compared to dry snuff.—JNCI 1987; 79:1281-1286.
{"title":"Toxic and Carcinogenic Agents in Dry and Moist Snuff","authors":"Dietrich Hoffmann, John D Adams, Donald Lisk, Isabel Fisenne, Klaus D Brunnemann","doi":"10.1093/jnci/79.6.1281","DOIUrl":"https://doi.org/10.1093/jnci/79.6.1281","url":null,"abstract":"The oral use of snuff is causatively associated with cancer of the oral cavity. Since most epidemiologic studies to date relate to the long-term use of dry snuff, which has dominated the U.S. smokeless tobacco market in the past, the concentrations of several toxic and carcinogenic agents in the three most popular dry snuff brands have been compared with those in the five most popular moist snuff brands sold in the United States. All eight samples were analyzed for nitrate, alkaloids, polyphenols, volatile carbonyl compounds, lead, cadmium, selenium, and the carcinogenic compounds benzo[a]pyrene (CAS: 50-32-8), polonium-210 (CAS: 13981-52-7), volatile N-nitrosamines (VNAs), N-nitrosodiethanolamine (CAS: 1116-54-7), and the tobacco-specific N-nitrosamines (TSNAs). Most of the snuff brands were rich in nitrate (≥1.5%), total polyphenols (&gt;2%), and in nicotine (≥1.5%), which is the habituating factor in tobacco use. Concentrations of the VNAs were significantly above the permissible limits set for some food products; the concentrations of the TSNAs in both snuff types exceeded the levels of nitrosamines in other consumer products by at least two to three orders of magnitude. The extremely high levels of the TSNAs in snuff have remained unchanged during the last decade and present the major carcinogenic risk factor for the oral use of snuff. Polonium-210 contributes further to the carcinogenic risk associated with snuff. The chemical-analytical data presented in this study do not indicate marked differences in the carcinogenic potential of moist snuff compared to dry snuff.—JNCI 1987; 79:1281-1286.","PeriodicalId":501635,"journal":{"name":"Journal of the National Cancer Institute","volume":"4 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147462113","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kenneth G Manton, Eric Stallard, Max A Woodbury, Wilson B Riggan, John P Creason, Thomas J Mason
The spatial variation of site-specific cancer mortality rates at the county or state economic area level can provide a) insights into possible etiologic factors and b) the basis for more detailed epidemiologic studies. One difficulty with such studies, especially for rare cancer types, is that unstable local area rate estimates, resulting from small population sizes, can obscure the underlying spatial pattern of disease risk. This paper presents a methodology for producing more stable rate estimates by statistically weighting the local area rate estimate toward the experience at the national level. The methodology is illustrated by the analysis of the spatial variation of two cancer types, bladder and lung, for U.S. white males over the three decades 1950-79.—JNCI 1987; 78:805-815.
{"title":"Statistically Adjusted Estimates of Geographic Mortality Profiles","authors":"Kenneth G Manton, Eric Stallard, Max A Woodbury, Wilson B Riggan, John P Creason, Thomas J Mason","doi":"10.1093/jnci/78.5.805","DOIUrl":"https://doi.org/10.1093/jnci/78.5.805","url":null,"abstract":"The spatial variation of site-specific cancer mortality rates at the county or state economic area level can provide a) insights into possible etiologic factors and b) the basis for more detailed epidemiologic studies. One difficulty with such studies, especially for rare cancer types, is that unstable local area rate estimates, resulting from small population sizes, can obscure the underlying spatial pattern of disease risk. This paper presents a methodology for producing more stable rate estimates by statistically weighting the local area rate estimate toward the experience at the national level. The methodology is illustrated by the analysis of the spatial variation of two cancer types, bladder and lung, for U.S. white males over the three decades 1950-79.—JNCI 1987; 78:805-815.","PeriodicalId":501635,"journal":{"name":"Journal of the National Cancer Institute","volume":"51 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147462017","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
David M Ingram, Fiona C Bennett, David Willcox, N de Klerk
The hypothesis that dietary fat acts as a promotional agent for the development of breast cancer by influencing sex hormone levels was tested in a dietary intervention study. Thirty-three women in good health were randomly allocated to commence either a standard diet (deriving 40% of their energy from fat) or a low-fat diet (deriving 20% of their energy from fat). After 2 months, the women were crossed over to the alternative diet for another 2 months. Serum hormone and lipid levels were measured in the middle and at the end of each dietary period. In premenopausal women, the low-fat diet appeared to decrease levels of both non-protein-bound estradiol (1.48 down to 1.27%; P = .07) and non-protein-bound testosterone (1.06 down to 0.86%; P = .11). Cholesterol levels were lowered by the low-fat diet and were significantly associated with estradiol, testosterone, and dehydroepiandrosterone. High-density lipoprotein (HDL) cholesterol was associated with estradiol and prolactin. For the postmenopausal women, the low-fat diet lowered cholesterol and HDL cholesterol levels, but there were not the same associations with the hormones. These findings add weight to the concept that attention to diet may be a means of reducing the incidence of breast cancer in our community.—JNCI 1987; 79:1225-1229.
{"title":"Effect of Low-Fat Diet on Female Sex Hormone Levels","authors":"David M Ingram, Fiona C Bennett, David Willcox, N de Klerk","doi":"10.1093/jnci/79.6.1225","DOIUrl":"https://doi.org/10.1093/jnci/79.6.1225","url":null,"abstract":"The hypothesis that dietary fat acts as a promotional agent for the development of breast cancer by influencing sex hormone levels was tested in a dietary intervention study. Thirty-three women in good health were randomly allocated to commence either a standard diet (deriving 40% of their energy from fat) or a low-fat diet (deriving 20% of their energy from fat). After 2 months, the women were crossed over to the alternative diet for another 2 months. Serum hormone and lipid levels were measured in the middle and at the end of each dietary period. In premenopausal women, the low-fat diet appeared to decrease levels of both non-protein-bound estradiol (1.48 down to 1.27%; P = .07) and non-protein-bound testosterone (1.06 down to 0.86%; P = .11). Cholesterol levels were lowered by the low-fat diet and were significantly associated with estradiol, testosterone, and dehydroepiandrosterone. High-density lipoprotein (HDL) cholesterol was associated with estradiol and prolactin. For the postmenopausal women, the low-fat diet lowered cholesterol and HDL cholesterol levels, but there were not the same associations with the hormones. These findings add weight to the concept that attention to diet may be a means of reducing the incidence of breast cancer in our community.—JNCI 1987; 79:1225-1229.","PeriodicalId":501635,"journal":{"name":"Journal of the National Cancer Institute","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147462020","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Previously, human diploid fibroblasts from some donors infected in vitro by avian sarcoma virus (ASV) were transformed and found, by electron microscopy, to produce small numbers of virus particles that were infectious by bioassay; also, a line of human osteosarcoma cells infected with ASV developed additional characteristics of transformation and released a small number of infectious virus particles. In this study the complete proviral sequence was shown to be integrated in the genome of these cells. The env-related proteins gp85 and gp37 and the gag-related proteins pr76, pr60, and p19 can be detected in cytoplasmic extracts of ASV-infected human cells Comparable amounts of pp60v-src were found in human and avian cells infected with ASV. The associated kinase activity in infected human cells was dramatically increased as compared to that of uninfected controls; the enzyme had the same cation and substrate requirements as those from ASV-transformed avian cells. Replicating particles from infected human cells were purified and were significantly modified compared to those from avian hosts as shown by a) higher specific gravity, b) the presence of RSV gag-related but not env-related antigens, and c) the fact that the virus-associated reverse transcriptase preferred the divalent cations Mn2+ and Fe2+ over Mg2t—JNCI 1987; 78:817-829.
{"title":"Integration and Expression of Provirus in Human Cells Transformed by Avian Sarcoma Virus","authors":"Giancarlo Rabotti, Betty Teutsch, Marcei Mariller, Nadine Pavloff, Françoise Mongiat, Josiane Auger, Marianne Semmel","doi":"10.1093/jnci/78.5.817","DOIUrl":"https://doi.org/10.1093/jnci/78.5.817","url":null,"abstract":"Previously, human diploid fibroblasts from some donors infected in vitro by avian sarcoma virus (ASV) were transformed and found, by electron microscopy, to produce small numbers of virus particles that were infectious by bioassay; also, a line of human osteosarcoma cells infected with ASV developed additional characteristics of transformation and released a small number of infectious virus particles. In this study the complete proviral sequence was shown to be integrated in the genome of these cells. The env-related proteins gp85 and gp37 and the gag-related proteins pr76, pr60, and p19 can be detected in cytoplasmic extracts of ASV-infected human cells Comparable amounts of pp60v-src were found in human and avian cells infected with ASV. The associated kinase activity in infected human cells was dramatically increased as compared to that of uninfected controls; the enzyme had the same cation and substrate requirements as those from ASV-transformed avian cells. Replicating particles from infected human cells were purified and were significantly modified compared to those from avian hosts as shown by a) higher specific gravity, b) the presence of RSV gag-related but not env-related antigens, and c) the fact that the virus-associated reverse transcriptase preferred the divalent cations Mn2+ and Fe2+ over Mg2t—JNCI 1987; 78:817-829.","PeriodicalId":501635,"journal":{"name":"Journal of the National Cancer Institute","volume":"13 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147462075","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The Lewis (Le) phenotype of both erythrocytes and sera and serum CA19-9 levels were studied in 49 patients with pancreatic carcinoma, in 37 with gastric cancer, in 22 with colorectal cancer, in 21 with bile duct carcinoma, and in 19 with hepatocellular carcinoma. The Le phenotype was determined in sera with the use of the dot-immunobinding assay and on erythrocytes. The localizations of the Le antigen and CA19-9 were studied in pancreatic tissues from 22 patients with pancreatic carcinoma. The prevalence of Le(a-,b-) on erythrocytes was significantly higher in patients with pancreatic carcinoma than in normal controls. Nineteen of 21 patients with pancreatic carcinoma, whose Le phenotype on erythrocytes was Le(a-,b-), had Le antigen in tissues and sera, and they had a raised serum CA19-9 level. The remaining 2 patients were of the Le(a-,b-) phenotype for both erythrocytes and sera, and their serum CA19-9 levels were below 6 U/ml. Neither Le antigen nor CA19-9 could be localized in tissues of these 2 patients. Two patients with gastric cancer, 6 with colorectal cancer, and 6 with bile duct carcinoma had Le antigen in sera in spite of having Le(a-,b-) on erythrocytes. These results indicate that the Le phenotype on erythrocytes can undergo a change not infrequently in patients with pancreatic carcinoma as well as in patients with other gastrointestinal cancers, but patients with the Le(a-,b-) phenotype in sera cannot synthesize CA19-19.—JNCI 1987; 79:1261-1268.
{"title":"Loss of Lewis Antigen Expression on Erythrocytes in Some Cancer Patients With High Serum CA19-9 Levels","authors":"Ken Hirano, Shigeyuki Kawa, Hisao Oguchi, Takeshi Kobayashi, Hiroaki Yonekura, Hiroyuki Ogata, Tatsuji Homma","doi":"10.1093/jnci/79.6.1261","DOIUrl":"https://doi.org/10.1093/jnci/79.6.1261","url":null,"abstract":"The Lewis (Le) phenotype of both erythrocytes and sera and serum CA19-9 levels were studied in 49 patients with pancreatic carcinoma, in 37 with gastric cancer, in 22 with colorectal cancer, in 21 with bile duct carcinoma, and in 19 with hepatocellular carcinoma. The Le phenotype was determined in sera with the use of the dot-immunobinding assay and on erythrocytes. The localizations of the Le antigen and CA19-9 were studied in pancreatic tissues from 22 patients with pancreatic carcinoma. The prevalence of Le(a-,b-) on erythrocytes was significantly higher in patients with pancreatic carcinoma than in normal controls. Nineteen of 21 patients with pancreatic carcinoma, whose Le phenotype on erythrocytes was Le(a-,b-), had Le antigen in tissues and sera, and they had a raised serum CA19-9 level. The remaining 2 patients were of the Le(a-,b-) phenotype for both erythrocytes and sera, and their serum CA19-9 levels were below 6 U/ml. Neither Le antigen nor CA19-9 could be localized in tissues of these 2 patients. Two patients with gastric cancer, 6 with colorectal cancer, and 6 with bile duct carcinoma had Le antigen in sera in spite of having Le(a-,b-) on erythrocytes. These results indicate that the Le phenotype on erythrocytes can undergo a change not infrequently in patients with pancreatic carcinoma as well as in patients with other gastrointestinal cancers, but patients with the Le(a-,b-) phenotype in sera cannot synthesize CA19-19.—JNCI 1987; 79:1261-1268.","PeriodicalId":501635,"journal":{"name":"Journal of the National Cancer Institute","volume":"9 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147462124","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Anna M Richter, Barbara Kelly, Jack Chow, Daniel J Liu, G H Neil Towers, David Dolphin, Julia G Levy
Phototoxicity of benzoporphyrin derivative (BPD) has been tested in vitro and compared with that of hematoporphyrin (HP). After 1-hour activation with visible light, BPD was 10 times more cytotoxic than HP toward human adherent cell lines: A549 lung cancer, Calu-1 lung carcinoma, and CCD-19Lu normal lung, killing 100% of cells at the concentration of 70 ng/ml. Under the same conditions, BPD was 10-70 times more cytotoxic than HP toward nonadherent cells and cell lines. Tested were human leukemia cell lines HL60, K562, and KG1, normal human lymphocytes, and mouse mastocytoma cell line P815. The concentrations required to kill 100% of cells varied between 10 and 500 ng BPD/ml and between 0.2 and 10 μg HP/ml. The difference between the nonadherent cell lines in respect to their sensitivity to phototoxicity of both BPD and HP seemed to be related to the cell sizes, with the smallest cells being the most vulnerable. The most attractive characteristic of BPD in addition to its powerful phototoxicity is its maximum absorption around 700 nm, which is in the range of wavelengths penetrating tissues the best. This characteristic alone could make BPD a drug of choice in cancer photodynamic therapy when the safety of its use is ensured. Preliminary tests in vivo have shown that DBA/2J mice can tolerate a single ip injection of 20-60 μg BPD as well as the same dose of HP. The biodistribution and toxicity studies of BPD are under way in our laboratory.—JNCI 1987; 79:1327-1332.
{"title":"Preliminary Studies on a More Effective Phototoxic Agent Than Hematoporphyrin","authors":"Anna M Richter, Barbara Kelly, Jack Chow, Daniel J Liu, G H Neil Towers, David Dolphin, Julia G Levy","doi":"10.1093/jnci/79.6.1327","DOIUrl":"https://doi.org/10.1093/jnci/79.6.1327","url":null,"abstract":"Phototoxicity of benzoporphyrin derivative (BPD) has been tested in vitro and compared with that of hematoporphyrin (HP). After 1-hour activation with visible light, BPD was 10 times more cytotoxic than HP toward human adherent cell lines: A549 lung cancer, Calu-1 lung carcinoma, and CCD-19Lu normal lung, killing 100% of cells at the concentration of 70 ng/ml. Under the same conditions, BPD was 10-70 times more cytotoxic than HP toward nonadherent cells and cell lines. Tested were human leukemia cell lines HL60, K562, and KG1, normal human lymphocytes, and mouse mastocytoma cell line P815. The concentrations required to kill 100% of cells varied between 10 and 500 ng BPD/ml and between 0.2 and 10 μg HP/ml. The difference between the nonadherent cell lines in respect to their sensitivity to phototoxicity of both BPD and HP seemed to be related to the cell sizes, with the smallest cells being the most vulnerable. The most attractive characteristic of BPD in addition to its powerful phototoxicity is its maximum absorption around 700 nm, which is in the range of wavelengths penetrating tissues the best. This characteristic alone could make BPD a drug of choice in cancer photodynamic therapy when the safety of its use is ensured. Preliminary tests in vivo have shown that DBA/2J mice can tolerate a single ip injection of 20-60 μg BPD as well as the same dose of HP. The biodistribution and toxicity studies of BPD are under way in our laboratory.—JNCI 1987; 79:1327-1332.","PeriodicalId":501635,"journal":{"name":"Journal of the National Cancer Institute","volume":"126 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147462126","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Thomas B Leonard, M Elizabeth Graichen, James A Popp
The hepatocarcinogenicity of 2,4-dinitrotoluene [(2,4-DNT) CAS: 121-14-2], 2,6-DNT (CAS: 606-20-2), and a representative technical-grade DNT (TDNT) containing 76% 2,4-DNT and 18% 2,6-DNT was studied in male F344 rats. Rats were fed diets containing 2,4-DNT, 2,6-DNT, or TDNT at concentrations that resulted in doses of 27 mg/kg/day for 2,4-DNT, 7 or 14 mg/kg/day for 2,6-DNT, and 35 mg/kg/day for TDNT. The carcinogenic effects were evaluated after 1 year of treatment. Administration of 2,6-DNT produced hepatocellular carcinomas in 100 and 85% of animals receiving 14 and 7 mg/kg, respectively. In contrast to the 2,6-DNT results, feeding of 2,4-DNT for 1 year caused no hepatic tumors. Treatment with both isomers (TDNT) resulted in a 47% incidence of hepatocellular tumors. The majority of tumors had a trabecular pattern, and pulmonary metastases were present in the 14- and 7-mg/kg 2,6-DNT-fed groups. These results have demonstrated that 2,6-DNT is a potent and complete hepatocarcinogen and that 2,4-DNT, under these conditions, is nonhepatocarcinogenic. In addition, these data indicate that 2,6-DNT accounts for the majority of the carcinogenic activity of TDNT.—JNCI 1987; 79:1313-1319.
{"title":"Dinitrotoluene Isomer-Specific Hepatocarcinogenesis in F344 Rats","authors":"Thomas B Leonard, M Elizabeth Graichen, James A Popp","doi":"10.1093/jnci/79.6.1313","DOIUrl":"https://doi.org/10.1093/jnci/79.6.1313","url":null,"abstract":"The hepatocarcinogenicity of 2,4-dinitrotoluene [(2,4-DNT) CAS: 121-14-2], 2,6-DNT (CAS: 606-20-2), and a representative technical-grade DNT (TDNT) containing 76% 2,4-DNT and 18% 2,6-DNT was studied in male F344 rats. Rats were fed diets containing 2,4-DNT, 2,6-DNT, or TDNT at concentrations that resulted in doses of 27 mg/kg/day for 2,4-DNT, 7 or 14 mg/kg/day for 2,6-DNT, and 35 mg/kg/day for TDNT. The carcinogenic effects were evaluated after 1 year of treatment. Administration of 2,6-DNT produced hepatocellular carcinomas in 100 and 85% of animals receiving 14 and 7 mg/kg, respectively. In contrast to the 2,6-DNT results, feeding of 2,4-DNT for 1 year caused no hepatic tumors. Treatment with both isomers (TDNT) resulted in a 47% incidence of hepatocellular tumors. The majority of tumors had a trabecular pattern, and pulmonary metastases were present in the 14- and 7-mg/kg 2,6-DNT-fed groups. These results have demonstrated that 2,6-DNT is a potent and complete hepatocarcinogen and that 2,4-DNT, under these conditions, is nonhepatocarcinogenic. In addition, these data indicate that 2,6-DNT accounts for the majority of the carcinogenic activity of TDNT.—JNCI 1987; 79:1313-1319.","PeriodicalId":501635,"journal":{"name":"Journal of the National Cancer Institute","volume":"12 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147462157","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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