GLORIA

GEOMAR Library Ocean Research Information Access

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • American Association for Cancer Research (AACR)  (52)
Material
Publisher
  • American Association for Cancer Research (AACR)  (52)
Language
Years
Subjects(RVK)
  • 1
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Research Vol. 72, No. 8_Supplement ( 2012-04-15), p. 1110-1110
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 72, No. 8_Supplement ( 2012-04-15), p. 1110-1110
    Abstract: In clinical practice, the main dilemma to a successful ovarian cancer therapy is the development of drug resistance. The mounting evidence demonstrated that microRNAs (miRNAs) not only controlled cell proliferation, invasion and metastasis but also therapeutic resistance of ovarian cancer cell. Recently, we isolated CP70sps(CP70 side population spheres) from CP70 ovarian cancer cell line and proved that CP70sps exhibited more resistant to cisplatin than CP70. This phenomenon was correlated to other study which supported that side population of cancer cells was responsible for chemoresistance. In this study, we compared the expression of miRNAs between CP70sps and CP70 to investigate the role of miRNAs in cisplatin resistance of ovarian cancer cells. Our miRNA array and quantitative RT-PCR data showed that CP70sps expressed lower level of miR-29a/b/c family than CP70 cells and CP70sps4wks cells which were repopulation of CP70sps in attached condition. After knockdown of miR-29a/b/c family by miRNA inhibitors, reduction of miR-29a/b/c family enhanced cisplatin resistance of CP70 cells. However, there was no effect on cell cycle and proliferation rate in both CP70 cells and A2780, a parental cisplatin-sensitive cell line of CP70 cells. Downregulation of miR-29a/b/c family contributed cells to escape cisplatin-induced cell death through COL1A1 upregulation. Moreover, reduction of miR-29a/b/c increased phosphorylation of ERK1/2 and GSK3β to transduce survival signaling and reduced active form casepase-9 to avoid cell apoptosis. Furthermore, we found that either ectopic expression of miR-29 alone or combination of miR-29 with cisplatin treatment efficaciously reduced tumorigenicity of CP70 cells in immunodeficiency mice. Finally, we ascertained that the ovarian cancer patients with high expression of miR-29a had better overall survival rate. Taken together, our data demonstrated that the miR-29 family was a sensitizer for cisplatin treatment and might be associated with tumorigenecity of ovarian cancer cells. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1110. doi:1538-7445.AM2012-1110
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 2
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2019
    In:  Clinical Cancer Research Vol. 25, No. 13 ( 2019-07-01), p. 4063-4078
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 25, No. 13 ( 2019-07-01), p. 4063-4078
    Abstract: Neuroblastoma is a pediatric malignancy of the sympathetic nervous system with diverse clinical behaviors. Genomic amplification of MYCN oncogene has been shown to drive neuroblastoma pathogenesis and correlate with aggressive disease, but the survival rates for those high-risk tumors carrying no MYCN amplification remain equally dismal. The paucity of mutations and molecular heterogeneity has hindered the development of targeted therapies for most advanced neuroblastomas. We use an alternative method to identify potential drugs that target nononcogene dependencies in high-risk neuroblastoma. Experimental Design: By using a gene expression–based integrative approach, we identified prognostic signatures and potentially effective single agents and drug combinations for high-risk neuroblastoma. Results: Among these predictions, we validated in vitro efficacies of some investigational and marketed drugs, of which niclosamide, an anthelmintic drug approved by the FDA, was further investigated in vivo. We also quantified the proteomic changes during niclosamide treatment to pinpoint nucleoside diphosphate kinase 3 (NME3) downregulation as a potential mechanism for its antitumor activity. Conclusions: Our results establish a gene expression–based strategy to interrogate cancer biology and inform drug discovery and repositioning for high-risk neuroblastoma.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2019
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 3
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 3761-3761
    Abstract: Background: Many phosphoproteins are among the targeted pathways of cancer signal transduction and are therefore candidates for cancer biomarkers. However, the collection procedures of biospecimens might affect the expression of the phosphoproteins significantly because the time interval between surgical removal of tissues and fixation, i.e. warm ischemia time, are variable. This study aimed to evaluate the stability of phosphoprotein expression under the differential tissue processing time. Materials and Methods: Specimens were obtained from patients who received mastectomy at National Taiwan University Hospital. Each specimen was cut into 5 pieces, stored at 4oC for 10 minutes, 2, 4, 6, and 24 hours before further processing. At each assigned time point, a small section of the specimen was fixed immediately in 10% buffered formalin, then paraffin embedded for immunohistochemical stains (IHC) of phospho-Akt (p-Akt) and phospho-Erk (p-Erk). The remaining specimens were snap frozen in liquid nitrogen, followed by homogenization in RIPA buffer. Western blot analysis was performed for phospho-Akt (p-Akt), total Akt, phospho-Erk (p-Erk), total Erk, phospho-STAT3 (p-STAT3), and total STAT3 staining. Results: Western blot analysis showed that the expression of p-Erk declined significantly as early as 2 hours. The expression of p-Akt was relatively stable and decreased slightly after 24 hours. The expression of p-STAT3 gave variable results. The expression of total Akt, Erk, and STAT3 remain unchanged at each assigned time point. The immunohistochemical expression of p-ERK declined in a time-dependent manner whereas no obvious p-Akt decrease was detected. Conclusions: Our results indicate that the expression of some phosphoproteins by IHC may be affected by warm ischemia time. Caution should be given to the interpretation of the results of these biomarkers. (The study was supported by the grant NSC 98-3112-B-002-038) 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 3761.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
    RVK:
    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
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 4
    In: Cancer Prevention Research, American Association for Cancer Research (AACR), Vol. 6, No. 5 ( 2013-05-01), p. 495-505
    Abstract: Curcumin has been shown to possess potent chemopreventive and antitumor effects on prostate cancer. However, the molecular mechanism involved in curcumin's ability to suppress prostate cancer cell invasion, tumor growth, and metastasis is not yet well understood. In this study, we have shown that curcumin can suppress epidermal growth factor (EGF)- stimulated and heregulin-stimulated PC-3 cell invasion, as well as androgen-induced LNCaP cell invasion. Curcumin treatment significantly resulted in reduced matrix metalloproteinase 9 activity and downregulation of cellular matriptase, a membrane-anchored serine protease with oncogenic roles in tumor formation and invasion. Our data further show that curcumin is able to inhibit the induction effects of androgens and EGF on matriptase activation, as well as to reduce the activated levels of matriptase after its overexpression, thus suggesting that curcumin may interrupt diverse signal pathways to block the protease. Furthermore, the reduction of activated matriptase in cells by curcumin was also partly due to curcumin's effect on promoting the shedding of matriptase into an extracellular environment, but not via altering matriptase gene expression. In addition, curcumin significantly suppressed the invasive ability of prostate cancer cells induced by matriptase overexpression. In xenograft model, curcumin not only inhibits prostate cancer tumor growth and metastasis but also downregulates matriptase activity in vivo. Overall, the data indicate that curcumin exhibits a suppressive effect on prostate cancer cell invasion, tumor growth, and metastasis, at least in part via downregulating matriptase function. Cancer Prev Res; 6(5); 495–505. ©2013 AACR.
    Type of Medium: Online Resource
    ISSN: 1940-6207 , 1940-6215
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2013
    detail.hit.zdb_id: 2422346-3
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 5
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2013
    In:  Cancer Research Vol. 73, No. 8_Supplement ( 2013-04-15), p. 3886-3886
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 73, No. 8_Supplement ( 2013-04-15), p. 3886-3886
    Abstract: Background: Brain metastasis is a formidable challenge in lung cancer treatment. The incidence has been increasing recently because of the advances of treatment which leads to prolonged survival of many patients. Methods: We established xenograft model of brain metastasis. Repeated rounds of in vivo selection and ex vivo primary cultures of the brain metastases resulted in a cell line with a high propensity to metastasize to the brain. Brain-tropism was confirmed by bioluminescence study. Gene expression profiles between parental lung cancer cells (PC9) and brain-tropic cells (PC9-Br) was compared by Agilent Gene Expression Microarray followed by Ingenuity Pathway Analysis. The biologic effects and clinical implications of the candidate molecules were further investigated. Results: Significant activation of IGF and WNT signaling pathways was detected in PC9-Br, as compared with the parental cells. We selected IGF pathway as the first step to explore the potential therapeutic implication. Western blot and RT-PCR validated the results of IGF2 overexpression and activated IGF1R (pIGF1R) in PC9-Br cells. In vitro drug sensitivity tests showed that PC9-Br, in comparison to parental cells, was more resistant to erlotinib, an EGFR TKI (IC50: 30nM for PC9 and 189nM for PC9-Br). Knocking down IGF2 expression in PC9-Br reversed the drug resistance, while adding IGF2 to PC9 enhanced the resistance. In clinical samples, there was a significantly higher expression of pIGF1R in 26 brain metastases as compared to their paired primary lung tumors (mean of H score differences=40.96, 95% C.I.=10.96∼70.96, P=0.0094). Conclusions: IGF signaling pathway is activated in brain-tropic lung cancer cells and could potentially be a therapeutic target for brain metastasis. Acknowledgement: This study was supported by Research Grant 101-M2002 from the National Taiwan University Hospital. Citation Format: Pei-Fang Wu, Ching-Hung Lin, Wen-Chang Huang, Wen-Chi Feng, Yen-Shen Lu, Chih-Hsin Yang, Ann-Lii Cheng. Activated insulin-like growth factor (IGF) signaling pathway is a potential therapeutic target for brain metastasis from lung 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 3886. doi:10.1158/1538-7445.AM2013-3886
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2013
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 6
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 21, No. 1 ( 2015-01-01), p. 193-200
    Abstract: Purpose: We aimed to identify serum metabolites as potential valuable biomarkers for lung cancer and to improve risk stratification in smokers. Experimental Design: We performed global metabolomic profiling followed by targeted validation of individual metabolites in a case–control design of 386 lung cancer cases and 193 matched controls. We then validated bilirubin, which consistently showed significant differential levels in cases and controls, as a risk marker for lung cancer incidence and mortality in a large prospective cohort composed of 425,660 participants. Results: Through global metabolomic profiling and following targeted validation, bilirubin levels consistently showed a statistically significant difference among healthy controls and lung cancer cases. In the prospective cohort, the inverse association was only seen in male smokers, regardless of smoking pack-years and intensity. Compared with male smokers in the highest bilirubin group ( & gt;1 mg/dL), those in the lowest bilirubin group ( & lt;0.75 mg/dL) had 55% and 66% increase in risks of lung cancer incidence and mortality, respectively. For every 0.1 mg/dL decrease of bilirubin, the risks for lung cancer incidence and mortality increased by 5% and 6% in male smokers, respectively (both P & lt; 0.001). There was a significant interaction between low serum bilirubin level and smoking on lung cancer risk (Pinteraction = 0.001). Conclusion: Low levels of serum bilirubin are associated with higher risks of lung cancer incidence and mortality in male smokers and can be used to identify higher risk smokers for lung cancer. Clin Cancer Res; 21(1); 193–200. ©2014 AACR.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2015
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 7
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 29, No. 6_Supplement_1 ( 2020-06-01), p. A114-A114
    Abstract: Background: Prostate cancer (PCa) is a clinically and molecularly heterogeneous disease, with differences in incidence and mortality among and between racial groups, which grade and stage only partially predict. Prostate cancer patient-derived xenografts (PCPDXs) are essential for studying PCa biology and testing new therapeutics in models that we expect to be reflective of the clinical setting. To date, PCPDXs have been difficult to establish due to lack of solid tumor content and poor uptake rates in mice. In the present study, we established and characterized the first PCPDX from a highly aggressive and metastatic tumor sample from a patient of African ancestry. Methods: We collected the PCa sample from the patient at the time of surgery after initiating stage-specific standard-of-care treatment. Tissue was minced and implanted into the kidney capsule of 8- to 10-week-old SCID mice. Once the explant was established, tissue was collected and formalin-fixed, paraffin-embedded for histologic evaluation. An initial section was stained using hematoxylin and eosin and another section was stained by PIN4 (p63, CKBE12, racemase) for immunohistochemical (IHC) analysis to confirm diagnosis of PCa. To obtain genetically estimated indicators of race, we performed ancestral genotyping. We evaluated response to chemical castration with 10mg/kg enzalutamide administered 5 days per week by oral gavage. Tumor growth was measured with calipers every day. Results: We established a PCPDX from a core prostate sample taken from a patient diagnosed with adenocarcinoma of the prostate (Gleason 10), metastatic to lymph nodes and penis undergoing a pelvic exenteration. Ancestral genotyping estimated 90% African ancestry. IHC staining showed this model to be highly tumorigenic and PSA negative. Passaged tumors took in 15 out of 15 SCID mice and reached 10mm3 within 3 weeks. This model does not show a significant decrease in growth in response to treatment with the androgen receptor inhibitor, enzalutamide. Further characterization using IHC, RNA and whole-exome sequencing, castration, drug treatment, and assays for metastatic potential are currently under way. Conclusions: Establishing this PCPDX provides a unique model of metastatic, androgen-independent PCa in a patient of African ancestry. Prior to this study, there had yet to be a PCPDX model derived from a patient of African ancestry. We established this PCPDX from a Gleason 10 PCa, supporting previous data of success in grafting this type of aggressive PCa into a mouse. It has a very high take rate and growth rate relative to other PCa models. Such a model will enable interrogation of PCa from a patient of African ancestry. Once a larger panel of PCPDXs from racially diverse patients is established, we will be able to achieve a more complete characterization of this disease and use such models to develop new biomarkers and therapeutic agents. Ultimately, these tools will improve outcomes for all men with aggressive PCa and reduce PCa disparities for patients of African ancestry. Citation Format: Brendon M. Patierno, Wayne Glover, Wen-Chi Foo, Jason A. Somarelli, Kathryn E. Ware, Lingfan Xu, Yanjing Li, Xufeng Chen, Daniel J. George, Rick A. Kittles, Andrew J. Armstrong, Shannon J. McCall, Jiaoti Huang, Jennifer A. Freedman, Steven R. Patierno, David S. Hsu. Characterization of a metastatic prostate cancer xenograft derived from a patient of African ancestry [abstract]. In: Proceedings of the Eleventh AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2018 Nov 2-5; New Orleans, LA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2020;29(6 Suppl):Abstract nr A114.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
    detail.hit.zdb_id: 2036781-8
    detail.hit.zdb_id: 1153420-5
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 8
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 74, No. 19_Supplement ( 2014-10-01), p. LB-298-LB-298
    Abstract: Background: Previous lung cancer models were mostly based on case control studies and used limited epidemiological risk factors. The clinical utility was hampered due to lack of added value beyond smoking history. In this study, we developed a series of lung cancer risk prediction models using extensive data, including lab testing data, from a large prospective cohort in Taiwan. In particular, we developed a risk prediction model within heavy smokers with ≧30 pack years that could further stratify this group and improve the screening efficiency of Low Dose Computed Tomography (LDCT). Methods: The cohort participants were divided into equal training and validation sets, by using variables from personal history and standard lab tests. Cox proportional hazards regression and goodness of fit were used to generate area under the curve (AUC). Results: A total of 1,774 incident lung cancer cases were identified among 505,030 participants recruited in a 14-year period during 1994-2007. We developed a “History only” model that included smoking status, body mass index (BMI), family history, and personal history; a “lab only” model that included blood in sputum, lung function test and serum biomarkers like carcinoembryonic antigen (CEA), bilirubin, and alpha fetoprotein (AFP); and an integrative model with all these variables. The AUC for “history only” model was 0.837, “lab only” model, 0.839, and integrative model, 0.862. We also developed integrative models for ever-smokers and never-smokers with AUCs of 0.872 and 0.801, respectively. Furthermore, since LDCT is recommended for heavy smokers with ≥ 30 smoking pack-years but with a high false positive rate, we developed a risk model in this group to further stratify this group. A total of 454 incident lung cancer cases were identified among 23,582 heavy smokers. Six variables are significantly associated with lung cancer risk: age, smoking status (current or former), smoking intensity (number of packs smoked in a day), BMI, lung function test and CEA. Current smokers, who smoked & gt;1 pack per day, with BMI & lt;25, lowest lung function and highest CEA, had the highest risk. The number of smokers needed to screen to identify one lung cancer (NNS) could decrease to 13 in this high-risk heavy smokers group from 52 in heavy smokers as a whole, a four-fold increase in risk identification. Highest risks were found among smokers with CEA ≧3.8 ug/L (NNS between 13 and 37) and smokers with lung function MMF & lt;43 ml/sec (NNS between 13 and 25). Conclusion: Routinely collected lab data can significantly improve lung cancer risk prediction models. An integrative lung cancer risk prediction model among heavy smokers with ≧30 pack years can stratify subjects with a 3-4 fold difference in lung cancer risk for LDCT screening. The model found decreased lung function and high CEA values, along with detailed smoking history and low BMI, offered a unique predictive ability to improve the efficiency of LDCT screening. Citation Format: Xifeng Wu, Chi Pang Wen, Yuanqing Ye, MinKwang Tsai, Xia Pu, Wong-Ho Chow, Chad Huff, Sonia Cunningham, Maosheng Huang, Shiuan Bei Wu, Chwen Keng Tsao, Jian Gu. The use of lung cancer risk prediction model to stratify heavy smokers: The power of routinely collected lab data. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr LB-298. doi:10.1158/1538-7445.AM2014-LB-298
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2014
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 9
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2018
    In:  Cancer Epidemiology, Biomarkers & Prevention Vol. 27, No. 7_Supplement ( 2018-07-01), p. A79-A79
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 27, No. 7_Supplement ( 2018-07-01), p. A79-A79
    Abstract: Background: Prostate cancer (PCa) is a clinically and molecularly heterogeneous disease, with differences in incidence and mortality among and between racial groups, which are only partially predicted by grade and stage. Age-adjusted incidence and mortality rates for PCa among African American (AA) men are 1.6- and 2.4-fold greater, respectively, than among white men. Preclinical models of AA PCa, including cell lines and xenografts, are severely lacking. This work addresses the urgent need to generate such models for study of the biology of AA PCa and for testing of novel therapeutic agents in models that are expected to be reflective of the clinical setting. Methods: To generate AA PCa patient-derived primary cell lines, we have used the fibroblast feeder cell system established at Georgetown University. In this method, human tumor cells are cocultivated with irradiated mouse fibroblasts in medium with addition of ROCK inhibitor. For generation of AA PCa patient-derived xenografts, we have collected sections of human prostate tumors, minced, suspended, and implanted in the renal capsule of immunodeficient mice. Tumor specimens have been collected and formalin-fixed, paraffin-embedded for histologic evaluation. Sections of such blocks have been stained using hematoxylin and eosin. DNA from the tumor specimens has been used to perform ancestral genotyping. Results: We have established eight AA PCa patient-derived primary cell lines and two AA PCa patient-derived xenografts. The AA PCa patient-derived primary cell lines have grown throughout the feeder layer and directly onto the plastic of the flasks. Currently, these lines are growing without addition of fibroblast feeder cells. The two AA PCa patient-derived xenografts have been passaged beyond three generations and key histologic features have been found to be consistent between the patient tumor and the patient-derived explant. In addition, African ancestry of the patient has been confirmed by ancestral genotyping. Further studies to more fully characterize the AA PCa patient-derived primary cell lines and xenografts at the pathologic, biologic, and molecular levels are currently under way. Procurement of individual AA PCa patient tissues continues for establishment of additional AA PCa patient-derived primary cell lines and xenografts. Conclusions: Strategies designed to maximize PCa specimen availability and tumor content enable the establishment of AA PCa patient-derived primary cell lines and xenografts. Such preclinical models of AA PCa will enable a more rigorous interrogation of the molecular mechanisms underlying AA PCa and aid in the development of new biomarkers and therapeutic agents for AA PCa. Citation Format: Brendon Patierno, Wayne Glover, Thomas Ribar, Rick Kittles, Wen-Chi Foo, Shannon McCall, Jiaoti Huang, Daniel George, Jennifer Freedman, Steven Patierno, Kris Wood, David Hsu. Establishment of African American prostate cancer patient-derived primary cell lines and xenografts [abstract]. In: Proceedings of the Tenth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2017 Sep 25-28; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2018;27(7 Suppl):Abstract nr A79.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2018
    detail.hit.zdb_id: 2036781-8
    detail.hit.zdb_id: 1153420-5
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 10
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Research Vol. 72, No. 8_Supplement ( 2012-04-15), p. 5509-5509
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 72, No. 8_Supplement ( 2012-04-15), p. 5509-5509
    Abstract: Models predicting liver cancer are only available for the high risk population with hepatitis carriers but not for the general population. we developed risk prediction models for liver cancer using data collected from a large health screening program in Taiwan with long term follow up. The cohort included 444,023 subjects at baseline. During a median follow up time of 7.4 years, 1,668 subjects developed liver cancer. Epidemiologic data, medical history and routine blood panel including serum transaminases data were collected with optional additional testing for HBV or HCV status. Liver cancer cases were ascertained by computerized record linkage with both the National Cancer Registry and the National Death Certification profiles in Taiwan. Stepwise Cox regression analysis was performed to identify significant predictors in the multivariate models. Individualized risk of developing liver cancer in 10 years was calculated from baseline probability and relative risk profile estimated from the Cox regression model. Models were developed separately to provide risk prediction for subjects who chose to have HCV tested (130,533 subjects at baseline and 416 liver cancer cases) and who chose otherwise (313,490 subjects and 1,252 liver cancer cases). Since the results for both sub-cohorts are comparable and we only reported results for the sub-cohort with HCV tested. In the sub-cohort with HCV tested, the model with only questionnaire data identified significant main effects for male gender, older age, prior history of diabetes, pack year of smoking, alcohol use, and physical inactivity. This epidemiologic model had an AUC of 0.798 (95% CI=0.772-0.815) for 10-year risk prediction. With only data from measures of Transaminases, the model achieved an AUC of 0.927 (95% CI=0.911-0.938), a significant increase as compared to the model with only epidemiologic variables. The addition of HBV improved the AUC to 0.936 (95% CI=0.913-0.958). Similar results were obtained for sub-cohort without HCV testing. The addition of HCV status in combination with HBV status, the AUC improve to 0.941 (95% CI=0.918-0.967). Among models using key history and blood panels, the use of serum Transaminases only, available in routine health check-ups, was able to provide most information needed in predicting liver cancer in the general public. Additional testing of HBV and /or HCV further increased the prediction power. This simple transaminase-based model for the general public can be valuable in clinical practice for identifying high risk individuals. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 5509. doi:1538-7445.AM2012-5509
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...