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Ann G Schwartz

Publications and source records attributed to Ann G Schwartz.

At least 19 recordsLinked to original sources
PubMed2025

Stratifying Lung Adenocarcinoma Risk with Multi-ancestry Polygenic Risk Scores in East Asian Never-Smokers.

BACKGROUND: Lung adenocarcinoma (LUAD) in never-smokers is a major public health burden, especially among East Asian women. Polygenic risk scores (PRSs) are promising for risk stratification but are primarily developed in European-ancestry populations. We aimed to develop and validate single- and multi-ancestry PRSs for East Asian never-smokers to improve LUAD risk prediction. METHODS: PRSs were developed using genome-wide association study summary statistics from East Asian (8,002 cases; 20,782 controls) and European (2,058 cases; 5,575 controls) populations. Single-ancestry models included PRS-25, PRS-CT, and LDpred2; multi-ancestry models included LDpred2+PRS-EUR128, PRS-CSx, and CT-SLEB. Performance was evaluated in independent East Asian data from the Female Lung Cancer Consortium (FLCCA) and externally validated in the Nanjing Lung Cancer Cohort (NJLCC). We assessed predictive accuracy via AUC, with 10-year and (age 30-80) absolute risks estimates. RESULTS: The best multi-ancestry PRS, using East Asian and European data via CT-SLEB (clumping and thresholding, super learning, empirical Bayes), outperformed the best East Asian-only PRS (LDpred2; AUC=0.629, 95% CI:0.618,0.641), achieving an AUC of 0.640 (95% CI:0.629,0.653) and odds ratio of 1.71 (95% CI:1.61,1.82) per SD increase. NJLCC Validation confirmed robust performance (AUC =0.649, 95% CI: 0.623, 0.676). The top 20% PRS group had a 3.92-fold higher LUAD risk than the bottom 20%. Further, the top 5% PRS group reached a 6.69% lifetime absolute risk. Notably, this group reached the average population 10-year LUAD risk at age 50 (0.42%) by age 41, nine years earlier. CONCLUSIONS: Multi-ancestry PRS approaches enhance LUAD risk stratification in East Asian never-smokers, with consistent external validation, suggesting future clinical utility.

East Asian never smokers↗
PubMed2025

Genetic analysis in African ancestry populations reveals genetic contributors to lung cancer susceptibility.

Striking disparities in lung cancer exist, with Black/African American individuals disproportionately affected by lung cancer, yet the genetic architecture in African ancestry individuals is poorly understood. We aimed to address this by performing a comprehensive genetic association study of lung cancer, incorporating local ancestry, across 6,490 African ancestry individuals (2,390 individuals with lung cancer and 4,100 control subjects). We identified a single genome-wide significant (p < 5 &#xd7; 10-8) locus, 15q25.1 (lead SNP rs17486278, OR [95% CI] = 1.34 [1.23-1.45], p = 4.52 &#xd7; 10-12), that has consistently shown a strong association with lung cancer across populations. Additionally, we identified nine suggestive (p < 1 &#xd7; 10-6) loci. Four of these loci (3p12.1, 8q22.2, 14q11.2, and 18q22.3) have no prior reported associations with lung cancer. We performed a multi-ancestry lung cancer meta-analysis using prior large-scale summary statistics from European and Asian ancestry populations, incorporating our African ancestry results. The meta-analysis identified 17 genome-wide significant loci, including an association with locus 4q35.2 (p = 1.22 &#xd7; 10-8), a genomic region that has been previously linked to forced expiratory volume. Genome-wide SNP-based heritability for lung cancer was 16% among African ancestry individuals. Follow-up in silico functional analyses identified genetically regulated gene expression (GReX) of nine genes (AC012184.3, ADK, CCDC12, CHRNA3, EML4, PSMA4, SNRNP200, TMEM50A, and ZYG11A) associated with lung cancer risk and biological pathways relevant to cancer and lung function. Cumulatively, these findings further elucidate the genetic architecture of lung cancer in African ancestry individuals, confirming prior loci and revealing new loci.

Female↗
PubMed2007

Identification of a novel tumor suppressor gene p34 on human chromosome 6q25.1.

In this study, we observed loss of heterozygosity (LOH) in human chromosomal fragment 6q25.1 in sporadic lung cancer patients. LOH was observed in 65% of the 26 lung tumors examined and was narrowed down to a 2.2-Mb region. Single-nucleotide polymorphism (SNP) analysis of genes located within this region identified a candidate gene, termed p34. This gene, also designated as ZC3H12D, C6orf95, FLJ46041, or dJ281H8.1, carries an A/G nonsynonymous SNP at codon 106, which alters the amino acid from lysine to arginine. Nearly 73% of heterozygous lung cancer tissues with LOH and the A/G SNP also exhibited loss of the A allele. In vitro clonogenic and in vivo nude mouse studies showed that overexpression of the A allele exerts tumor suppressor function compared with the G allele. p34 is located within a recently mapped human lung cancer susceptibility locus, and association of the p34 A/G SNP was tested among these families. No significant association between the less frequent G allele and lung cancer susceptibility was found. Our results suggest that p34 may be a novel tumor suppressor gene involved in sporadic lung cancer but it seems not to be the candidate familial lung cancer susceptibility gene linked to chromosomal region 6q23-25.

Alleles↗
PubMed2006

The molecular epidemiology of lung cancer.

Lung cancer is the leading cause of cancer mortality worldwide. There have been only slight improvements in early diagnosis and survival, reflecting limited advances in screening and treatment for lung cancer. The identification of host differences in susceptibility to lung carcinogens, in particular to cigarette smoke, is essential in predicting who is at highest risk. Susceptibility differences in the form of rare, high-penetrance genes are suggested from studies of familial aggregation of lung cancer and a linkage study. Studies focused on more common, low-penetrance genes in the tobacco smoke metabolism pathways (phase I and phase II enzymes) and DNA repair pathways are reviewed, as are inflammation and cell cycle-related genes and DNA adducts as intermediate biomarkers. Also reviewed are studies of epigenetic mechanisms, such as methylation, as alternative sources of variation in host susceptibility. Studies of molecular epidemiology in lung cancer survival are discussed briefly. In the future, studies that focus on complex interactions between multiple genes and environmental exposures within pertinent pathways are needed. New technological advances in genotyping will help move the field forward.

Carcinogens↗
PubMed2006

Polymorphisms in genes related to bacterial lipopolysaccharide/peptidoglycan signaling and gastric precancerous lesions in a population at high risk for gastric cancer.

As Helicobacter pylori (HP) is a Gram-negative bacterium, we investigated the associations between several functional polymorphisms in genes involved in lipopolysaccharide (LPS) signaling and the prevalence of various stages of gastric premalignant lesions in a Venezuelan population. The two NOD2 polymorphisms, del3020insC and Gly908Arg, were too infrequent to study their associations with gastric lesions. The risk of intestinal metaplasia (IM) was significantly increased among subjects with the CD14 T-260 allele compared to those without this allele. A similar, but nonsignificant increase in risk for dysplasia was observed among homozygotes of this allele. There was no association between TLR4 Asp299Gly polymorphism and any type of lesions, except for a slight nonsignificant increase in risk of IM associated with the AA genotype among subjects with a higher histological HP score. These results suggest that genetic polymorphisms in HP LPS signaling may be implicated in the development of intermediate stages of gastric premalignant lesions.

Adult↗
PubMed2006

Host-bacterial interaction in the development of gastric precancerous lesions in a high risk population for gastric cancer in Venezuela.

Helicobacter pylori (HP) infection affects over 50% of the world's population. The prevalence is over 90% in populations at high risk for gastric cancer, but clinical outcomes of the infection are highly variable and thus host genetic factors have been suggested to play a role in its outcomes in addition to bacterial factors. In this study, we examined the effects of common functional genetic polymorphisms of several proinflammatory cytokines known to be overexpressed in HP-infected gastric mucosa on the risk of various stages of gastric premalignant lesions. The odds ratios (ORs) and 95% confidence intervals (CI) for atrophic gastritis, intestinal metaplasia and dysplasia were estimated by multinominal logistic regression analysis among 2,033 Venezuelan subjects. There was a significant effect of IL8 -251A allele on the prevalence of dysplasia (p = 0.021). The OR associated with the A-allele was 1.34 (95% CI: 0.82-2.18) for heterozygotes and 2.00 (95% CI: 1.13-3.56) for homozygotes, compared with the TT genotype. Furthermore, there was a statistically significant interaction between the number of A-alleles and HP cag A genotype (p = 0.009), suggesting that the A-allele increased the risk of dysplasia only when cag A was present. The OR for the AA compared with TT genotype was 3.22 (95% CI: 1.60-6.52) in this group. There were no associations with other proinflammatory cytokines studied, i.e., IL1 beta, IL6, monocyte chemoattractant protein 1 (MCP1) and TNF alpha, or with other stages of premalignant lesions. The present study provides important evidence suggesting host-bacterial interactions in the development of gastric precancerous lesions.

Alleles↗
PubMed2006

Breast cancer risk estimates for relatives of white and African American women with breast cancer in the Women's Contraceptive and Reproductive Experiences Study.

PURPOSE: Family history is a well-recognized risk factor for breast cancer. Familial aggregation and segregation analyses have estimated breast cancer risk based on family history primarily for white women; such information is limited for African American (AA) women. The purpose of this report is to update breast cancer risk estimates associated with a family history of breast cancer for white and AA women. METHODS: We used family cancer history from 2,676 white and 1,525 AA women with breast cancer (probands) in the population-based National Institute of Child Health and Human Development's Women's Contraceptive and Reproductive Experiences (CARE) Study to estimate age-specific breast cancer risks in their first degree adult female relatives. Cumulative hazard curves were calculated for relatives of all probands using Cox proportional hazards models, and were stratified by the proband's race and age at diagnosis and number of relatives affected. RESULTS: Breast cancer risks for white and AA women with a family history of the disease are similar through age 49 years, but diverge afterwards, with higher risks by age 79 in white women than in AA women (17.5% [SE, 0.9%] v 12.2% [SE, 1.1%]; P < .001). These risks increase as the number of affected first degree relatives increases, reaching 25.2% (SE, 3.4%) and 16.9% (SE, 4.0%) in white and AA women with more than one affected relative, respectively (P = .3). CONCLUSION: We found age-related racial differences in breast cancer risk in women with a family history of breast cancer and have updated risk estimates for white and AA women for clinical use.

Adult↗
PubMed2006

Genetic polymorphisms in anti-inflammatory cytokine signaling and the prevalence of gastric precancerous lesions in Venezuela.

OBJECTIVES: The aim of the study was to assess the effects of genetic polymorphisms in anti-inflammatory mediators, i.e., IL10, IL4 and IL4R on the prevalence of gastric precancerous lesions and their interactions with other environmental factors. METHODS: The study population consisted of 2,033 Venezuelan subjects known to have extremely high Helicobacter Pylori (HP) infection rates. The odds ratios (OR) and 95% confidence intervals (CI) associated with these polymorphisms were estimated by multinominal logistic regression models for gastric precursor lesions. RESULTS: We found a 60% increase in risk of intestinal metaplasia (IM) and dysplasia combined (OR 1.62, 95% CI: 1.10-2.38) among the carriers of the IL10-1082 low activity allele. This increased risk was more pronounced for dysplasia than for IM. On the other hand, homozygotes with the low activity allele of the A398G polymorphism in the IL4R gene had a modest increase in risk of atrophic gastritis (OR = 1.52, 95% CI: 1.05-2.21), compared with homozygotes of the high activity allele. There were no statistically significant synergetic interactions between these polymorphisms and environmental risk factors (low fruit intake, high starchy vegetable intake and cigarette smoking) for these lesions. CONCLUSION: While the results of the present study suggest roles of genetic variability in these anti-inflammatory mediators in different stages of gastric carcinogenesis, there is high likelihood that they were chance findings due to multiple comparisons.

Adult↗
PubMed2005

Nuclear estrogen receptor beta in lung cancer: expression and survival differences by sex.

PURPOSE: A role for estrogens in determining lung cancer risk and prognosis is suggested by reported sex differences in susceptibility and survival. Archival lung tissue was evaluated for the presence of nuclear estrogen receptor (ER)-alpha and ER-beta and the relationship between ER status, subject characteristics, and survival. EXPERIMENTAL DESIGN: Paraffin-embedded lung tumor samples were obtained from 214 women and 64 men from two population-based, case-control studies as were 10 normal lung autopsy samples from patients without cancer. Nuclear ER-alpha and ER-beta expression was determined by immunohistochemistry. Logistic regression was used to identify factors associated with ER positivity and Cox proportional hazards models were used to measure survival differences by ER status. RESULTS: Neither tumor (0 of 94) nor normal (0 of 10) lung tissue stained positive for ER-alpha. Nuclear ER-beta positivity was present in 61% of tumor tissue samples (170 of 278; 70.3% in men and 58.3% in women) and 20% of normal tissue samples (2 of 10; P = 0.01). In multivariate analyses, females were 46% less likely to have ER-beta-positive tumors than males (odds ratio, 0.54; 95% confidence interval, 0.27-1.08). This relationship was stronger and statistically significant in adenocarcinomas (odds ratio, 0.40; 95% confidence interval, 0.18-0.89). Women with ER-beta-positive tumors had a nonsignificant 73% (P = 0.1) increase in mortality, whereas men with ER-beta-positive tumors had a significant 55% (P = 0.04) reduction in mortality compared with those with ER-beta-negative tumors. CONCLUSIONS: This study suggests differential expression by sex and influence on survival in men of nuclear ER-beta in lung cancer, particularly in adenocarcinomas.

Adenocarcinoma↗
PubMed2005

Familial lung cancer: genetic susceptibility and relationship to chronic obstructive pulmonary disease.

Lung cancer continues to be the leading cause of cancer death, and although most lung cancer is attributable to cigarette smoking, underlying genetic susceptibility is suggested by studies demonstrating familial aggregation. The first family linkage study of lung cancer has identified linkage of lung, laryngeal, and pharyngeal cancer in families to a region on chromosome 6q23-25. Because lung cancer and chronic obstructive pulmonary disease (COPD) are known to aggregate in families beyond shared risk associated with smoking, the linkage results are compared and contrasted with results from genomewide linkage and association studies and candidate gene studies searching for genes for lung cancer, lung function, and COPD. Linkage on chromosome 6q to both lung cancer and lung function, and on 12 to lung cancer, COPD, and lung function, together with overlap in candidate genes for these outcomes, suggests that future research into underlying genetic mechanisms of lung disease would benefit from broadening the collection of family history data and better defining the "high risk" population. As familial risk of lung disease is better defined, referral into screening programs and prevention trials can be better targeted to reach families with both a history of lung cancer and COPD.

Genetic Linkage↗
PubMed2005

Risk of lung cancer among white and black relatives of individuals with early-onset lung cancer.

CONTEXT: Evidence exists that lung cancer aggregates in families and recent findings of a chromosomal region linked to lung cancer susceptibility support a genetic component to risk. Family studies of early-onset lung cancer patients offer a unique opportunity to evaluate lifetime risk of lung cancer in relatives. OBJECTIVE: To measure lung cancer aggregation and estimate lifetime risk among relatives of early-onset cases and population-based controls. DESIGN AND SETTING: Familial aggregation and cumulative risk estimates from interview data of incident cases and concurrently ascertained controls between 1990 and 2003 in metropolitan Detroit, Mich. PARTICIPANTS: The study included 7576 biological mothers, fathers, and siblings of 692 early-onset cases and 773 frequency-matched controls. One third of the population was black. MAIN OUTCOME MEASURES: Cumulative lifetime risk of lung cancer, stratified by race and smoking behavior in relatives of early-onset cases and controls. RESULTS: Smokers with a family history of early-onset lung cancer in a first-degree relative had a higher risk of developing lung cancer with increasing age than smokers without a family history. An increase in risk occurs after age 60 years in these individuals, with 17.1% (SE 2.4%) of white case relatives and 25.1% (SE 5.8%) of black case relatives diagnosed with lung cancer by age 70 years. Relatives of black cases were at statistically significant increased risk of lung cancer compared with relatives of white cases (odds ratio, 2.07, 95% confidence interval, 1.29-3.32) after adjusting for age, sex, pack-years, pneumonia, and chronic obstructive lung disease. CONCLUSIONS: First-degree relatives of black individuals with early-onset lung cancer have greater risk of lung cancer than their white counterparts, and these risks are further amplified by cigarette smoking. These data provide estimates of lung cancer risk that can be used to offer counseling to family members of patients with early-onset lung cancer.

Adult↗
PubMed2005

Multiplicity of abnormal promoter methylation in lung adenocarcinomas from smokers and never smokers.

The prevalence of methylation of the p16, DAPK and RASSF1A genes was investigated in lung adenocarcinoma from smokers, former uranium miners and never smokers. The association between a common genetic alteration in adenocarcinoma, mutation of the K-ras gene and methylation of these genes, as well as survival was examined. Adenocarcinomas from 157 smokers, 46 never smokers and 34 former uranium miners were evaluated for methylation of the p16, DAPK and RASSF1A genes using the methylation-specific PCR assay. Comparisons were also made to prevalences of methylation of the MGMT gene and mutation of the K-ras gene previously examined in these tumors. The prevalence of methylation for all genes was similar between adenocarcinomas from smokers and never smokers, although the prevalence for methylation of the p16 gene tended to be higher in smokers compared to never smokers. A significantly higher prevalence for p16 methylation was seen in central vs. peripheral lung tumors. At least 1 gene was methylated in 35% of stage I tumors, whereas 2 and >/=3 genes were methylated in 40% and 16% of tumors, respectively. Methylation of all genes was independent of K-ras mutation, whereas methylation of the DAPK and RASSF1A genes was positively associated. Environmental tobacco smoke, the strongest lung cancer risk factor among never smokers, induces adenocarcinoma in part through inactivation of the p16, DAPK and RASSF1A genes. Adenocarcinomas may develop through 2 distinct processes: multiple gene inactivations through promoter hypermethylation and activation of the K-ras gene.

Adenocarcinoma↗
PubMed2005

Racial differences in the familial aggregation of breast cancer and other female cancers.

Although breast cancer familial aggregation has been studied in Caucasians, information for African-Americans is scant. We used family cancer history from the Women's Contraceptive and Reproductive Experiences study to assess the aggregation of breast and gynecological cancers in African-American and Caucasian families. Information was available on 41,825 first and second-degree relatives of Caucasian and 28,956 relatives of African-American participants. We used a cohort approach in which the relative's cancer status was the outcome in unconditional logistic regression and adjusted for correlated data using generalized estimating equations. Race-specific models included a family history indicator, the relative's age, and type. Relative risk (RR) estimates for breast cancer were highest for first-degree relatives, and the overall RR for breast cancer among case relatives was 1.96 (95% CI = 1.68-2.30) for Caucasian and 1.78 (95% CI = 1.41-2.25) for African-Americans. The effect of CARE participants' reference age on their relatives' breast cancer risk was greatest among first-degree relatives of African-American patients with RRs (95% CI) for ages <45 and > or =45 of 2.97 (1.86-4.74) and 1.48 (1.14-1.92), respectively. Among Caucasians, first-degree relatives of case subjects were at greater risk for ovarian cancer, particularly relatives younger than 45 years (RR (95% CI) = 2.06 (1.02-4.12)), whereas African-American first-degree relatives of case subjects were at increased cervical cancer risk (RR (95% CI) = 2.17 (1.22-3.85). In conclusion, these racially distinct aggregation patterns may reflect different modes of inheritance and/or environmental factors that impact cancer risk.

Adult↗
PubMed2005

Examining population stratification via individual ancestry estimates versus self-reported race.

Population stratification has the potential to affect the results of genetic marker studies. Estimating individual ancestry provides a continuous measure to assess population structure in case-control studies of complex disease, instead of using self-reported racial groups. We estimate individual ancestry using the Federal Bureau of Investigation CODIS Core short tandem repeat set of 13 loci using two different analysis methods in a case-control study of early-onset lung cancer. Individual ancestry proportions were estimated for "European" and "West African" groups using published allele frequencies. The majority of Caucasian, non-Hispanics had >50% European ancestry, whereas the majority of African Americans had <20% European ancestry, regardless of ancestry estimation method, although significant overlap by self-reported race and ancestry also existed. When we further investigated the effect of ancestry and self-reported race on the frequency of a lung cancer risk genotype, we found that the frequency of the GSTM1 null genotype varies by individual European ancestry and case-control status within self-reported race (particularly for African Americans). Genetic risk models showed that adjusting for individual European ancestry provided a better fit to the data compared with the model with no group adjustment or adjustment for self-reported race. This study suggests that significant population substructure differences exist that self-reported race alone does not capture and that individual ancestry may be confounded with disease status and/or a candidate gene risk genotype.

Black People↗
PubMed2005

Evaluation of African-American and white racial classification in a surveillance, epidemiology, and end results cancer registry.

OBJECTIVES: This study evaluated the validity of registry-reported race for individuals who participated in research studies conducted since 1980 through the Metropolitan Detroit Cancer Surveillance System (MDCSS), a Surveillance, Epidemiology, and End Results (SEER) Program registry. METHODS: 5329 individuals who self-identified as African American or White and were classified in the MDCSS registry as African American or White were included. Self-identified and registry-reported race were compared, and associations between demographics and racial misclassification were examined. RESULTS: Most self-identified African Americans and Whites were correctly classified (sensitivity=98.5%, specificity=99.7%). Males were two times more likely to be misclassified than females [odds ratio (OR)=2.13, 95% confidence interval (CI): 1.06-4.29]. Individuals diagnosed with cancer after 1990 were two times more likely to be misclassified than those diagnosed before 1990 (OR= 2.17, 95% CI: 1.07-4.42). African Americans were four times more likely to be misclassified than Whites (OR=4.39, 95% CI: 2.24-8.60). CONCLUSIONS: Misclassification in the MDCSS registry of African Americans as Whites, and vice versa, is relatively low. Additional studies should evaluate misclassification of African Americans and Whites as other races and/or ethnicities in the SEER registry.

Black or African American↗
PubMed2004

Chest radiography for the diagnosis of acute aortic syndrome.

PURPOSE: We sought to assess the diagnostic accuracy of routine chest radiography for the acute aortic syndrome (dissection, intramural hematoma, penetrating ulcer, or nondissecting aneurysm). METHODS: During a 6-year period, 216 patients (143 men, 73 women; mean [+/- SD] age, 58 +/- 17 years) underwent chest radiography for suspected acute aortic syndrome. Chest films were re-evaluated blindly for aortic disease, based on an overall impression using standard criteria such as widening of the aortic contour and mediastinal shadow. Findings were matched to tomographic images, anatomical inspection, or both, as the criterion standard; aortic disease was confirmed in 109 (50%) of the patients. RESULTS: Chest radiography had a sensitivity of 64% (70/109) and a specificity of 86% (92/107) for aortic disease. Sensitivity was 67% (38/57) for overt aortic dissection, 61% (22/36) for nondissecting aneurysm, and 63% (10/16) for intramural hemorrhage or penetrating ulcer. However, sensitivity was lower for pathology confined to the proximal aorta (47% [21/45]) than for disease involving distal aortic segments (77% [49/64]). A receiver operating characteristic curve analysis of aortic diameters failed to identify a threshold for the diagnosis of aortic disease. CONCLUSION: Chest radiography is of limited value for diagnosing the acute aortic syndrome, particularly for conditions confined to the ascending aorta. Since a definitive diagnosis is required in any patient with clinically suspected acute aortic syndrome, routine chest radiography should be replaced by tomographic aortic imaging.

Acute Disease↗
PubMed2004

Microsatellite alterations in african americans with head and neck cancer.

OBJECTIVE: To determine the genetic differences between African Americans (AA) and Non-African Americans (NAA) with head and neck squamous cell carcinoma (HNSCC). METHODS: DNA was obtained from tumor tissues and peripheral blood from 18 AA and 19 NAA patients with HNSCC. Microsatellite analysis using a fluorescent technique was performed on chromosomal arms 1p, 3p, 4q, 9p, 13q, and 17p. Statistical analyses were performed on the molecular and clinical outcome data. RESULTS: Based on the Surveillance, Epidemiologic, and End Result (SEER) data from southeast Michigan, the incidence rate of HNSCC in AA has been higher than for NAA, and the overall 5-year relative survival rate is lower for AA than NAA (36.2% vs. 47.6%). In this study, we found that the rate of loss of heterozygosity of chromosomal arms 1p, 3p, 4q, 9p, 13q, and 17p ranged from 68.8% to 83.3% for HNSCC in AA and from 66.7% to 90.0% in NAA. The difference in the rates of microsatellite alterations in chromosomal arms 3p, 4q, and 9p between AA and NAA were between 12.5% and 20% and were not statistically significant. CONCLUSION: The incidence and clinical outcomes for AA with HNSCC are different from that of NAA in southeast Michigan. In our group of patients with HNSCC, differences in rates of microsatellite alterations and survival were found between AA and NAA; however, these differences were not statistically significant. We conclude that genetic difference, as determined by the rates of microsatellite alterations, is not predictive of outcome difference between AA and NAA HNSCC patients.

Adult↗