Biomedical subjects

M R Spitz

Publications and source records attributed to M R Spitz.

At least 91 records · Page 5Linked to original sources

PubMed1997

Molecular epidemiology and retinoid chemoprevention of head and neck cancer.

Head and neck cancer is a major worldwide health problem; it has been estimated that approximately 900,000 people were diagnosed with this disease in 1995. Patients are generally treated with surgery and/or radiation therapy. Treatment, especially of patients with early stage (I or II) head and neck squamous cell carcinoma, is often successful. A serious concern, however, is the fact that these patients subsequently develop second primary tumors at an annual rate of 4%-7%. Molecular analyses of premalignant and malignant tissues have produced strong evidence that clonal genetic alterations occur during the early stage of aerodigestive tract carcinogenesis. Although the roles of tobacco and diet in head and neck carcinogenesis have been the subjects of epidemiologic investigations for many years, it has only recently become possible to integrate information regarding genetic susceptibility factors into the development of comprehensive risk models for these cancers. The molecular and epidemiologic studies provide the foundation on which clinical trials can be designed to evaluate the role of retinoids and other compounds in the reversal of premalignancy and the prevention of second primary tumors (i.e., in chemoprevention). This translational approach has led to studies of the utility of intermediate end point markers, such as the nuclear retinoic acid receptors, in chemoprevention strategies. Given the rapid advances occurring in this area of research, it may soon be possible to use these biomarkers to identify patients who are most at risk for developing head and neck cancer and who are most likely to benefit from chemopreventive interventions.

Biomarkers, Tumor↗

PubMed1997

Polymorphisms in the glutathione S-transferase class mu and theta genes interact and increase susceptibility to lung cancer in minority populations (Texas, United States).

The genes coding for separate isoforms of both the human glutathione S-transferase class mu and class theta enzymes (GSTM1 and GSTT1) are polymorphic with a variable ethnic distribution. These enzymes detoxify reactive epoxides, including carcinogens produced by tobacco smoke. Because of this, the null polymorphism in the GSTM1 gene (coding for the glutathione S-transferase class mu enzyme) has been studied widely as a possible source of inherited susceptibility to smoking-related lung cancer. The more recently described null polymorphism in the GSTT1 gene also could contribute to an increased risk of smoking-related lung cancer. As the incidence of lung cancer is known to differ by ethnicity, we have conducted a case-control study in the United States of 108 African-Americans (Blacks) and 60 Mexican-Americans (Hispanics) with lung cancer and 132 African-American (Black) and 146 Mexican-American (Hispanic) controls to investigate the association of the GSTT1 and GSTM1 polymorphisms with lung cancer in minority populations. In the unadjusted data, there was a borderline significant association of the GSTM1 null polymorphism with lung cancer in Mexican-Americans (odds ratio [OR] = 1.8, 95 percent confidence interval [CI] = 1.0-3.3 ) that was not observed in African-Americans. The GSTT1 null polymorphism also had a higher prevalence in cases than controls in both racial/ethnic groups, but this increase was not statistically significant. When the data were analyzed using logistic regression controlling for age, gender, race, and smoking, no significant association of either trait with lung cancer was observed, with ORs for both traits of approximately 1.3. However, when the prevalence of individuals who were null for both polymorphisms was compared by case status, a significant interaction was observed. Logistic regression models showed the OR for the association of lung cancer and the presence of both null polymorphisms compared with one (either GSTT1 or GSTM1) or no null genotype to be 2.9 (P < 0.04). These results suggest that there may be carcinogenic intermediates in cigarette smoke that are substrates for both the GSTT1 and GSTM1 enzymes, and that lung cancer risk is increased more than additively for individuals who have both GSTT1 and GSTM1 null polymorphisms.

Black People↗

PubMed1997

Ethnic variation in the prevalence of a common NAD(P)H quinone oxidoreductase polymorphism and its implications for anti-cancer chemotherapy.

The NAD(P)H quinone oxidoreductase (NQO1:EC 1.6.99.2) is an important biotransformation enzyme system that is also known to metabolize important novel chemotherapeutic compounds. The gene that codes for this enzyme has recently been found to be polymorphic in humans. Here, we describe the ethnic distribution of the polymorphism and note that this may have implications for anti-tumour drug development and use.

Antineoplastic Agents↗

PubMed1997

Case-control assessment of diet and lung cancer risk in African Americans and Mexican Americans.

In this case-control study we determined whether dietary differences underlie some of the ethnic and sex differences in US lung cancer rates. We examined the relationship between diet and lung cancer development in 137 lung cancer cases (93 African Americans and 44 Mexican Americans) and 187 controls (78 African Americans and 109 Mexican Americans). Cases reported a higher daily mean total fat intake (p < 0.001), whereas controls had a higher daily mean intake of dietary fiber (p < 0.001) and fruits (p = 0.02). Ethnic differences in diet were also observed: Mexican Americans consumed less total fat (p < 0.02) and more fiber (p < 0.001) and vegetables (p = 0.08) than African Americans. Additionally, men consumed more total fat (p = 0.08) and less fiber (p = 0.001), fruits (p < 0.001), and vegetables (p = 0.002) than women. Multivariable analysis, after adjustment for the effects of pack-years of smoking, age, total energy intake, sex, and ethnicity, demonstrated a positive association between high total fat consumption and lung cancer risk (p < 0.01) and an inverse association between high fruit consumption and lung cancer risk (p = 0.05). In conclusion, our findings support the hypothesis that diet, particularly high fat consumption and low fruit and vegetable consumption, contributes (independent of cigarette smoking) to the excess lung cancer risk in African-American men, who have the highest lung cancer rates in the United States.

Black or African American↗

PubMed1997

Associations between cytochrome P4502E1 genotype, mutagen sensitivity, cigarette smoking and susceptibility to lung cancer.

Cytochrome P4502E1 (CYP2E1) is involved in the metabolic activation of carcinogenic N-nitrosoamines. We therefore assessed the genotype frequencies of PstI or RsaI CYP2E1 restriction fragment length polymorphisms and another susceptibility marker, mutagen sensitivity, in 137 lung cancer cases (92 African American and 45 Mexican American) and 206 controls (114 African American and 92 Mexican American) identified in a molecular epidemiological study of lung cancer. The CYP2E1 c1/c1 genotype was found in 86.7% of Mexican American cases, 70.6% of Mexican American controls, 89.1% of African American cases and 86.8% of African American controls. By multivariate analysis, this genotype was found to be associated with a 14.0-fold increased risk of lung cancer in Mexican Americans but not in African Americans; a 9.9-fold increased risk of lung cancer in Mexican American former smokers, but not in non-smokers or current smokers; a 15-fold increased risk of lung cancer in Mexican American males, but not in females. Patients with the susceptible genotype appeared to have developed cancer at an earlier age and with lower cigarette pack-year of exposure than did patients with the c1/c2 or c2/c2 genotypes. Stratified analysis suggested a greater than multiplicative interaction between cigarette smoking and CYP2E1 c1/c1 genotype, although not statistically significant. The odds ratios (ORs) for the CYP2E1 c1/c1 genotype, cigarette smoking and both risk factors combined were 1.3, 6.7 and 16.3, respectively. The association between CYP2E1 c1/c1 genotype and pack-years of smoking followed the same pattern. The interaction between mutagen sensitivity and CYP2E1 c1/c1 genotype was especially strong in former smokers (the ORs for the CYP2E1 c1/c1 genotype, mutagen sensitivity and both risk factors combined were 3.9, 5.4 and 23.0, respectively). Therefore, the data suggest that individuals who lack a c2 allele might be at higher risk for developing lung cancer.

Alleles↗

PubMed1997

Health care's double standard: the prevention dilemma.

Curative services often have been judged by their perceived value, while preventive services have been held to a more rigorous standard of documentation. The dilemma for preventive services is not driven by evidence of their cost-ineffectiveness relative to curative services, but by the paucity of evidence of any type. The issues are whether preventive services of different types are perceived as having value, by what criteria these perceptions are measured, and by whom they are determined. We examine five key constituencies, the measures by which the value of prevention is judged, and the implications for the funding of prevention activities.

Attitude to Health↗

PubMed1997

Lung cancer in Mexican-Americans and African-Americans is associated with the wild-type genotype of the NAD(P)H: quinone oxidoreductase polymorphism.

Age-adjusted incidence rates for lung cancer are significantly lower for Hispanics compared with non-Hispanic whites or African-Americans; differences in genetic susceptibility have been postulated as one explanation for these ethnic differences. Recently, a polymorphism of the gene encoding NAD(P)H quinone oxidoreductase (NQO1) has been described. NQO1 is a cytosolic enzyme catalyzing the two-electron reduction of quinone substrates, which is thought to be involved in both metabolic activation and detoxification of carcinogenic agents that could be involved in lung carcinogenesis. The polymorphic variant of the gene (a C-to-T transition at base pair 609) is associated with reduced NQO1 activity and resistance to anticancer agents requiring reductive activation. We studied 177 untreated lung cancer cases and 297 community controls, examining the prevalence of the NQO1 wild-type and variant alleles to assess whether the polymorphism was associated with lung cancer. Cases and controls were individuals of Mexican-American (n = 222) or African. American (n = 252) ethnicity recruited from the Houston and San Antonio areas. Overall cases were more likely to carry two copies of the wild-type NQO1 allele compared with controls (odds ratio, 1.79; P = 0.002). When cases and controls were stratified by ethnicity, the wild-type genotype was found to be approximately 2-fold more common among African-Americans (P < 0.001) than among Mexican-Americans. Multivariate analyses indicated a significant association of the wild-type genotype with lung cancer risk after controlling for the effects of age, gender, ethnicity, and smoking status (odds ratio, 1.80; 95% CI:1.09-2.97; P = 0.02). These results indicate a significant ethnic variation in the occurrence of the NQO1 base pair 609 transition and demonstrate an association of the wild-type genotype with lung cancer risk. Given the known role of NQO1 in the activation of potential lung carcinogens, the NQO1 polymorphism should be investigated further as a possible genetic risk factor for lung cancer among minority populations.

Adult↗

PubMed1997

Evaluation of sister chromatid exchange and chromosome breaks in a cohort of untreated Hodgkin's disease patients.

Cytogenetic biomarkers, chromosomal breaks [spontaneous breaks (SB) and bleomycin-induced breaks (BIB)], and sister chromatid exchange (SCE) have been shown to be sensitive cytological assays to defect susceptibility to DNA-damaging effects. However, little information is available on how environmental factors and demographic and clinical characteristics influence variation among individuals. We sought to characterize interindividual variability in a cohort of 105 untreated adult Hodgkin's disease patients. SB, BIB, and SCE data were integrated with epidemiological data by using linear regression analysis. Age, sex, ethnicity, education, histology, history of mononucleosis, and family history of cancer showed no association with any biomarker. In univariate analysis, alcohol intake was significantly associated with high SCEs (P = 0.005) and SBs (P = 0.02). Current smoking was associated only with high frequencies of SCE (P = 0.05). Advanced stage of disease was related with high SBs (P = 0.01). BIBs were not associated with any of the variables studied. In multivariate modeling, current alcohol intake was associated with high SCEs (P = 0.04) and SBs (P = 0.01). Former smokers had higher SBs than nonsmokers did (P = 0.02). A small positive correlation was found among each pair of markers. The higher SCEs and SBs in patients who smoke and consume alcohol indicate the need for evaluating these exposures when interpreting these biomarkers.

Adult↗

PubMed1997

A clinical trial to evaluate the effect of vitamin C supplementation on in vitro mutagen sensitivity. The University of Texas M. D. Anderson Clinical Community Oncology Program Network.

Mutagen sensitivity, as measured by an in vitro assay, has been described as a risk factor for the development of several tobacco-related epithelial cancers. In vitro studies have indicated that sensitivity to the clastogenic effects of bleomycin on chromosomes was reduced with the introduction of ascorbic acid in a dose-dependent relationship. We report the results of a randomized clinical trial to determine whether increasing levels of oral ascorbic acid could reduce the levels of mutagen sensitivity. For this study, we recruited 228 healthy smokers from 21 centers around the country through the Clinical Community Oncology Program. Each individual was randomly assigned to one of four daily regimens: placebo, 1 g of ascorbic acid, 2 g of ascorbic acid, or 4 g of ascorbic acid. Treatments were administered for 16 weeks. Assessment of mutagen sensitivity was made at baseline and at weeks 4, 16, and 20 (4 weeks after cessation of treatment). Serum ascorbic acid levels were measured at baseline and at weeks 4 and 16. Demographic and risk factor data were collected at baseline and at each-measurement point. Analyses measured the differences of mutagen sensitivity levels across the four treatment arms, as well as investigating the correlation between serum ascorbic acid level and mutagen sensitivity levels in individuals. We did not find a dose-response relationship between ascorbic acid intake and mutagen sensitivity. Additionally, we did not find an association between serum ascorbic acid levels and mutagen sensitivity.

Administration, Oral↗

PubMed1997

Identifying and recruiting healthy control subjects from a managed care organization: a methodology for molecular epidemiological case-control studies of cancer.

Case-control studies with stringent matching criteria require large pools of healthy subjects from which to select matched controls. This paper describes a successful method of identifying a large pool of potential control subjects to participate in two molecular epidemiological case-control studies of lung cancer, each enrolling 400 case subjects and 400 control subjects. These studies are not population based, and the study base is not well-defined. Therefore, potential control subjects are being identified and recruited through 20 area clinic sites of a large multispecialty health maintenance organization. Because the research focus is driven by genetic hypotheses and we are controlling for multiple smoking-related variables, representativeness is of lesser concern. To identify potential control subjects, a one-page questionnaire is distributed to patients in the waiting room to assess contact information as well as data relevant to the case-control matching process. An average of 2,228 questionnaires are returned monthly toward a target pool of 40,000; of these, 59% of the respondents fulfill eligibility criteria as a control subject for one of the studies and are not averse to being contacted in the future for the purpose of research. When compared to former smokers and never smokers, current smokers in the control population were least likely to refuse further contact. A collaborative arrangement with a managed care organization offers a feasible mechanism through which researchers can access a large, ethnically diverse population of potential control subjects.

Adolescent↗

PubMed1997

Correlates of mutagen sensitivity in patients with upper aerodigestive tract cancer.

Although tobacco and alcohol use are the major determinants of upper aerodigestive tract carcinogenesis, not all smokers develop cancer. This phenomenon is due to individual variation in genetic susceptibility to carcinogens. One explanation may be differences in mutagen sensitivity (as measured by the in vitro bleomycin-induced mutagen sensitivity assay) in patients with squamous cell carcinoma of the upper aerodigestive tract. Antioxidant supplementation has also been shown to decrease DNA damage and thus may also inhibit carcinogenesis. In this study, we examined whether smoking, alcohol intake, and dietary antioxidant intake were correlated with mutagen sensitivity. The 612 patients evaluated are part of an ongoing multicenter Phase III trial of 13-cis retinoic acid for the prevention of second primary tumors. We found that patients with pharyngeal cancers were more likely than patients with oral cavity or larynx cancers to be mutagen sensitive. There were no significant differences in the distribution of mutagen sensitivity by sex or alcohol use. Never smokers were significantly more likely (61.1%) to be mutagen sensitive than current smokers (35.6%). Dietary consumption of the micronutrients alpha-carotene, beta-carotene, lutein, lycopene, and vitamin C was not correlated with mutagen sensitivity. Therefore, we suggest that mutagen sensitivity is an independent marker of cancer risk not affected by other known risk factors.

Adult↗

PubMed1996

Reduced DNA repair capacity in lung cancer patients.

Although lung cancer is the paradigm of a tobacco-induced malignancy, host-specific factors modulate susceptibility to tobacco carcinogenesis. Variations in DNA repair may influence the rate of removal of DNA damage and of fixation of mutations. To test the hypothesis that genetically determined DNA repair capacity (DRC) modulates lung cancer susceptibility, we conducted a pilot case-control study of 51 patients with newly diagnosed, previously untreated lung cancer and 56 controls identified from local community centers and frequency matched to the cases on age, sex, and ethnicity. The subjects were ascertained and interviewed for an ongoing molecular epidemiological investigation of lung cancer susceptibility. We measured DRC in the subjects' peripheral blood lymphocytes by using the host-cell reactivation assay, which measures cellular reactivation of a reporter gene damaged by exposure to 75 microM benzo(a)pyrene diol epoxide. The mean level of DRC in cases (3.3%) was significantly lower than that in controls (5.1%) (P < 0.01). Only nine cases (18%) had DNA repair levels greater than the median value of repair in the controls. This median level of DRC in controls was used as the cutoff value for calculating the odds ratios. After adjustment for age, sex, ethnicity, and smoking status, the cases were five times more likely than the controls to have reduced DRC (odds ratio, 5.7; 95% confidence interval, 2.1-15.7). Younger cases (< 65 years) and smokers were more likely than controls to have reduced DRC. These findings suggest that individuals with reduced DRC are at an increased risk of developing lung cancer.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗

PubMed1996

Lung carcinoma in former smokers.

BACKGROUND: A reduction in the risk of lung carcinoma and a lower death rate among former smokers (FS) compared with current smokers (CS) have been documented in numerous U.S. and international studies. The main objective of our study was to compare the differences in demographic and clinical characteristics in groups stratified by smoking status and gender to evaluate the effect of smoking history and cessation on age at lung carcinoma diagnosis and on specific histologic type. METHODS: We conducted a cross-sectional study of lung cancer at The University of Texas M.D. Anderson Cancer Center from January 1986 to December 1990 and from January 1992 to December 1993. This study included 1039 patients age 19-88 with confirmed primary lung carcinoma who responded to self-administered risk factor questionnaires. Among them, 497 patients (47.83%) were CS, 444 patients (42.73%) were FS, 98 patients (9.43%) had never smoked (NS), and 840 patients (80.8%) were heavy smokers (more than 20 pack-years). RESULTS: The median age at lung carcinoma diagnosis for FS was slightly later than that for CS. The histologic type of lung carcinoma for those who had quit smoking more than 20 years previously was not significantly different from that of NS, but was significantly different from that of CS (P < 0.05) and from those who quit smoking fewer than 10 years previously (P < 0.10). CS was a positive predictor for both small cell carcinoma (odds ratio [OR] = 8.79) and squamous cell carcinoma (OR = 2.11) and negatively associated with adenocarcinoma (OR = 0.50), whereas FS was a positive predictor only for small cell carcinoma (OR = 5.50). The variable of pack-years was negatively associated with adenocarcinoma and positively associated with small cell carcinoma in all patients combined and in women, and was also positively associated with squamous carcinoma in all patients after adjustment by smoking status. CONCLUSIONS: These results indicate that smoking cessation or less life-time smoking exposure affects the distribution of specific histologic subtypes of lung cancer, especially for women, and that smoking cessation may postpone the age at which lung cancer occurs.

Adenocarcinoma↗

PubMed1996

Benzo(a)pyrene diol epoxide-induced chromosomal aberrations and risk of lung cancer.

Benzo(a)pyrene is considered a classic DNA-damaging carcinogen and is one of a multitude of polycyclic aromatic hydrocarbons commonly found in tobacco smoke and in the ambient environment. In this report, we describe the characteristics of chromosomal aberrations induced in vitro by activated benzo(a)pyrene diol epoxide (BPDE) in lymphocyte cultures of 172 normal individuals ages 19-95 years and present the analysis of a pilot case-control study of 33 lung cancer patients and 96 selected controls without history of cancer and frequency matched on age (50-85 years) to the cases. The BPDE-induced chromosomal aberrations were predominantly single chromatid breaks, with few isochromatid breaks or exchange figures. In the 172 normal subjects, the frequencies of both spontaneous and BPDE-induced chromatid breaks were not correlated with age, sex, ethnicity, or tobacco use. However, the frequency of BPDE-induced chromatid breaks was significantly correlated with the frequency of spontaneous chromatid breaks (r = 0.19, P < 0.05). In addition, Hispanics had significantly higher mean BPDE-induced chromatid breaks than did non-Hispanic whites (P < 0.01). From the case-control analyses, the frequency of BPDE-induced chromosomal aberrations was significantly higher in cases (mean, 0.67 breaks/cell) than in controls (mean, 0.41 breaks/cell; P < 0.0001). An adjusted odds ratio of 6.53 (95% confidence interval, 3.74-11.4) for lung cancer was associated with increased frequency of these chromosomal aberrations. The higher rate of BPDE-induced chromosomal aberrations may be due to inefficient DNA repair. These findings warrant additional molecular epidemiological studies. The BPDE mutagen sensitivity assay will facilitate epidemiological studies of genetic susceptibility to smoking-related cancers.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗

PubMed1996

In vitro induction of benzo(a)pyrene diol epoxide-DNA adducts in peripheral lymphocytes as a susceptibility marker for human lung cancer.

Given the same exposure, DNA adduct profiles can be considered as a phenotypic marker for carcinogen metabolism and DNA repair, which may reflect individual susceptibility to chemical carcinogenesis. Based on this notion, we have established a straightforward assay that measures induced DNA adducts in peripheral lymphocytes exposed in vitro to a model carcinogen, benzo(a)pyrene diol epoxide (BPDE) by 32P-postlabeling. To test the hypothesis that the levels of induced DNA adducts are a predictor for cancer risk, we conducted a pilot study of 21 lung cancer patients and 41 healthy frequency-matched controls. We found that the peripheral lymphocytes of cancer patients tended to accumulate higher levels of BPDE-DNA adducts than controls did (mean +/- SE of relative adduct labeling x 10(7) value; 59.6 +/- 12.0 versus 39.4 +/- 6.1 for cases and controls, respectively; P = 0.09). Using the tertile relative adduct labeling value of controls (10 adducts/10(7) nucleotides) as the cutoff point, 18 of 21 cases and 23 of 41 controls distributed above this level (odds ratio, 4.7; 95% confidence interval, 1.2-18.5). In logistic regression analysis, the level of induced adduct was an independent risk factor (odds ratio, 6.4; 95% confidence interval, 1.3-29.4) after adjustment for the potential confounding factors, i.e., age, sex, ethnicity, and smoking. Stratified analyses showed that greater differences in DNA adduct levels induced by BPDE between cases and controls were observed in individuals younger than 65 years and in nonsmokers. Despite the small sample size, the significant association between the level of BPDE-induced DNA adducts and risk for lung cancer suggests that this assay is a promising method for further investigations.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗

PubMed1996

Genetic susceptibility to head and neck squamous cell carcinoma.

BACKGROUND: In addition to influences of exposure to carcinogenic compounds, the development of cancer may depend on an individual intrinsic cancer susceptibility. Biomarkers for cancer susceptibility can be powerful additions to epidemiologic analyses. PURPOSE: This multicenter, case-control analysis combines previously published data and new data to substantiate the value of mutagen sensitivity as a biomarker of susceptibility to head and neck squamous cell carcinoma and, more importantly, to gain insight into the interaction between susceptibility and exposure to carcinogens. METHODS: Mutagen sensitivity (mean number of chromatid breaks per cell of cultured lymphocytes treated with bleomycin in the late S-G2 phase of the cell cycle) was determined in 313 patients with head and neck cancer and in 334 control subjects at two major U.S. medical institutions and one European institution, yielding a unique study population. The ages of the case and control subjects, as well as their history of use of tobacco and alcohol, were also recorded. The relationships between variables were analyzed by use of Student's t tests, Spearman's rank correlations, and multiple linear regression. For estimation of cancer risk, crude odds rations (ORs) were measured and multiple logistic regression was performed. All P values were based on two-sided tests. RESULTS: There were no differences across institutions in the distribution of mutagen sensitivity (Kruskal-Wallis test) for both case subjects and control subjects. Values for case subjects were consistently and significantly (P<.0001) higher than values for control subjects in the overall analyses. Age and tobacco or alcohol use did not influence the outcome in terms of mutagen-sensitivity values for either the case or the control subjects. A mean number of breaks per cell dichotomized at 1.0 was found to be the best predictor of a hypersensitive phenotype. For nonsensitive, heavy smokers, the OR was 11.5 (95% confidence interval [CI] = 5.0-26.6). This risk increased dramatically in mutagen-hypersensitive, heavy smokers to 44.5 (95% CI = 17.4-114.0). Multiple logistic regression analysis confirmed these results, and a significant trend was found (P<.01) for the dose-dependent increase in cancer risk by smoking. The consumption of alcohol potentiated the effects of smoking, resulting in an OR of 57.5 (95% CI = 17.5-188.0) in hypersensitive persons. CONCLUSIONS: Mutagen sensitivity was found to be a biomarker of cancer susceptibility. This study underscores the importance of utilizing both susceptibility markers and the exposure data for the identification of persons at high risk of developing cancer. IMPLICATIONS: More accurate risk estimation can define susceptible subgroups who might be targeted for intensive behavioral interventions, surveillance through screening, and enrollment in chemoprevention programs.

Adult↗

PubMed1996

Sex chromosome abnormalities in lung cancer patients.

Chromosomal analyses of lymphocytes from lung cancer patients and normal subjects revealed that the X and the Y chromosomes have both structural and numerical abnormalities in higher frequency in patients compared to the controls. These abnormalities included chromatid/isochromatid breaks, translocations, ring formation, and selective nondisjunctions, resulting in multisomies of either the X or Y chromosomes. Possible significance of these genetic abnormalities are discussed in relation to lung cancer patients.

Adult↗

PubMed1996

Month-of-birth and incidence of acute lymphoblastic leukemia in children.

As a means of examining the virus-relatedness of acute lymphoblastic leukemia (ALL) in children, we investigated the association between month-of-birth and the occurrence of ALL in 1487 children aged 0-15 years at the time of diagnosis. Our hypothesis being that evidence of seasonal variation in births of ALL cases would suggest exposure to a transmissible etiologic agent during the perinatal period. The data were obtained from the Surveillance, Epidemiology, and End Results (SEER) Program and consisted of children diagnosed during the years 1973-1986. Aggregate monthly incidence rates of ALL stratified by month-of-birth, for each SEER site, all sites combined, and for broad geographic regions were calculated. No evidence for an association between month-of-birth and childhood ALL was found.

Adolescent↗