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  • 1
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    The effect of anti-IGF1 therapy on muscle mass in metastatic pancreatic cancer.
    American Society of Clinical Oncology (ASCO) ; 2013
    In:  Journal of Clinical Oncology Vol. 31, No. 15_suppl ( 2013-05-20), p. 4064-4064
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 31, No. 15_suppl ( 2013-05-20), p. 4064-4064
    Abstract: 4064 Background: IGF-1 plays a role in the growth of multiple tumor types, including pancreatic cancer. IGF-1 also serves as a growth factor for muscle. The impact of therapeutic targeting of IGF-1 on muscle mass is unknown. Methods: We evaluated muscle mass at L3 in patients enrolled in a randomized phase II study of MK-0646 (M), a monoclonal antibody directed against the IGF-1 protein, in patients with metastatic pancreatic cancer (MPC). We used the Slice-o-matic (ver 4.3) software to segregate CT images into muscle and fat components and measured muscle area (cm2) at baseline and after 2 and 4 months of treatment. Patients received either gemcitabine with erlotinib (G+E), G+E+M, or G+M. Differences between the groups were compared using t-tests. Results: 58 patients had both baseline and 2 month imaging available for analysis. Of these, 44 received M and 14 had G+E only. Baseline muscle mass between the two groups was similar: 146 cm2 and 142 cm2, respectively (P=0.47). After two months of treatment, both groups demonstrated decrease in muscle mass: 134 cm2 (8% loss) vs. 130 cm2 (6% loss) (P= 0.19). Of the 37 patients who had either PR or SD at 2 months, there was a non-significant increase in muscle mass loss among the patients receiving M (7.8% vs. 4.5%, p=.31). At 4 months, those remaining patients in the M group lost 6% (n=14) of muscle mass compared to 3% in the non-M group (n=5) (P=0.54). Each 1% loss of muscle mass increased the odds of dropout by 13% (p=.03, CI 1.0-27%) and predicted for poor survival (p=HR 1.08, p=.02). Conclusions: MPC patients can be expected to lose muscle mass even while having clinical benefit (PR or SD) from chemotherapy. Muscle loss correlated with a risk of study drop-out and death. There was a non-significant trend towards greater muscle mass loss in patients on anti-IGF-1R therapy. However, it is unclear if this loss translates into functional differences between patients. Clinical trial information: NCT00769483.
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/jco.2013.31.15_suppl.4064
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2013
    detail.hit.zdb_id: 2005181-5
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  • 2
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    The association between statin use and hepatocellular cancer outcome.
    American Society of Clinical Oncology (ASCO) ; 2013
    In:  Journal of Clinical Oncology Vol. 31, No. 4_suppl ( 2013-02-01), p. 165-165
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 31, No. 4_suppl ( 2013-02-01), p. 165-165
    Abstract: 165 Background: Preclinical evidence supports anti-tumoral activity of statins. Several observational studies have shown inverse association between statin use and hepatocellular cancer (HCC) incidence. However, little is known as to whether statins can delay the progression of HCC. Therefore, we investigated the association between statin use and the outcome of patients with HCC. Methods: 644 patients diagnosed with pathologically confirmed HCC were followed up from 2000 till 2011. Survival analysis was done using Cox regression model. Results: The mean age of the HCC cohort was 63.1 years (SD, ±11.5). 73.4% were men and 65.5% were Caucasians. 70.7% were diagnosed at TNM stage III and IV. 52.6% had no evidence of hepatitis B or C virus infection. 81.7% had local and systemic therapy, while 18.3% underwent surgical resection. The median survival of HCC patients was 19.2 months. 10.7% of patients reported statin use. We observed significant difference in overall survival between statin non-users and users; the median overall survival (95% CI) were 18.5 (16.4-20.5) months and 25.4 (19.8-31.1) months, respectively (log rank test p = 0.04). 30% mortality reduction was observed in statin users versus non-users (HR = 0.7, 95% CI, 0.5-0.9). This significant association was also observed in patients who received systemic and local therapy (p = 0.04). HCC patient without liver cirrhosis showed 40% mortality reduction (HR = 0.6, 95% CI, 0.4-0.9, P = 0.04) while patient with liver cirrhosis did not. History of hepatitis did not affect the association. Even after controlling for various clinical variables including age, sex, race, staging, HCV, HBV, liver cirrhosis, treatment, alcohol use and diabetes, statin use was still associated with favorable overall survival in HCC patients (HR = 0.7, 95% CI, 0.5-0.9, P=0.03). Conclusions: This is the largest study to date to evaluate the effect of statins on the outcomes of HCC patients. We found that statin use may reduce the risk of death in patients with HCC. Validation of our finding is warranted in a large prospective study.
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/jco.2013.31.4_suppl.165
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2013
    detail.hit.zdb_id: 2005181-5
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  • 3
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    Development and validation of a scoring system using insulin-like growth factor to assess hepatic reserve in hepatocellular carcinoma.
    American Society of Clinical Oncology (ASCO) ; 2014
    In:  Journal of Clinical Oncology Vol. 32, No. 3_suppl ( 2014-01-20), p. 231-231
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 32, No. 3_suppl ( 2014-01-20), p. 231-231
    Abstract: 231 Background: The Child-Turcotte-Pugh (CTP) score fails to accurately predict survival in hepatocellular carcinoma (HCC), yet remains the standard tool for assessing the liver reserve and guiding therapeutic decisions. CTP relies partially on subjective clinical grading of encephalopathy and ascites. Since liver production of insulin-like growth factor-1 (IGF-1) is significantly reduced in chronic liver diseases and HCC, we hypothesized that IGF-1 could be a valid surrogate for hepatic reserve to replace the subjective parameters in CTP score. Methods: We tested plasma IGF-1 in the training set (n=310). Recursive partitioning identified three optimal IGF-1 ranges that correlated with survival: 〉 50 ng/mL = 1 point; 26-50 ng/mL = 2 points; and 〈 26 ng/mL = 3 points. We modified the CTP score by replacing ascites and encephalopathy with plasma IGF-1, subjected both scores to log-rank analysis, and quantified the prognostic values with C-statistics to compare the scores’ performance. We prospectively validated the score in 150 patients from MDACC; in addition to 180 patients from Korea. Results: The IGF score significantly predicted OS of all classes (p 〈 0·001). In the training cohort, C-indices for CTP and IGF scores were 0·57 and 0·61, respectively (p=0·003 per the U-statistic). Similarly, C-indices in MDACC validation cohort were 0·56 and 0·63 (p=0·02 per the U-statistic), and in Korean cohort were 0·58 and 0·60 (p=0·03 per the U-statistic). Conclusions: The new IGF score is simple and blood-based, and validated well on multiple independent HCC cohorts. It could identify a subpopulation of patients who may benefit from active therapy because of their preserved hepatic reserve, as distinct from patients for whom therapy can be deferred or avoided.
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/jco.2014.32.3_suppl.231
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2014
    detail.hit.zdb_id: 2005181-5
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  • 4
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    Pancreatic injury, genetic variation of PNPLA3 , and risk of pancreatic cancer.
    American Society of Clinical Oncology (ASCO) ; 2013
    In:  Journal of Clinical Oncology Vol. 31, No. 4_suppl ( 2013-02-01), p. 141-141
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 31, No. 4_suppl ( 2013-02-01), p. 141-141
    Abstract: 141 Background: Similar to primary liver cancer, obesity, diabetes mellitus and hepatitis B virus infection have been associated with increased risk of pancreatic cancer (PC) development. A genome-wide association study has reported that a polymorphic variant of the patatin-like phospholipase domain containing 3 (PNPLA3) gene was associated with a higher susceptibility to fatty liver and liver cancer. The relationship between this variation and PC has not been previously examined. We investigated the correlation in the degree of organ damage between the liver and the pancreas in patients with PC. In addition, we examined the effect of PNPLA3genetic variation (rs738409: C 〉 G) on PC development. Methods: Using resources of our case-control study in MD Anderson Cancer Center, we analyzed 544 pathologically confirmed PC patients and 498 healthy controls. Cases and controls were frequency matched by age, gender, and race. Multivariate logistic regression analysis was performed to adjust for the confounding factors. Medical records of PC patients were reviewed for pancreatic and liver fatty changes. Results: We found that 18.8% of PC patients had evidence of pancreatic steatosis, fibrosis, or pancreatitis. Fatty liver was observed in 14.5% of PC patients which was frequently detected in patients with pancreatitis (p=0.002). A significant correlation between pancreatitis and cirrhosis was observed in PC patients with a prior history of obesity but not in patients without a history of obesity (p=0.001). On the other hand, we observed no significant association between PNPLA3 genotype and risk of PC. The adjusted odds ratio (OR) was 1.4 (95% confidence interval [CI], 0.7-2.7) for the homozygous variant GG genotype compared with the CC/CG genotypes. Conclusions: We concluded that despite the similarities between the liver and the pancreas, genetic susceptibility to fatty infiltration and its effect on cancer development may differ between the two organs. Evaluation and assessment of nonalcoholic fatty pancreatic disease (NAFPD) in PC patients and genetic susceptibility of NAFPD may be warranted in future research.
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/jco.2013.31.4_suppl.141
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2013
    detail.hit.zdb_id: 2005181-5
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  • 5
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    Staging of advanced hepatocellular carcinoma patients in the targeted therapy era.
    American Society of Clinical Oncology (ASCO) ; 2012
    In:  Journal of Clinical Oncology Vol. 30, No. 4_suppl ( 2012-02-01), p. 209-209
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 30, No. 4_suppl ( 2012-02-01), p. 209-209
    Abstract: 209 Background: Several hepatocellular carcinoma (HCC) staging systems are currently available. However, they were all developed before the targeted therapy era prevailed in the last decade which has changed the natural history of the disease. Our study goal was to test the performance of different HCC staging systems in patients with HCC who were treated at our institution during the last decade. Methods: We prospectively enrolled 438 patients from early 2000 to late 2009. Baseline clinicopathologic parameters and staging were available, including the TNM, Cancer of the Liver Italian Program (CLIP), Barcelona Clinic Liver Cancer (BCLC), Okuda, and Chinese University Prognostic Index (CUPI). We performed survival and cox-regression analyses, and compared the staging systems’ predictive ability using Harrell's C-index. Finally, we performed a subgroup analysis of 3 independent cohorts based on whether or not they received sorafenib, whether or not they had hepatitis, and whether or not they had cirrhosis. Results: The overall survival was 13.9 months. Overall, CLIP score was the most predictive staging system with a C-index of 0.71. 187 patients were treated with targeted therapies and 138 were treated with sorafenib after it was approved in 2007. CLIP score was the most predictive staging system with a C-index of 0.71 in the no sorafenib group, and 0.74 in the sorafenib group. In hepatitis patients, CLIP topped amongst all staging systems with a C-index of 0.75, and in patients without hepatitis, despite all staging systems having a poor predictive ability, CLIP score still had the highest C-index of 0.67. Similarly, CLIP score had the best predictive ability in patients with and without pre-existing liver cirrhosis, with C-indices of 0.73 and 0.68 respectively. There was no statistically significant interaction between CLIP score and hepatitis status, and CLIP score and liver cirrhosis. Thus, overall the CLIP score was the best predictive system in all cohorts. Conclusions: Our results suggest that the CLIP score has the highest stratification ability in our advanced HCC patient population, including several subgroups. Our study confirms the utility of the CLIP score to stratify advanced HCC patients in clinical trials.
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/jco.2012.30.4_suppl.209
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2012
    detail.hit.zdb_id: 2005181-5
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  • 6
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    Association of diabetes and perineural invasion in pancreatic cancer
    Wiley ; 2012
    In:  Cancer Medicine Vol. 1, No. 3 ( 2012-12), p. 357-362
    Details
    In: Cancer Medicine, Wiley, Vol. 1, No. 3 ( 2012-12), p. 357-362
    Type of Medium: Online Resource
    ISSN: 2045-7634 , 2045-7634
    URL: Issue
    URL: Article
    DOI: 10.1002/cam4.2012.1.issue-3
    DOI: 10.1002/cam4.43
    Language: English
    Publisher: Wiley
    Publication Date: 2012
    detail.hit.zdb_id: 2659751-2
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  • 7
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    Metformin Use Is Associated with Better Survival of Diabetic Patients with Pancreatic Cancer
    American Association for Cancer Research (AACR) ; 2012
    In:  Clinical Cancer Research Vol. 18, No. 10 ( 2012-05-15), p. 2905-2912
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 18, No. 10 ( 2012-05-15), p. 2905-2912
    Abstract: Purpose: Accumulating evidence suggests that metformin has antitumor activity. The aim of this study was to determine whether metformin use has a survival benefit in patients with pancreatic cancer. Experimental Design: We conducted a retrospective study of patients with diabetes and pancreatic cancer treated at The University of Texas MD Anderson Cancer Center (Houston, TX). Information on diabetes history, including treatment modalities and clinical outcome of pancreatic cancer, was collected using personal interviews and medical record review. Survival analysis was carried out using a Kaplan–Meier plot, log-rank test, and Cox proportional hazards regression models. Results: Among the 302 patients identified, there were no significant differences in demographic or major clinical characteristics between the patients who had received metformin (n = 117) and those who had not (n = 185). The 2-year survival rate was 30.1% for the metformin group and 15.4% for the non-metformin group (P = 0.004; χ2 test). The median overall survival time was 15.2 months for the metformin group, and 11.1 months for the non-metformin group (P = 0.004, log-rank test). Metformin users had a 32% lower risk of death; the HR (95% confidence interval) was 0.68 (0.52–0.89) in a univariate model (P = 0.004), 0.64 (0.48–0.86) after adjusting for other clinical predictors (P = 0.003), and 0.62 (0.44–0.87) after excluding insulin users (P = 0.006). Metformin use was significantly associated with longer survival in patients with nonmetastatic disease only. Conclusions: Our finding that metformin use was associated with improved outcome of patients with diabetes and pancreatic cancer should be confirmed in independent studies. Future research should prospectively evaluate metformin as a supplemental therapy in this population. Clin Cancer Res; 18(10); 2905–12. ©2012 AACR.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-11-2994
    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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  • 8
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    Body Mass Index and Obesity- and Diabetes-Associated Genotypes and Risk for Pancreatic Cancer
    American Association for Cancer Research (AACR) ; 2011
    In:  Cancer Epidemiology, Biomarkers & Prevention Vol. 20, No. 5 ( 2011-05-01), p. 779-792
    Details
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 20, No. 5 ( 2011-05-01), p. 779-792
    Abstract: Background: The genetic factors predisposing individuals with obesity or diabetes to pancreatic cancer have not been identified. Aims: To investigate the hypothesis that obesity- and diabetes-related genes modify the risk of pancreatic cancer. Methods: We genotyped 15 single nucleotide polymorphisms of fat mass and obesity-associated (FTO), peroxisome proliferators-activated receptor gamma (PPARγ), nuclear receptor family 5 member 2 (NR5A2), AMPK, and ADIPOQ genes in 1,070 patients with pancreatic cancer and 1,175 cancer-free controls. Information on risk factors was collected by personal interview. Adjusted ORs (AOR) and 95% CIs were calculated using unconditional logistic regression. Results: The PPARγ P12A GG genotype was inversely associated with risk of pancreatic cancer (AOR, 0.21; 95% CI, 0.07–0.62). Three NR5A2 variants that were previously identified in a genome-wide association study were significantly associated with reduced risk of pancreatic cancer, AORs ranging from 0.57 to 0.79. Two FTO gene variants and one ADIPOQ variant were differentially associated with pancreatic cancer according to levels of body mass index (BMI; Pinteraction = 0.0001, 0.0015, and 0.03). For example, the AOR (95% CI) for FTO IVS1-2777AC/AA genotype was 0.72 (0.55–0.96) and 1.54 (1.14–2.09) in participants with a BMI of less than 25 or 25 kg/m2 or more, respectively. We observed no significant association between AMPK genotype and pancreatic cancer and no genotype interactions with diabetes or smoking. Conclusion: Our findings suggest the PPARγ P12A GG genotype and NR5A2 variants may reduce the risk for pancreatic cancer. A positive association of FTO and ADIPOQ gene variants with pancreatic cancer may be limited to persons who are overweight. Impact: The discovery of genetic factors modifying the risk of pancreatic cancer may help to identify high-risk individuals for prevention efforts. Cancer Epidemiol Biomarkers Prev; 20(5); 779–92. ©2011 AACR.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    URL: Article
    DOI: 10.1158/1055-9965.EPI-10-0845
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2011
    detail.hit.zdb_id: 2036781-8
    detail.hit.zdb_id: 1153420-5
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  • 9
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    Abstract C26: Development and validation of a scoring system using insulin-like growth factor to assess hepatic reserve in hepatocellular carcinoma.
    American Association for Cancer Research (AACR) ; 2013
    In:  Molecular Cancer Therapeutics Vol. 12, No. 11_Supplement ( 2013-11-01), p. C26-C26
    Details
    In: Molecular Cancer Therapeutics, American Association for Cancer Research (AACR), Vol. 12, No. 11_Supplement ( 2013-11-01), p. C26-C26
    Abstract: Background: The Child-Turcotte-Pugh (CTP) score inaccurately predicts survival in patients with chronic liver disease, including hepatocellular carcinoma (HCC), yet remains the standard tool for assessing hepatic reserve and guiding therapeutic decisions. CTP scoring relies on objective laboratory values for albumin, bilirubin, and prothrombin time and subjective clinical grading of hepatic encephalopathy and ascites. Since liver production of insulin-like growth factor 1 (IGF-1) is significantly reduced in patients with cirrhosis, we hypothesized that IGF-1 could be a valid surrogate for hepatic reserve to replace the subjective parameters in CTP score. Methods: We prospectively enrolled patients and collected data and retrospectively tested plasma IGF-1 levels in four independent cohorts: two HCC cohorts from the United States, n=310 (training set) and n=99 (validation set 1); one HCC cohort from Korea, n=188 (validation set 2); and one cirrhosis cohort from Egypt, n=71 (validation set 3). Recursive partitioning identified within the training set three optimal IGF-1 ranges that correlated with survival: & gt;50 ng/mL = 1 point; 26-50 ng/mL = 2 points; and & lt;26 ng/mL = 3 points. We modified the CTP score by replacing ascites and encephalopathy grading with IGF-1 value, subjected both the resulting IGF score and the CTP score to log-rank analysis, and quantified the prognostic values with C-statistics to compare the scores’ performance in all cohorts. Results: The IGF score was significantly more accurate in predicting survival and improved the stratification of all CTP classes in the training and validation cohorts. Conclusion: The new IGF score is simple and blood-based, and validated well on multiple independent HCC cohorts. It could identify a subpopulation of patients who may benefit from active therapy because of their preserved hepatic reserve, as distinct from patients for whom therapy can be deferred or avoided. Citation Information: Mol Cancer Ther 2013;12(11 Suppl):C26. Citation Format: Ahmed O. Kaseb, Lianchun Xiao, Rania Naguib, Wafaa El-Shikh, Manal Hassan, Hesham Hassabo, Jeong-Hoon Lee, Jung-Hwan Yoon, Hyo-Suk Lee, Young Kwang Chae, James L. Abbruzzese, Jeffrey Morris. Development and validation of a scoring system using insulin-like growth factor to assess hepatic reserve in hepatocellular carcinoma. [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; 2013 Oct 19-23; Boston, MA. Philadelphia (PA): AACR; Mol Cancer Ther 2013;12(11 Suppl):Abstract nr C26.
    Type of Medium: Online Resource
    ISSN: 1535-7163 , 1538-8514
    URL: Article
    DOI: 10.1158/1535-7163.TARG-13-C26
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2013
    detail.hit.zdb_id: 2062135-8
    SSG: 12
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  • 10
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    Can we identify patients with cancer at high risk for cachexia? A prospective study in pancreatic cancer (PC).
    American Society of Clinical Oncology (ASCO) ; 2012
    In:  Journal of Clinical Oncology Vol. 30, No. 4_suppl ( 2012-02-01), p. 219-219
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 30, No. 4_suppl ( 2012-02-01), p. 219-219
    Abstract: 219 Background: Identifying PC patients at high risk for cachexia may allow for early intervention to prevent it. Symptoms such as pain, nausea and anorexia may predict weight loss. Inflammatory cytokines are also associated with cachexia. We evaluated the ability of each to predict weight loss in newly diagnosed PC patients. Methods: Using the M. D. Anderson Symptom Inventory (MDASI), we assessed baseline symptoms in untreated advanced or metastatic PC patients. The survey assesses severity of symptoms on a 0-10 scale. Baseline serum levels of IL-1a, IL-1b, IGF-1, CXCL-12, CXCL-16, CRP, IL-6, IL-8, VEGF, CEA, and CA 19-9 were measured via ELISA. Using STATA (version 12), we generated multivariable logistic regression models with a backward selection procedure. This allowed us to evaluate all potential univariate correlates with 5% and 10% weight loss at P 〈 .1 to create a multivariate model containing variables of p 〈 .05. Student t-test was used to compare the mean values of cytokines across different strata. Results: We evaluated 72 patients (33M/39F). Weight loss of 〉 5% or death was observed in 44 patients (62%) and 〉 10% or death in 24 (34%). 61 pts (30M/31F) survived sixty days after the start of treatment with 5% and 10% weight loss seen in 33 (54%) and 13 (21%), respectively. Baseline severe loss of appetite was most strongly associated with weight loss (OR 15.3, p=.005), compared to those with a moderate loss of appetite (OR 4.7, p=.058), nausea (OR 9.4, p=.048), or shortness of breath (OR 7.4, p=.063). Neither diarrhea nor vomiting correlated with weight loss, nor did age, tumor markers, or treatment with platinum drugs, opiates, or erlotinib. Baseline cytokine levels were available for 23 patients. Mean CXCL-16 (p=.05) and IL-6 (p=.045) levels were greater in patients with weight loss. Serum erythropoietin levels may be negatively associated with weight loss (p=0.06). An analysis of the remaining patients’ samples will be available at the meeting. Conclusions: Both alterations in serum cytokines and specific symptoms may predict the development of cachexia. A more robust analysis of circulating cytokines may allow us to design interventions which prevent or delay cachexia in patients with advanced pancreatic cancer.
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/jco.2012.30.4_suppl.219
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2012
    detail.hit.zdb_id: 2005181-5
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