927 resultados para Geography|Health Sciences, Public Health|Health Sciences, Epidemiology|Health Sciences, Oncology
Resumo:
Advances in therapy for colorectal cancer have been hampered by development of resistance to chemotherapy. The Src family of protein tyrosine kinases has been associated with colorectal cancer development and progression. Activation of the prototypic member of the family, Src, occurs in advanced colorectal cancer and is associated with a worse outcome. This work tests the hypotheses that Src activation contributes to chemoresistance in some colon tumors and that this resistance can be overcome by use of Src inhibitors. The aims of the proposal were to (1) determine if constitutive Src activation is sufficient to induce oxaliplatin resistance; (2) evaluate the role of reactive oxygen species (ROS) in the activation of Src after oxaliplatin treatment; (3) determine the frequency of Src activation in liver metastases after oxaliplatin treatment; and (4) evaluate the safety, preliminary efficacy, and pharmacodynamics of the combination of dasatinib with oxaliplatin-based therapy in patients with metastatic colorectal cancer. ^ Using a panel of colon cancer cell lines and murine models, I demonstrate that administration of oxaliplatin, a commonly utilized chemotherapy for colorectal cancer, results in an increased activation of Src. The activation occurs acutely in some, but not all, colorectal carcinoma cell lines. Cell lines selected for oxaliplatin resistance are further increased in Src activity. Treatment of cell lines with dasatinib, a non-selective pharmacologic inhibitor of the Src family kinases synergistically killed some, but not all cell lines. Cell lines with the highest acute activation of Src after oxaliplatin administration were the most sensitive to the combination therapy. Previous work demonstrated that siRNA to Src increased sensitivity to oxaliplatin, suggesting that the effects of dasatinib are primarily due to its ability to inhibit Src in these cell lines. ^ To examine the mechanism underlying these results, I examined the effects of reactive oxygen species (ROS), as previous studies have demonstrated that platinum chemotherapeutics result in intracellular oxidative stress. I demonstrated that oxaliplatin-induced reactive oxygen species were higher in the cell lines with Src activation, relative to those in which Src was not activated. This oxaliplatin-induced Src activation was blocked by the administration of anti-oxidants, thereby demonstrating that synergistic killing between dasatinib and oxaliplatin was associated with the ability of the latter to generate ROS. ^ In a murine model of colorectal cancer metastasis to the liver, the combination of dasatinib and oxaliplatin was more effective in reducing tumor volume than either agent alone. However, when oxaliplatin resistant cell lines were treated with a combination of oxaliplatin and AZD0530, an inhibitor in the clinic with increased specificity for Src, no additional benefit was seen, although Src was activated by oxaliplatin and Src substrates were inhibited. The indolent growth of oxaliplatin-resistant cells, unlike the growth of oxaliplatin resistant tumors in patients, precludes definitive interpretation of these results. ^ To further explore Src activation in patients with oxaliplatin exposure and resistance, an immunohistochemistry analysis of tumor tissue from resected liver metastases of colorectal cancer was performed. Utilizing a tissue microarray, staining for phosphorylated Src and FAK demonstrated strong staining of tumor relative to stromal and normal liver. In patients recently exposed to oxaliplatin, there was increased FAK activation, supporting the clinical relevance of the prior preclinical studies. ^ To pursue the potential clinical benefit of the combination of Src inhibition with oxaliplatin, a phase IB clinical trial was completed. Thirty patients with refractory metastatic colorectal cancer were treated with a combination of 5-FU, oxaliplatin, an epidermal-growth factor receptor monoclonal antibody, and dasatinib. The recommended phase II dose of dasatinib was established, and toxicities were quantified. Pharmacodynamic studies demonstrated increased phosphorylation of the Src substrate paxillin after dasatinib therapy. Tumor biopsies were obtained and Src expression levels were quantitated. Clinical benefit was seen with the combination, including a response rate of 20% and disease control rate of 56%, prompting a larger clinical study. ^ In summary, although Src is constitutively activated in metastatic colorectal cancer, administration of oxaliplatin chemotherapy can further increase its activity, through a reactive oxygen species dependent manner. Inhibition of Src in combination with oxaliplatin provides additional benefit in vitro, in preclinical animal models, and in the clinic. Further study of Src inhibition in the clinic and identification of predictive biomarkers of response will be required to further advance this promising therapeutic target. ^
Resumo:
Background. It is important to understand the association between diet and risk of pancreatic cancer in order to better understand the etiology of pancreatic cancer.^ Objectives. Describe the dietary patterns of cases of adenocarcinoma of the pancreas and non-cancer controls and evaluate the odds of having a healthy eating pattern among cases and non-cancer controls.^ Design and Methods. An ongoing hospital-based case-control study was conducted in Houston, Texas from 2000-2008 with 678 pancreatic adenocarcinoma cases and 724 controls. Participants completed a food frequency questionnaire and a risk factor questionnaire. Dietary patterns were derived by principal component analysis and associations between dietary patterns and pancreatic cancer risk were assessed using unconditional logistic regression.^ Results. Two dietary patterns were derived: fruit-vegetable and high fat-meat. There were no statistically significant associations between the fruit-vegetable pattern and pancreatic cancer. An inverse association was seen between the high fat-meat pattern and pancreatic cancer risk when comparing those in the upper intake quintile to those scoring in the lowest quintile after adjusting for demographic and risk factor variables (OR=0.67, p=0.03). In sex-stratified analysis adjusted for demographic and risk factor variables, females scoring in the upper intake quintile of the fruit-vegetable pattern had a 49% lower risk of pancreatic cancer compared to females scoring in the lowest quintile (OR=0.51, p=0.03). An inverse relationship was also seen for the high fat-meat pattern when comparing females in the upper intake quintile to females in the lowest quintile (OR=0.50, p=0.03). In males, neither dietary pattern was significantly associated with pancreatic cancer.^ Conclusions. The current findings for the fruit-vegetable pattern are similar to those of previous studies and support the hypothesis that there is an inverse association between a “healthy” diet (comprised of fruits, vegetables, and whole grains) and risk of having pancreatic cancer (in females only). However, the inverse relationship with the high fat-meat pattern and risk of pancreatic cancer is contrary to other results. Further research on dietary patters and pancreatic cancer risk may lead to better understanding of the etiologic cause of pancreatic cancer.^
Resumo:
The objectives of this dissertation were to determine the quality of life in women with ovarian cancer and the association of their physical and emotional well-being with the number of symptoms, duration of symptoms, and the scores of common symptoms of ovarian cancer; to study the prevalence of complementary and alternative medicine techniques for symptom relief and its association with the number of symptoms, age, education, insurance, comorbidity, and satisfaction with medical care they received, and their pre-diagnostic experience of symptoms.^ This study was based on a secondary data analysis of a study of early detection of ovarian cancer. A sample of 139 women with ovarian cancer was recruited and was administered a questionnaire comprised of questions on their quality of life, their symptoms and what they did about the symptoms, whether they used any complementary and alternative medicine techniques, and other medical conditions they had. Out of this sample, 53 patients underwent in-depth interviews relating to their symptoms before the diagnosis and their experiences with the health care system leading to the ovarian cancer diagnosis. ^ In article #1, ovarian cancer patients were observed to have significantly poorer quality of life on all subscales and summary scores except pain, compared to that of the general population of US women. Physical well-being scores were negatively associated with the number of symptoms before diagnosis and a significant negative association of comorbidity index was observed with physical well-being. Higher education and increase in time since diagnosis was found to have better physical scores. Emotional well-being scores showed marginally significant associations with number of symptoms and bloating. ^ In article #2, a thematic content analysis of the ovarian cancer patients’ interviews revealed that on recognition of their symptoms women first assumed their symptoms to be a normal transient occurrence due to a pre-existing disease condition, or due to some other disease. A series of misattributions of their symptoms on their and their doctors’ part impacted their health care seeking.In article #3, a significantly greater likelihood of CAM use with an increase in the number of symptoms was observed.^ Based on the foregoing results, it is important to educate women on possible signs of ovarian cancer and also to educate doctors about the results of current research regarding ovarian cancer diagnosis. This will help to avoid a delay in getting a diagnosis and improve women’s quality of life. It emphasizes the diagnosis of ovarian cancer in earlier stages by more sensitive screening techniques. This study emphasizes the importance of consideration of comorbidity in any quality of life research. Additionally, educating women in the safe use of CAM techniques carries immense significance because the efficacy and safety of many of the currently advertized CAM products has not been scientifically validated. Further research is needed to confirm the findings of this study. ^
Resumo:
Background: Pancreatic cancer is the fourth most common cause of cancer death in the United States. Despite advances in cancer treatment, prognosis of pancreatic cancer remains extremely poor with survival rates of 24% and 5% in 1 and 5 years, respectively. Many patients with pancreatic cancer have a history of diabetes and are treated with various antidiabetic regimens including metformin. In multiple retrospective studies, metformin has been associated with decreased risk of cancer and cancer-related mortality. Metformin has also been reported to inhibit the growth of cancer cells, both in vitro and in vivo.^ Methods: We conducted a retrospective cohort study to examine the survival benefit of metformin in diabetic patients with pancreatic cancer at MD Anderson Cancer Center (MDACC). A dataset of 397 patients who carried the diagnosis of "Diabetes Mellitus" and "Pancreatic Cancer" at MD Anderson were screened for this study. ^ Results: Mean age of patients at diagnosis of cancer was 64.0 ± 8.7 years (range 37-84). The majority of the patients were male (65.6%) and of Caucasian race (78.5%). The most common antidiabetic regimen used were insulin and metformin (in 39.1% and 38.7%, respectively). Patients' cancer were staged as resectable in 34.1%, locally advanced unresectable in 29.1%, and disseminated disease in 36.7% of cases. Overall 1-year and 3-year survival rates for all stages combined were 51.8% and 7.6%, respectively. Earlier stage, metformin use, low CA19-9 level, better ECOG performance status, surgical intervention, negative surgical margins, and smaller tumor size were associated with longer survival. Metformin use was associated with a 33% decrease in risk of death (HR: 0.67; 95% CI: 0.51-0.88). Multivariate Cox proportional hazard regression showed hazard ratio of 1.77 (95% CI 1.49-2.10) for cancer stage, 0.65 (95% CI 0.49-0.86) for metformin use, and 1.68 (95% CI 1.26-2.23) for CA 19-9 level above population median. ^ Conclusion: Our study suggests that metformin may improve the outcome in diabetic patients with pancreatic cancer independently of other known prognostic factors. Pancreatic cancer carries extremely poor prognosis; metformin may provide a suitable adjunct therapeutic option for pancreatic cancer in patients with and without diabetes mellitus.^
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DNA ligase and DNA polymerase play important roles in DNA replication, repair, and recombination. Frequencies of spontaneous and chemical- and physical-induced mutations are correlated to the fidelity of DNA replication. This dissertation elucidates the mechanisms of the DNA ligation reaction by DNA ligases and demonstrates that human DNA ligase I and DNA polymerase $\alpha$ are the molecular targets for two metal ions, Zn$\sp{2+}$ and Cd$\sp{2+},$ and an anticancer drug, F-ara-ATP.^ Human DNA ligases were purified to homogeneity and their AMP binding domains were mapped. Although their AMP-binding domains are similar, there could be difference between the two ligases in their DNA binding domains.^ The formation of the AMP-DNA intermediate and the successive ligation reaction by human DNA ligases were analyzed. Both reactions showed their substrate specificity for ligases I and II, required Mg2+, and were inhibited by ATP.^ A protein inhibitor from HeLa cells and specific for human DNA ligase I but not ligase II and T4 ligase was discovered. It reversibly inhibited DNA ligation activity but not the AMP-binding activity due to the formation of a reversible ligase I-inhibitor complex.^ F-ara-ATP inhibited human DNA ligase I activity by competing with ATP for the AMP-binding site of DNA ligase I, forming a ligase I-F-ara-AMP complex, as well as when it was incorporated at 3$\sp\prime$-terminus of DNA nick by DNA polymerase $\alpha.$^ All steps of the DNA ligation reaction were inhibited by Zn$\sp{2+}$ and Cd$\sp{2+}$ in a concentration-dependent manner. Both ions did not show the ability to change the fidelity of DNA ligation reaction catalyzed by human DNA ligase I. However, Zn$\sp{2+}$ and Cd$\sp{2+}$ showed their contradictory effects on the fidelity of the reaction by human DNA polymerase $\alpha.$ Zn$\sp{2+}$ decreased the frequency of misinsertion but less affected that of mispair extension. On the contrary, Cd$\sp{2+}$ increased the frequencies of both misinsertion and mispair extension at very low concentration. Our data provided strong evidence in the molecular mechanisms for the mutagenicity of zinc and cadmium, and were comparable with the results previously reported. ^
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The clinical application of chemopreventive agents is expected to prevent the appearance of cancer by arresting carcinogenesis or reversing it in the precancerous stages. The hypothesis of the present investigations was that chemopreventive agents (retinoids and antioxidant vitamins) may counteract the clastogenic effects of bleomycin in vitro in both lymphoblastoid cell lines and primary lymphocyte cultures and that a similar phenomenon can be detected in lymphocytes from individuals treated with 13-cis-retinoic acid. The efficacy of 13-cis-retinoic acid, n-(4-hydroxyphenyl)-retinamide, ascorbic acid, n-acetyl-l-cysteine, alpha-tocopherol, and alpha-tocopherol-acid succinate was tested against bleomycin-induced chromosomal breakage.^ The results provided direct evidence of the concentration-related protective effects of these agents against bleomycin-induced clastogenicity in cultures of human lymphoblastoid cell lines in vitro. Similar anticlastogenic protection was demonstrated with 13-cis-retinoic acid, ascorbic acid, n-acetyl-l-cysteine, and alpha-tocopherol-acid succinate in primary lymphocyte cultures in vitro. The in vitro anticlastogenic effect of 13-cis-retinoic acid was also demonstrated in lymphocyte cultures from peripheral blood samples from patients treated with this retinoid.^ An important consideration is that the concentrations used in the present investigations are comparable to those achieved in clinical situations.^ The in vitro anticlastogenic effect of these retinoids and antioxidants may constitute an important element of their chemopreventive properties. The results corroborate the hypothesis that these compounds may be effective in clinical chemoprevention trials. The bleomycin-assay may also be used as a short-term test to evaluate the antimutagenic effects of various agents. ^
Resumo:
Urines from patients administered mutagenic antineoplastic drugs were significantly mutagenic in the Ames assay, and hence may pose a genotoxic hazard to hospital personnel or family members caring for the patient. The urines were tested for mutagenicity in several different strains of Salmonella typhimurium that were uvr positive or negative (TA98, TA100, TA102, UTH8413, UTH8414). The urines were fractionated by high pressure liquid chromatography (HPLC) and the fractions assayed for mutagenicity in the strains in which the whole urine was mutagenic. Only fractions of urines containing the parent compound (cisplatin, doxorubicin, or mitomycin) were mutagenic; no other fraction showed significant mutagenicity. However, urine containing cyclophosphamide had two fractions that were mutagenic. One fraction, the fraction containing cyclophosphamide, required metabolic activation for mutagenicity. The other fraction did not require activation for mutagenicity.^ The chemical and mutagenic stability of these urines at room temperature was assayed over a 14 day period. The parent compound degraded within the first seven days, but the urines remained mutagenic. Cis-platinum was chemically stable in the urine; however, the urine decreased in mutagenicity. The decrease was probably the result of stable ligands binding to the platinum.^ Inactivation methods were developed to reduce the genotoxic hazard. Urine containing cisplatin was inactivated by complexing the cisplatin with diethyldithiocarbamate (DDTC). Oxidation with NaOCl of urines containing mitomycin and doxorubicin (sodium thiosulfate must be added to the doxorubicin urine) results in mutagenic inactivation. Inactivation of urine containing cyclophosphamide requires oxidation with alkaline potassium permaganate and trapping of active degradation products with sodium thiosulfate. Urines containing these drugs can be inactivated, but not always by the same method that inactivates the drug alone in solution. Therefore, in the future development of inactivation methods, both chemical and mutagenic assays are necessary to determine effectiveness. Methods of inactivation of mutagenic excreta developed in this study are both effective and practical. ^
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BACKGROUND Although one out of every five gastrointestinal cancer patients needs transitional care (home-based skilled care or placement in skilled nursing or rehabilitation facilities) following treatment, few studies have examined outcomes in this population compared to patients who return home without assistance. This study has two primary goals: 1. To evaluate long-term cancer-specific outcomes in colorectal cancer patients utilizing transitional care compared to those that return home without assistance following therapy 2. To compare results using standard regression techniques and propensity scores. ^ METHODS Patients undergoing curative surgery for colorectal adenocarcinoma will be identified using data from a tertiary care Veterans Administration hospital. Survival and recurrence will then be determined from VA records and the Social Security Death Index. ^ The association between transitional care utilization and overall and disease-free survival will be evaluated using Cox proportional hazards regression to adjust for confounding factors. Predictors of transitional care utilization will be assessed using multiple logistic regression to generate a propensity score which will also be used to assess differences in survival based on transitional care use. ^ POTENTIAL SIGNIFICANCE If transitional care utilization is associated with worse survival and recurrence following therapy then it will be important to subsequently assess the mechanism in order to target interventions to improve outcomes. If there is no difference in cancer-specific outcomes, then this project can potentially highlight benefits of supportive therapy following colorectal cancer resection.^
Resumo:
Ovarian cancer is the leading cause of cancer-related death for females due to lack of specific early detection method. It is of great interest to find molecular-based biomarkers which are sensitive and specific to ovarian cancer for early diagnosis, prognosis and therapeutics. miRNAs have been proposed to be potential biomarkers that could be used in cancer prevention and therapeutics. The current study analyzed the miRNA and mRNA expression data extracted from the Cancer Genome Atlas (TCGA) database. Using simple linear regression and multiple regression models, we found 71 miRNA-mRNA pairs which were negatively associated between 56 miRNAs and 24 genes of PI3K/AKT pathway. Among these miRNA and mRNA target pairs, 9 of them were in agreement with the predictions from the most commonly used target prediction programs including miRGen, miRDB, miRTarbase and miR2Disease. These shared miRNA-mRNA pairs were considered to be the most potential genes that were involved in ovarian cancer. Furthermore, 4 of the 9 target genes encode cell cycle or apoptosis related proteins including Cyclin D1, p21, FOXO1 and Bcl2, suggesting that their regulator miRNAs including miR-16, miR-96 and miR-21 most likely played important roles in promoting tumor growth through dysregulated cell cycle or apoptosis. miR-96 was also found to directly target IRS-1. In addition, the results showed that miR-17 and miR-9 may be involved in ovarian cancer through targeting JAK1. This study might provide evidence for using miRNA or miRNA profile as biomarker.^
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Hereditary breast and ovarian cancer (HBOC) is an inherited cancer syndrome that is associated with mutations in the BRCA1 and BRCA2 genes. Carriers of BRCA mutations, both men and women, are at an increased risk for developing certain cancers. Carriers are most notably at an increased risk to develop breast and ovarian cancers; however an increased risk for prostate cancer, melanoma, and pancreatic cancers has also been associated with these mutations. In 2009 the American Congress of Obstetricians and Gynecologists (ACOG) released a practice bulletin stating that evaluating a patient’s risk for HBOC should be a routine part of obstetric and gynecologic practice. A survey was created and completed by 83 obstetricians and gynecologists in the greater Houston, TX area. The survey consisted of four sections designed to capture demographic information, attitudes towards HBOC and BRCA testing, utilization of BRCA testing, and the overall knowledge of respondents with regards to HBOC and BRCA testing. This study found that the majority of participants indicated that they felt that obstetricians and gynecologists should have the primary responsibility of identifying patients who may be at increased risk of carrying a BRCA mutation. Moreover, this study found that the majority of participants indicated that they felt comfortable or very comfortable in identifying patients at an increased risk of carrying a BRCA mutation. However, only about a quarter of participants indicated that they order BRCA genetic testing one to two times per month or more. Lastly, this study demonstrates that the overall knowledge of HBOC and BRCA testing among this population of obstetricians and gynecologists is poor. The results of this study stress the need for more education regarding HBOC, genetic testing, and strategies for identifying patients that may be at risk for having a mutation in a BRCA gene. Furthermore, it reiterates the importance of raising awareness to current practice guidelines and recommendations that can assist obstetricians and gynecologist to better identify and manage patients that may be at an increased risk of having HBOC.
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Oncologic specialty societies and multidisciplinary collaborative groups have dedicated considerable effort to developing evidence-based quality indicators (QIs) to facilitate quality improvement, accreditation, benchmarking, reimbursement, maintenance of certification, and regulatory reporting. In particular, radiation oncology as a field has a long history of organized quality assessment efforts, and continues to work toward developing consensus quality standards in the face of continually evolving technologies and standards of care. The present report provides a comprehensive review of the current state of quality assessment in radiation oncology, with an emphasis on recent quality improvement efforts. Specifically, this report aims to highlight implications of the healthcare quality movement for radiation oncology and review existing efforts to define and measure quality in the field, with particular focus on dimensions of quality that are specific to radiation oncology within the "big picture" of oncologic quality improvement efforts.^
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The ECM of epithelial carcinomas undergoes structural remodeling during periods of uncontrolled growth, creating regional heterogeneity and torsional stress. How tumors maintain ECM integrity in the face of dynamic biophysical forces is still largely unclear. This study addresses these deficiencies using mouse models of human lung adenocarcinoma. Spontaneous lung tumors were marked by disorganized basement membranes, dense collagen networks, and increased tissue stiffness. Metastasis-prone lung adenocarcinoma cells secreted fibulin-2 (Fbln2), a matrix glycoprotein involved in ECM supra-molecular assembly. Fibulin-2 depletion in tumor cells decreased the intra-tumoral abundance of matrix metalloproteinases and reduced collagen cross-linking and tumor compressive properties resulting in inhibited tumor growth and metastasis. Fbln2 deposition within intra-tumoral fibrotic bands was a predictor of poor clinical outcome in patients. Collectively, these findings support a feed-forward model in which tumor cells secrete matrix-stabilizing factors required for the assembly of ECM that preferentially favors malignant progression. To our knowledge, this is the first evidence that tumor cells directly regulate the integrity of their surrounding matrix through the secretion of matrix-stabilizing factors such as fibulin-2. These findings open a new avenue of research into matrix assembly molecules as potential therapeutic targets in cancer patients.
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Early-stage lung cancer incidence among older adults is expected to increase due to demographic trends and CT-based screening, yet optimal treatment of lung cancer in the elderly remains controversial. There are several accepted strategies for treating lung cancer including surgery, conventional radiation, and stereotactic ablative body radiotherapy (SABR). However, there are currently no randomized controlled trials to help distinguish the comparative effectiveness of these various strategies. This is an unfortunate omission as lung cancer causes the most deaths among all cancers in the United States (as well as the entire world). SABR holds particular promise as it is a completely non-invasive, ambulatory technique for achieving cure without an operation, thus avoiding the risks of surgery and the associated pre-operative and post-operative costs. To provide fair view of the potential effect on SABR on controlling lung cancer in the United States, a systematic review of SABR with a focus on its achieved outcomes, toxicities, and comparison to conventional radiation and surgical options is presented. ^
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This report describes the development of a Markov model for comparing percutaneous radiofrequency ablation (RFA) and stereotactic body radiation therapy (SBRT) in terms of their cost-utility in treating isolated liver metastases from colorectal cancer. The model is based on data from multiple retrospective and prospective studies, available data on different utility states associated with treatment and complications, as well as publicly available Medicare costs. The purpose of this report is to establish a well-justified model for clinical management decisions. In comparison with SBRT, RFA is the most cost-effective treatment for this patient population. From the societal perspective, SBRT may be an acceptable alternative with an ICER of $28,673/QALY. ^
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This study investigated the characteristics of a clinic that affect how satisfied survivors of childhood cancer are with their medical care. Questionnaire and interview data from the Passport for Care: Texas Implementation project collected between January 2011 to April 2012 were analyzed. Eleven clinics in Texas participated. Questionnaire respondents were childhood cancer survivor patients who had been off therapy for at least 2 years, or their parents. Interview respondents were clinical providers or research staff at the participating clinics. The outcomes evaluated were answers to a single question on satisfaction with care and a composite Percent Satisfaction Score created from seven other questionnaire items that were correlated (Spearman Rho >0.3) with the question on satisfaction. The following characteristics were also evaluated: sex, age, race, education, and type of cancer. The following clinic indicators were evaluated: type of clinic (general vs. dedicated cancer survivor clinics), number of providers, number of survivors, ratio of survivors/providers, distribution of handouts, distribution of treatment summaries, and use of Children's Oncology Group (COG) guidelines. ^ The only demographic characteristic that affected satisfaction was race. A Kruskal-Wallis test showed a statistically significant difference (Chi-square 6.129, 2 d.f., p = 0.0467). To analyze this further, Wilcoxon Rank Sum test of pairings of the three groups were performed. A Bonferroni correction for multiple testing was applied, with p = 0.017 indicating significance at alpha = 0.05. There was no significant difference between the White and Hispanic groups or between the Hispanic and "Other" groups. For the White and "Other" groups there was a significant difference for the satisfaction item (p = 0.0123) but not for the Percent Satisfaction Score (p = 0.0289). These results suggest that race may influence satisfaction and should be evaluated further in future studies. ^ None of the clinic indicators affected the Percent Satisfaction Score. Going to a clinic that distributed patient information handouts (Wilcoxon Rank Sum p = 0.048) and going to a clinic with >=100 survivors (Wilcoxon Rank Sum p = 0.021) were associated with increased satisfaction. The population of childhood cancer survivors is a growing group of individuals with special health needs. In the future survivors will likely seek medical care in a variety of clinical settings, so it is important to investigate features to improve patient satisfaction with clinical care.^