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  • American Association for Cancer Research (AACR)  (97)
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  • 1
    Online-Ressource
    Online-Ressource
    Abstract B94: Pharmacogenetics of retinoid chemoprevention in head and neck cancer patients: Modulation of response by common genetic variation in the mTOR signaling pathway
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Prevention Research Vol. 3, No. 1_Supplement ( 2010-01-07), p. B94-B94
    Details
    In: Cancer Prevention Research, American Association for Cancer Research (AACR), Vol. 3, No. 1_Supplement ( 2010-01-07), p. B94-B94
    Kurzfassung: Patients diagnosed with early stage head and neck squamous cell carcinoma (HNSCC) have a high risk of developing second primary tumors (SPT) or recurrence following curative purpose therapy. To prevent these occurrences, several chemoprevention agents have been developed, including 13-cis-retinoid acid (13-cRA). However, results from clinical trials have remained inconclusive and suggest that biomarkers may be needed to select patients who will receive benefit from therapy. The mTOR signaling pathway plays a major role in the regulation of cell growth, cell survival, and apoptosis. We hypothesized that genetic variation in this pathway may serve as prognostic factors for the development of SPT/recurrence and affect response to chemoprevention therapy. We genotyped 137 SNPs from genes within this pathway in 450 HNSCC patients who received 13-cRA or placebo as part of the Retinoid Head and Neck Second Primary Trial. Genotypes were then analyzed for association with risk of SPT/recurrence to identify biomarkers for prognosis and treatment response. Twenty-two genetic loci were significant prognostic factors for SPT/recurrence in the placebo treatment group. Of these, nine were SNPs within the tuberous sclerosis 1 (TSC1) gene and most often resulted in an increased SPT/recurrence risk for the majority of patients carrying the wild-type genotype. Two of these alleles (rs4962225 and rs7035940) were in strong linkage disequilibrium and resulted in a high risk of SPT/recurrence (HR: 1.92, 95% CI: 1.15–3.23) and a significant 18 month survival disadvantage (Log-rank P = 0.026) in those carrying the wild-type genotype. These results indicate that this locus may be a potential target for chemoprevention. Intriguingly, although 13-cRA did not show a reduction in SPT/recurrence risk overall, response to this therapy was significantly different depending on the patient's genetic background for these potential targets. A significant modulation of SPT/recurrence risk in those who received 13-cRA was observed for seven of the prognostic TSC1 SNPs. The majority of the population with the wild-type genotype were conferred the protective effect of 13-cRA, indicating that the high-risk group for SPT/recurrence were being effectively treated by this chemoprevention intervention. Individuals carrying the wild-type genotype for either TSC1 rs4962225 or rs7035940 were at a 43% reduced risk (95% CI: 0.37–0.88). However those who carried at least one variant allele did not receive the benefit of 13-cRA treatment and were at an increased risk (HR: 1.91, 95% CI: 1.10–3.32). These results indicate that genetic variation within the mTOR pathway, particularly TSC1, could potentially be used to better identify patients who are at high-risk of SPT/recurrence and also those who are candidates for chemoprevention therapy based on their favorable genetic background. Citation Information: Cancer Prev Res 2010;3(1 Suppl):B94.
    Materialart: Online-Ressource
    ISSN: 1940-6207 , 1940-6215
    URL: Article
    DOI: 10.1158/1940-6207.PREV-09-B94
    Sprache: Englisch
    Verlag: American Association for Cancer Research (AACR)
    Publikationsdatum: 2010
    ZDB Id: 2422346-3
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  • 2
    Online-Ressource
    Online-Ressource
    Abstract A105: Genetic variations in sonic pathway genes as predictors of bladder cancer risk
    American Association for Cancer Research (AACR) ; 2008
    In:  Cancer Prevention Research Vol. 1, No. 7_Supplement ( 2008-11-01), p. A105-A105
    Details
    In: Cancer Prevention Research, American Association for Cancer Research (AACR), Vol. 1, No. 7_Supplement ( 2008-11-01), p. A105-A105
    Kurzfassung: A105 BACKGROUND The hedgehog (Hh) signaling pathway plays a crucial role in normal embryonic development. However, abnormal activation of the pathway later in life has been demonstrated in a variety of human diseases, including bladder cancer. METHODS We genotyped 171 potentially functional single nucleotide polymorphisms (SNPs) and tagging SNPs among seven Sonic Hedgehog pathway-related genes in a case-control study including 803 Caucasian bladder cancer patients and 803 matched controls. RESULTS The homozygous variant genotype of a SNP located in the Intron of Gli2 (rs4848123) was associated with a significantly increased bladder cancer risk [odds ratios (OR), 4.21; 95% confidence interval (95% CI), 1.15-15.44]. Likewise, the homozygous variant genotype of a 3’ UTR SNP (rs3823720) and a SNP in the Intron (rs10951671) of GLI3 was associated with a significantly increased bladder cancer risk (OR, 1.58, 95% CI, 1.10-2.26; and OR, 1.87, 95% CI, 1.14-3.06; respectively). To assess the cumulative effects, we performed a combined unfavorable genotype analysis that included all SNPs showing at least a borderline statistical significance. We found that, compared with the low-risk reference group with less than two unfavorable genotypes, the medium-risk group with two unfavorable genotypes exhibited a 1.29-fold (0.92-1.81) increased risk and the high-risk group with more than two unfavorable genotypes exhibited a 1.92-fold (1.36-2.71) increased risk (P(trend) & lt; 0.0001). CONCLUSION To our knowledge, this is the first epidemiologic study showing that sonic pathway-related genetic variants may affect bladder cancer risk individually and jointly. Citation Information: Cancer Prev Res 2008;1(7 Suppl):A105.
    Materialart: Online-Ressource
    ISSN: 1940-6207 , 1940-6215
    URL: Article
    DOI: 10.1158/1940-6207.PREV-08-A105
    Sprache: Englisch
    Verlag: American Association for Cancer Research (AACR)
    Publikationsdatum: 2008
    ZDB Id: 2422346-3
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  • 3
    Online-Ressource
    Online-Ressource
    Abstract A93: Genetic variations in aging related genes/pathways and colorectal cancer risk
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Prevention Research Vol. 5, No. 11_Supplement ( 2012-11-01), p. A93-A93
    Details
    In: Cancer Prevention Research, American Association for Cancer Research (AACR), Vol. 5, No. 11_Supplement ( 2012-11-01), p. A93-A93
    Kurzfassung: Advanced age is arguably the most important risk factor for developing cancer. About 77% of all cancers are diagnosed in individuals 55 years of age and older. Aging is especially a dominant risk factor for colorectal cancer (CRC), with 91% of cases diagnosed in individuals 50 years of age and older. A number of genes and signaling pathways have been indicated in the aging process in model organisms including mammals, e.g. the insulin/IGF-1 signaling pathway, mTOR pathway and telomere and telomerase pathway. Recently, genome-wide association studies also identified several single nucleotide polymorphisms (SNPs) associated with longevity. Therefore, we hypothesized that genetic variations of the genes and pathways related to aging might be associated with CRC risk. We systematically identified 189 putative functional SNPs in 109 aging-related genes and 20 longevity-associated SNPs from GWAS. In the discovery phase, we genotyped these SNPs in 797 Caucasian CRC cases and 797 matched healthy control subjects. In main effect analysis, 10 SNPs were significantly associated with altered CRC risk. When evaluating combined effects of these SNPs, we found a significant gene dosage effect for increased CRC risk with increasing number of unfavorable genotypes. Compared with individuals carrying fewer than three unfavorable genotypes, individuals with six and more than six of these unfavorable genotypes exhibited a 2.06-fold (95% CI: 1.24-3.43, P = 0.006) and a 2.44-fold (95% CI: 1.76-3.38, P = 7.56×10−8) increased risk of CRC, respectively (P for trend 1.25×10−9). Higher order gene-gene interaction analysis also revealed potential relationships among SNPs in TP53, ERCC2, GPR133, PRKAG3, TEP1, TSC1 and LMNA that further defined risk groups for CRC. Our results suggest that genetic polymorphisms in aging-related genes and pathways may modify CRC susceptibility both individually and jointly. Replication is currently underway to validate these findings. Citation Format: Fanmao Zhang, Cathy Eng, Moubin Lin, Michelle A.T. Hildebrandt, Yonggang He, Jie Lin, Maosheng Huang, Jian Gu, Xifeng Wu. Genetic variations in aging-related genes/pathways and colorectal cancer risk. [abstract]. In: Proceedings of the Eleventh Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2012 Oct 16-19; Anaheim, CA. Philadelphia (PA): AACR; Cancer Prev Res 2012;5(11 Suppl):Abstract nr A93.
    Materialart: Online-Ressource
    ISSN: 1940-6207 , 1940-6215
    URL: Article
    DOI: 10.1158/1940-6207.PREV-12-A93
    Sprache: Englisch
    Verlag: American Association for Cancer Research (AACR)
    Publikationsdatum: 2012
    ZDB Id: 2422346-3
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  • 4
    Online-Ressource
    Online-Ressource
    Genetic Variations in the Sonic Hedgehog Pathway Affect Clinical Outcomes in Non–Muscle-Invasive Bladder Cancer
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Prevention Research Vol. 3, No. 10 ( 2010-10-01), p. 1235-1245
    Details
    In: Cancer Prevention Research, American Association for Cancer Research (AACR), Vol. 3, No. 10 ( 2010-10-01), p. 1235-1245
    Kurzfassung: Sonic hedgehog (Shh) pathway genetic variations may affect bladder cancer risk and clinical outcomes. Therefore, we genotyped 177 single-nucleotide polymorphisms (SNP) in 11 Shh pathway genes in a study including 803 bladder cancer cases and 803 controls. We assessed SNP associations with cancer risk and clinical outcomes in 419 cases of non–muscle-invasive bladder cancer (NMIBC) and 318 cases of muscle-invasive and metastatic bladder cancer (MiMBC). Only three SNPs (GLI3 rs3823720, rs3735361, and rs10951671) reached nominal significance in association with risk (P ≤ 0.05), which became nonsignificant after adjusting for multiple comparisons. Nine SNPs reached a nominally significant individual association with recurrence of NMIBC in patients who received transurethral resection (TUR) only (P ≤ 0.05), of which two (SHH rs1233560 and GLI2 rs11685068) were replicated independently in 356 TUR-only NMIBC patients, with P values of 1.0 × 10−3 (SHH rs1233560) and 1.3 × 10−3 (GLI2 rs11685068). Nine SNPs also reached a nominally significant individual association with clinical outcome of NMIBC patients who received Bacillus Calmette-Guérin (BCG; P ≤ 0.05), of which two, the independent GLI3 variants rs6463089 and rs3801192, remained significant after adjusting for multiple comparisons (P = 2 × 10−4 and 9 × 10−4, respectively). The wild-type genotype of either of these SNPs was associated with a lower recurrence rate and longer recurrence-free survival (versus the variants). Although three SNPs (GLI2 rs735557, GLI2 rs4848632, and SHH rs208684) showed nominal significance in association with overall survival in MiMBC patients (P ≤ 0.05), none remained significant after multiple-comparison adjustments. Germ-line genetic variations in the Shh pathway predicted clinical outcomes of TUR and BCG for NMIBC patients. Cancer Prev Res; 3(10); 1235–45. ©2010 AACR.
    Materialart: Online-Ressource
    ISSN: 1940-6207 , 1940-6215
    URL: Article
    DOI: 10.1158/1940-6207.CAPR-10-0035
    Sprache: Englisch
    Verlag: American Association for Cancer Research (AACR)
    Publikationsdatum: 2010
    ZDB Id: 2422346-3
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  • 5
    Online-Ressource
    Online-Ressource
    Abstract B40: Genetic variations in PI3K-AKT-mTOR pathway and bladder cancer risk
    American Association for Cancer Research (AACR) ; 2008
    In:  Cancer Prevention Research Vol. 1, No. 7_Supplement ( 2008-11-01), p. B40-B40
    Details
    In: Cancer Prevention Research, American Association for Cancer Research (AACR), Vol. 1, No. 7_Supplement ( 2008-11-01), p. B40-B40
    Kurzfassung: B40 Bladder cancer is a complex disease involving multiple genes interacting with each other and/or with environment factors in the tumorigenesis process. We examined 245 SNPs of 22 genes of PI3K-AKT-mTOR pathway which is an essential cellular pathway controlling cell growth, proliferation and survival. We used a case-control design with 803 cases and 803 controls systematically evaluate single nucleotide polymorphisms (SNPs) in this pathway as predicators of bladder cancer risk, in close interaction with environmental factors. In individual SNP analysis, increased bladder cancer risk was significantly associated with 20 SNPs (AKT3: rs12045585, RHEB: rs1920978, RPS6KA5: rs8018757, IRS2: rs9515120, TSC2: rs2073636 and rs8063461, and Raptor: rs11653499, rs9890502, rs8071015, rs7211818, rs9915378, rs9674559, rs7208536, rs7219896, rs4969444, rs2672890, rs7212142, rs9897968, rs2271608, and rs1062935) adjusting by age, gender and smoking status using logistic regression. We grouped the unfavorable SNPs into four categories based on the distribution of the control. Compared to the reference group, the second, third and fourth category showed 1.01 (95%CI: 0.76-1.34), 1.16 (95%CI: 0.89-1.50), and significantly 1.53 (95%CI: 1.14-2.07, P=0.005) fold increased risk of bladder cancer respectively (P for the trend: & lt;0.0001). Classification and regression tree (CART) analysis was performed to explore the high order gene-gene and gene-environment interaction. Further stratification, haplotype and diplotype analysis are still ongoing. This is the first study to address the role of germline genetic variation in this pathway as cancer susceptibility factors. The identification of novel genetic susceptibility markers for bladder cancer etiology will not only help understand the biology of bladder carcinogenesis, but also help identify high risk individuals for bladder cancer. These findings warrant further replication in independent populations. Citation Information: Cancer Prev Res 2008;1(7 Suppl):B40.
    Materialart: Online-Ressource
    ISSN: 1940-6207 , 1940-6215
    URL: Article
    DOI: 10.1158/1940-6207.PREV-08-B40
    Sprache: Englisch
    Verlag: American Association for Cancer Research (AACR)
    Publikationsdatum: 2008
    ZDB Id: 2422346-3
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  • 6
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    Online-Ressource
    Genome-Wide Meta-Analyses of Breast, Ovarian, and Prostate Cancer Association Studies Identify Multiple New Susceptibility Loci Shared by at Least Two Cancer Types
    American Association for Cancer Research (AACR) ; 2016
    In:  Cancer Discovery Vol. 6, No. 9 ( 2016-09-01), p. 1052-1067
    Details
    In: Cancer Discovery, American Association for Cancer Research (AACR), Vol. 6, No. 9 ( 2016-09-01), p. 1052-1067
    Kurzfassung: Breast, ovarian, and prostate cancers are hormone-related and may have a shared genetic basis, but this has not been investigated systematically by genome-wide association (GWA) studies. Meta-analyses combining the largest GWA meta-analysis data sets for these cancers totaling 112,349 cases and 116,421 controls of European ancestry, all together and in pairs, identified at P & lt; 10−8 seven new cross-cancer loci: three associated with susceptibility to all three cancers (rs17041869/2q13/BCL2L11; rs7937840/11q12/INCENP; rs1469713/19p13/GATAD2A), two breast and ovarian cancer risk loci (rs200182588/9q31/SMC2; rs8037137/15q26/RCCD1), and two breast and prostate cancer risk loci (rs5013329/1p34/NSUN4; rs9375701/6q23/L3MBTL3). Index variants in five additional regions previously associated with only one cancer also showed clear association with a second cancer type. Cell-type–specific expression quantitative trait locus and enhancer–gene interaction annotations suggested target genes with potential cross-cancer roles at the new loci. Pathway analysis revealed significant enrichment of death receptor signaling genes near loci with P & lt; 10−5 in the three-cancer meta-analysis. Significance: We demonstrate that combining large-scale GWA meta-analysis findings across cancer types can identify completely new risk loci common to breast, ovarian, and prostate cancers. We show that the identification of such cross-cancer risk loci has the potential to shed new light on the shared biology underlying these hormone-related cancers. Cancer Discov; 6(9); 1052–67. ©2016 AACR. This article is highlighted in the In This Issue feature, p. 932
    Materialart: Online-Ressource
    ISSN: 2159-8274 , 2159-8290
    URL: Article
    DOI: 10.1158/2159-8290.CD-15-1227
    Sprache: Englisch
    Verlag: American Association for Cancer Research (AACR)
    Publikationsdatum: 2016
    ZDB Id: 2607892-2
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  • 7
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    Online-Ressource
    Abstract 5229: Pathogenic germline mutations and risk of multiple myeloma
    American Association for Cancer Research (AACR) ; 2023
    In:  Cancer Research Vol. 83, No. 7_Supplement ( 2023-04-04), p. 5229-5229
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 83, No. 7_Supplement ( 2023-04-04), p. 5229-5229
    Kurzfassung: BACKGROUND: Multiple Myeloma (MM) is an incurable disease with no known germline high penetrant risk gene. The higher risk of MM among affected relatives suggests a genetic contribution to the etiology. To date, 24 common risk variants with low effect sizes were identified using genome-wide association studies, which account for 17% of heritability. However, a systematic analysis of the known rare alleles in cancer predisposition genes has not been undertaken so far in MM. We collaborated with six other academic centers across the United States to identify and select cases for analysis of germline predisposition of MM. METHODS: We performed whole exome, next-generation sequencing of 2,387 familial or early onset germline MM cases from the myeloma sequencing consortium (MMSEQ). We called 1.5 million variants and performed standard quality control of the data. We also obtained exome data on 1,285 cases from UK Biobank (UKBB) and 344,513 non-cancer controls (total=3,672 cases). We analyzed the ultra-rare, coding variants in 90 clinically relevant or putative candidates for cancer predisposition. We then used the automated variant curator PathoMAN to annotate and assert pathogenicity of each variant. We contrasted our results with assertions of pathogenicity from ClinVar and tested for gene association with MM. RESULTS: Overall, we observed several pathogenic or likely pathogenic variants, both singleton and recurrent founder mutations. In the MMSEQ, 8.7% of MM cases harbored a pathogenic variant in these known/putative cancer predisposition genes. Predominant group of pathogenic variants were observed within CHEK2 (19%), TP53 (8%), and ATM (5%). A case-control analysis revealed strong association with TP53 and weakly with ATM. In the familial/early onset MMSEQ cases, TP53 mutations were enriched 68 times more than in the UKBB controls. Our preliminary results suggest that known genes of cancer susceptibility such as TP53 and ATM may also play a role in myeloma risk. CONCLUSION: In a large study of multi-center MM cases, we identified a significant proportion of individuals who are carriers of known (solid) cancer predisposition genes. This study suggests that these known cancer predisposition genes may be relevant in a subset of MM cases. Citation Format: Michael T. Conry, Nicola Camp, Celine Vachon, Michelle Hildebrandt, Elizabeth E. Brown, Steven M. Lipkin, Judy Garber, Susan L. Slager, Samantha Stokes, Aaron D. Norman, Aalin Izhar, Sita Dandiker, Kylee Maclachlan, Kenneth Offit, Saad Usmani, Vijai Joseph. Pathogenic germline mutations and risk of multiple myeloma. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 5229.
    Materialart: Online-Ressource
    ISSN: 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2023-5229
    Sprache: Englisch
    Verlag: American Association for Cancer Research (AACR)
    Publikationsdatum: 2023
    ZDB Id: 2036785-5
    ZDB Id: 1432-1
    ZDB Id: 410466-3
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  • 8
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    Proinflammatory Macrophage Activation by the Polysialic Acid-Siglec-16 Axis Is Linked to Increased Survival of Patients with Glioblastoma
    American Association for Cancer Research (AACR) ; 2023
    In:  Clinical Cancer Research Vol. 29, No. 12 ( 2023-06-13), p. 2266-2279
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 29, No. 12 ( 2023-06-13), p. 2266-2279
    Kurzfassung: Interactions with tumor-associated microglia and macrophages (TAM) are critical for glioblastoma progression. Polysialic acid (polySia) is a tumor-associated glycan, but its frequency of occurrence and its prognostic value in glioblastoma are disputed. Through interactions with the opposing immune receptors Siglec-11 and Siglec-16, polySia is implicated in the regulation of microglia and macrophage activity. However, due to a nonfunctional SIGLEC16P allele, SIGLEC16 penetrance is less than 40%. Here, we explored possible consequences of SIGLEC16 status and tumor cell–associated polySia on glioblastoma outcome. Experimental Design: Formalin-fixed paraffin-embedded specimens of two independent cohorts with 70 and 100 patients with newly diagnosed glioblastoma were retrospectively analyzed for SIGLEC16 and polySia status in relation to overall survival. Inflammatory TAM activation was assessed in tumors, in heterotypic tumor spheroids consisting of polySia-positive glioblastoma cells and Siglec-16–positive or Siglec-16–negative macrophages, and by exposing Siglec-16–positive or Siglec-16–negative macrophages to glioblastoma cell–derived membrane fractions. Results: Overall survival of SIGLEC16 carriers with polySia-positive tumors was increased. Consistent with proinflammatory Siglec-16 signaling, levels of TAM positive for the M2 marker CD163 were reduced, whereas the M1 marker CD74 and TNF expression were increased, and CD8+ T cells enhanced in SIGLEC16/polySia double-positive tumors. Correspondingly, TNF production was elevated in heterotypic spheroid cultures with Siglec-16–expressing macrophages. Furthermore, a higher, mainly M1-like cytokine release and activating immune signaling was observed in SIGLEC16-positive as compared with SIGLEC16-negative macrophages confronted with glioblastoma cell–derived membranes. Conclusions: Collectively, these results strongly suggest that proinflammatory TAM activation causes the better outcome in patients with glioblastoma with a functional polySia-Siglec-16 axis.
    Materialart: Online-Ressource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-22-1488
    RVK:
    XA 36791
    Sprache: Englisch
    Verlag: American Association for Cancer Research (AACR)
    Publikationsdatum: 2023
    ZDB Id: 1225457-5
    ZDB Id: 2036787-9
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  • 9
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    Abstract 990: Patterns of racial disparities in health-related quality of life among colorectal cancer patients and relationship with survival
    American Association for Cancer Research (AACR) ; 2017
    In:  Cancer Research Vol. 77, No. 13_Supplement ( 2017-07-01), p. 990-990
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 77, No. 13_Supplement ( 2017-07-01), p. 990-990
    Kurzfassung: Distinct racial disparities are evident in CRC prognosis with Black patients experiencing worse outcomes than Hispanics and Whites. In a prior study of Health Related Quality of Life (HR-QoL) in a cohort of CRC patients, we observed that racial minority patients experienced lower HR-QoL scores compared to White CRC patients. Therefore, in this study, we focused on the identification of patterns of racial disparities in HR-QoL scores and relationship to differences in prognosis. White (N=450), Hispanic (N=366), and Black (N=316) CRC patients within 1 year of diagnosis at MD Anderson Cancer Center completed the SF-12 quality of life questionnaire to determine Mental Composite Summary (MCS) and Physical Composite Summary (PCS) scores. Participants also completed a questionnaire to collect epidemiology and sociodemographic variables. Vital status and histology information was obtained from the institutional tumor registry. Racial disparities were reported in HR-QoL with both Black and Hispanic patients reporting lower mean PCS and MCS scores compared to White patients, suggesting poorer HR-QoL in these populations. We observed differences in patterns of association between epidemiology and sociodemographic variables and poor HR-QoL by race. Hispanics who never married were at higher risk of poor physical HR-QoL (OR: 2.55(1.15-5.67), P=0.021) compared to married patients, which was not observed for White or Black CRC patients. Similarly, CRC patients with some college education was associated with a decreased risk of poor PCS, but only in Hispanics (OR: 0.26(0.13-0.52), P & lt;0.0001). White females have about two-fold risk of poor PCS (P=2.00 x 10-4) and MCS (P=2.21 x 10-4) scores compared to White males. This relationship was also observed for Black females OR: 2.28(1.35-3.84), but not Hispanic females. Among CRC patients reporting poor PCS ( & lt;50), significant differences in median survival times (MSTs) were observed by race. Hispanic patients had the highest MST at 85.4 months followed by Blacks (47.8 months) and Whites (43.2 months). A similar relationship was observed for poor MCS ( & lt;50) stratified by race with MST times of 81.9 months for Hispanics, 40.8 months for Blacks, and 54.1 months for Whites. In conclusion, we identified patterns of racial disparities in epidemiology and sociodemographic factors that correspond to poor baseline HR-QoL in CRC patients. We also demonstrated that a prognostic correlation exists between baseline HR-QoL and patient overall survival, and that this relationship is influenced by race. The patterns of racial disparity identified in this study can be an important tool for assessing the underlying mediators of HR-QoL in CRC patients and to further identify those who are particularly at risk for poor prognosis. Citation Format: Michelle A. T. Hildebrandt, Alem A. Belachew, Monica E. Reyes, Yuanqing Ye, Xifeng Wu. Patterns of racial disparities in health-related quality of life among colorectal cancer patients and relationship with survival [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 990. doi:10.1158/1538-7445.AM2017-990
    Materialart: Online-Ressource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2017-990
    RVK:
    XA 36000
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: American Association for Cancer Research (AACR)
    Publikationsdatum: 2017
    ZDB Id: 2036785-5
    ZDB Id: 1432-1
    ZDB Id: 410466-3
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  • 10
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    Abstract 3011: Determinants and prognostic value of quality of life in patients with pancreatic ductal adenocarcinoma
    American Association for Cancer Research (AACR) ; 2018
    In:  Cancer Research Vol. 78, No. 13_Supplement ( 2018-07-01), p. 3011-3011
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 78, No. 13_Supplement ( 2018-07-01), p. 3011-3011
    Kurzfassung: Background Quality of life (QOL) is impaired in pancreatic cancer patients. Our aim was to investigate the determinants and prognostic value of QOL after diagnosis in a hospital-based cohort of racially/ethnically diverse patients with pancreatic ductal adenocarcinoma (PDAC). Patients and methods QOL was prospectively assessed using the Short Form-12 version 1 in 2478 PDAC patients. The Physical Component Summary (PCS) and Mental Component Summary (MCS) were categorized into tertiles based on their distribution. Ordered logistic regression was adopted to compare the risk of having lower PCS and MCS by patient sociodemographic and clinical characteristics. The association of PCS and MCS with mortality was assessed by Cox regression. Results Compared with non-Hispanic whites, Hispanics were at significantly higher risk of having lower PCS (odds ratio [95%CI], 1.69 [1.26-2.26] ; P & lt; .001) and lower MCS (1.66 [1.24-2.23]; P & lt; .001). Patients diagnosed with stage III (1.80 [1.10-2.94]; P = .02) and stage IV (2.32 [1.50-3.59] ; P & lt; .001) were more likely to have lower PCS than were patients diagnosed with stage I. Other determinants included sex, age, drinking, smoking, education level, and comorbidities. The low tertile of PCS (hazard ratio [95%CI], 1.94 [1.72-2.18] ; P & lt; .001) and MCS (1.42 [1.26-1.59]; P & lt; .001) were each related to poor prognosis. Similar results were found for non-Hispanic Whites as compared to African Americans/Hispanics/others. Conclusion QOL after diagnosis is a significant prognostic indicator for patients with PDAC, and multiple factors determine QOL, suggesting possible means of intervention to improve QOL and outcomes of PDAC patients. Citation Format: Yang Deng, Huakang Tu, Jeanne A. Pierzynski, Ethan Miller, Maosheng Huang, Xiangjun Gu, David W. Chang, Yuanqing Ye, Michelle A. Hildebrandt, Alison P. Klein, Scott M. Lippman, Xifeng Wu. Determinants and prognostic value of quality of life in patients with pancreatic ductal adenocarcinoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 3011.
    Materialart: Online-Ressource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2018-3011
    RVK:
    XA 36000
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: American Association for Cancer Research (AACR)
    Publikationsdatum: 2018
    ZDB Id: 2036785-5
    ZDB Id: 1432-1
    ZDB Id: 410466-3
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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