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  • American Association for Cancer Research (AACR)  (52)
  • Wu, Xifeng  (52)
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  • American Association for Cancer Research (AACR)  (52)
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  • 1
    Online Resource
    Online Resource
    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
    Abstract: 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.
    Type of Medium: Online Resource
    ISSN: 1940-6207 , 1940-6215
    URL: Article
    DOI: 10.1158/1940-6207.PREV-09-B94
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
    detail.hit.zdb_id: 2422346-3
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  • 2
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    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
    Abstract: 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.
    Type of Medium: Online Resource
    ISSN: 1940-6207 , 1940-6215
    URL: Article
    DOI: 10.1158/1940-6207.PREV-08-A105
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2008
    detail.hit.zdb_id: 2422346-3
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  • 3
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    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
    Abstract: 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.
    Type of Medium: Online Resource
    ISSN: 1940-6207 , 1940-6215
    URL: Article
    DOI: 10.1158/1940-6207.PREV-12-A93
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
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  • 4
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    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
    Abstract: 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.
    Type of Medium: Online Resource
    ISSN: 1940-6207 , 1940-6215
    URL: Article
    DOI: 10.1158/1940-6207.CAPR-10-0035
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
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  • 5
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    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
    Abstract: 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.
    Type of Medium: Online Resource
    ISSN: 1940-6207 , 1940-6215
    URL: Article
    DOI: 10.1158/1940-6207.PREV-08-B40
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2008
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  • 6
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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
    Abstract: 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
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2017-990
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2017
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 7
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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
    Abstract: 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.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2018-3011
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2018
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
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  • 8
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    Abstract 4843: Genetic variants in Notch signaling pathway and ovarian cancer.
    American Association for Cancer Research (AACR) ; 2013
    In:  Cancer Research Vol. 73, No. 8_Supplement ( 2013-04-15), p. 4843-4843
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 73, No. 8_Supplement ( 2013-04-15), p. 4843-4843
    Abstract: The Notch signaling pathway drives proliferation, differentiation, apoptosis, cell fate choices, and has a key role in the regulation of stem cells in a variety of cancers. In this study, we applied a pathway-based approach to evaluate the associations between single nucleotide polymorphisms in Notch signaling pathway and ovarian cancer risk, survival, and response to chemotherapy. Towards this, we systematically genotyped 139 SNPs from 10 genes in the pathway in 339 Caucasian ovarian cancer cases and 349 Caucasian healthy controls. Individually, four SNPs were significantly associated with the ovarian cancer risk. The most significant SNP was NOTCH4: rs397081, with an adjusted odds ratio (OR) of 0.38 (95% CI = 0.22-0.66, P=0.00057). A highly significant gene-dosage effect was observed for these top variants (P for trend & lt; 0.00001) with those carrying ≥ 3 risk genotypes having a nearly 6-fold increase in risk (OR = 5.67, 95% CI = 2.58 - 12.44] . Classification and regression tree (CART) analysis further revealed potential higher order gene-gene interactions between these four SNPs, with the highest risk group having almost 7-fold increased risk. Ten SNPs were significantly associated with overall survival, of which the strongest association was identified for NOTCH4: rs3131290 (OR = 0.48, 95% CI = 0.27-0.84). Cumulative effect analysis showed that multiple adverse genotypes had a significant dose-dependent effect on overall survival. The median survival times for individuals carrying ≤3, 4 to 6, and ≥7 of these adverse genotypes were & gt;186.3, 62.82, and 28.58 months, respectively. Similarly, a significant association was identified between a poor response to platinum-based chemotherapy and the number of unfavorable SNPs (P for trend & lt; 0.0001). Our findings suggest that genetic variants in the Notch signaling pathway are associated with ovarian cancer risk and could serve as potential predictors of clinical outcomes in ovarian cancer patients. Citation Format: Enping Xu, Karen H. Lu, Michelle AT Hildebrandt, Maosheng Huang, Xifeng Wu, Dong Liang. Genetic variants in Notch signaling pathway and ovarian cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 4843. doi:10.1158/1538-7445.AM2013-4843
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2013-4843
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2013
    detail.hit.zdb_id: 2036785-5
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  • 9
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    Genetic Variants in the PI3K/PTEN/AKT/mTOR Pathway Predict Head and Neck Cancer Patient Second Primary Tumor/Recurrence Risk and Response to Retinoid Chemoprevention
    American Association for Cancer Research (AACR) ; 2012
    In:  Clinical Cancer Research Vol. 18, No. 13 ( 2012-07-01), p. 3705-3713
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 18, No. 13 ( 2012-07-01), p. 3705-3713
    Abstract: Purpose: The development of second primary tumors (SPT) or recurrence alters prognosis for curatively treated head and neck squamous cell carcinoma (HNSCC) patients. The 13-cis-Retinoic acid (13-cRA) has been tested as a chemoprevention agent in clinical trials with mixed results. Therefore, we investigated whether genetic variants in the PI3K/PTEN/AKT/mTOR pathway could serve as biomarkers to identify which patients are at high risk of an SPT/recurrence, while also predicting response to 13-cRA chemoprevention. Experimental Design: A total of 137 pathway single-nucleotide polymorphisms were genotyped in 440 patients from the Retinoid Head and Neck Second Primary Trial and assessed for SPT/recurrence risk and response to 13-cRA. Risk models were created based on epidemiology, clinical, and genetic data. Results: Twenty-two genetic loci were associated with increased SPT/recurrence risk, with six also being associated with a significant benefit following chemoprevention. Combined analysis of these high-risk/high-benefit loci identified a significant (P = 1.54 × 10−4) dose–response relationship for SPT/recurrence risk, with patients carrying four to five high-risk genotypes having a 3.76-fold [95% Confidence Interval (CI), 1.87–7.57] increase in risk in the placebo group (n = 215). Patients carrying four to five high-risk loci showed the most benefit from 13-cRA chemoprevention, with a 73% reduction in SPT/recurrence (95% CI, 0.13–0.58) compared with those with the same number of high-risk genotypes who were randomized to receive placebo. Incorporation of these loci into a risk model significantly improved the discriminatory ability over models with epidemiology, clinical, and previously identified genetic variables. Conclusions: These results show that loci within this important pathway could identify individuals with a high-risk/high-benefit profile and are a step toward personalized chemoprevention for HNSCC patients. Clin Cancer Res; 18(13); 3705–13. ©2012 AACR.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-11-3271
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
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  • 10
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    Abstract 3007: Hsa-miR-9 expression patterns are associated with metastatic recurrence in patients with clear cell renal cell carcinoma through hypermethylation of the gene in tumor tissue
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 8_Supplement ( 2010-04-15), p. 3007-3007
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 3007-3007
    Abstract: The long-term prognosis for patients with clear cell renal cell carcinoma (ccRCC) is dramatically altered by the development of metastatic recurrence. However, there are very few indicators that can predict which patient will develop a recurrence. MicroRNA gene expression has been shown to be associated with RCC development, and here we show that it can also help to identify patients at increased recurrence risk. We utilized genome-wide microRNA arrays to measure expression levels in tumors from 74 ccRCC patients and identified hsa-miR-9 as a candidate for recurrence risk (Hazard Ratio: 2.6, 95% Confidence Interval: 1.55-4.38) resulting in a reduction in median time to recurrence by 30 months (P-value = 0.0038). This observation was validated in a replication sample of an additional 254 ccRCC tumors. We further showed that the genes encoding for hsa-miR-9 were significantly hypermethylated in tumors compared to adjacent normal tissues (P-value & lt; 0.001 for both miR-9-1 and miR-9-3) resulting in decreased expression, and that the methylation of these genes was more significant in tumor DNA obtained from patients who developed a recurrence (P-value = 0.012 and 0.009 for miR-9-1 and miR-9-3, respectively). Furthermore, methylation of miR-9-1 and miR-9-3 were independently associated with a reduction in time to recurrence. Hsa-miR-9 has been shown to play a role in tumor development for other cancers, and our results demonstrate that it has similar functions in ccRCC while also playing a role in the development of metastatic recurrence. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3007.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM10-3007
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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