bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 3588: Treatment differences are associated with black-white disparities in advanced epithelial ovarian cancer
Authors: Howell Elizabeth A. , Egorova Natalia , Hayes Monica P. , Wisnivesky Juan , Franco Rebeca , Bickell Nina A. 
Published: August 2012

Abstract
Background: Racial differences in survival for ovarian cancer are well documented. Previous research suggests that black-white mortality disparities are partially explained by more advanced disease among black women. Whether differences in receipt of guideline recommended care (including both surgery and chemotherapy) also explain mortality differences between black and white women with advanced epithelial ovarian cancer is not known. Methods: Using the Surveillance, Epidemiology, and End Results (SEER) linked to Medicare claims for 1997-2007, we identified a cohort of 4363 women age 65 and older with histologically confirmed stage III or IV epithelial ovarian cancer. We evaluated long-term survival for black and white women in the entire fee-for-service Medicare population, and then in patients matched by propensity score to create two similar cohorts for comparison with Kaplan-Meier analysis. We investigated the association between race, stage, and survival among women who received guideline recommended care and those who received incomplete care. Adjusted analyses were conducted using Cox modeling. Results: Overall, black women with advanced epithelial ovarian cancer were more likely to die than white women; unadjusted hazard ratio (HR):1.29 (95% confidence interval [CI]: 1.12-1.48). Black women were more likely than white women to present with stage 4 disease (40% vs. 32%, p=0.02) and comorbid conditions (55% vs. 36%, p&lt;0.0001). Black women were less likely than white women to receive guideline recommended care (61% vs. 73%, p=0.0001) and women who received incomplete care had lower survival than women who received recommended care, unadjusted HR of 0.27 (95% CI: 0.25-0.29). In multivariable models including demographic factors, stage of disease, comorbidity, and extent of surgery, there was no racial difference in mortality among women who received guideline recommended care, HR for mortality for black women at 1.09 (95% CI: 0.90-1.13) or among women who received incomplete care, HR for black women at 1.15 (0.89-1.39). The survival analysis of patients matched by propensity score showed no difference between white and black women with recommended care (p=0.68) and no racial difference with incomplete care (p=0.87). Conclusions: Differences in receipt of guideline recommended care partially explain black-white mortality disparities among women with advanced epithelial ovarian cancer. Patients who receive incomplete treatment have worse prognosis. Our findings suggest a need to identify and rectify the cause for disparate treatment rates.
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 3588. doi:1538-7445.AM2012-3588
Abstract 3591: Triple negative (c-KIT, BRAF, NRAS) acral lentiginous melanoma in Hawaii: Molecular profiling in a multi-ethnic population
Authors: Morita Shane Y. , Lum Christopher A. , Davis James W. 
Published: August 2012

Abstract
Background: Acral lentiginous melanoma (ALM) is the least common subtype among patients with melanoma. There is a higher preponderance in the minority population. A different pathogenesis has been proposed for ALM. Previous studies have profiled the importance of c-KIT, BRAF and NRAS mutations in melanoma treatment and prognosis. However, characterization of these somatic mutations in a specific non-Caucasian ALM population has not been reported. The Pacific Basin provides a unique opportunity to study diseases in diverse ethnic groups, including Pacific Islanders and Filipinos. We sought to determine the frequency of a “triple negative” genotype in our multi-ethnic cohort. Methods: IRB approval was obtained for this molecular analysis. From 1999 to 2011, 12 non-Caucasian patients (8-Filipino, 3-Pacific Islander and 1-Vietnamese) histologically confirmed to have ALM were evaluated at a tertiary institution. Data including age, gender, tumor location, Breslow thickness, Clark level, ulceration, regression, and mitoses per mm squared were compiled. Direct sequencing (c-KIT [Exons 8,9,11,13,17,18], NRAS [Exons 2,3]) and real-time PCR (BRAF [Exon 15]) was performed on formalin-fixed/ paraffin-embedded archived biospecimens (primary lesions). Results: Our findings demonstrated that 7/12 (58%) patients exhibited the “triple negative” genotype. Mutually exclusive somatic mutations (4 c-KIT and 1 BRAF) were identified in the remaining 5/12 (42%) patients. Those in the “triple negative” group trended toward a deeper Breslow thickness, when compared to those with a mutation (depth 4.73 mm vs. 3.07 mm). Demographics of the entire non-Caucasian cohort included a mean age of 72.0 years old (range 52-87) and male gender 6/12 (50%). Tumor location principally involved the foot 10/12 (83%); mean Breslow thickness was 4.04 mm (range 2.20-7.75), Clark IV or higher 11/12 (92%), ulceration 8/12 (67%), regression 12/12 (100%), and mean mitoses per mm squared was 5.71 (range 0-30). Conclusions: Non-Caucasian patients with ALM were found to have a high prevalence of the “triple negative” genotype. Those within that group appeared to have thicker tumors. Nearly half of our cohort had thick primary lesions with a high propensity for ulceration. This is the first study to our knowledge that has profiled somatic mutations (c-KIT, BRAF, NRAS) in a multi-ethnic population of ALM patients and examined the histologic correlates of a “triple negative” genotype. This novel concept highlights the relevance of alternate pathways and molecular targets, such as PI3KCA in prognosis and therapy.
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 3591. doi:1538-7445.AM2012-3591
Abstract 3592: Risk factors of prostate cancer in African American men
Authors: Chornokur Ganna , Han Gang , Tanner Richard E. , Lin Hui-Yi , Gwede Clement , Kumar Nagi B. , Pow-Sang Julio , Phelan Catherine M. 
Published: August 2012

Abstract
Background. African American men have 1.6 times the incidence and 2.4 times the mortality rate of prostate cancer, compared to Caucasian men. Thus, prostate cancer constitutes one of the most striking racial health disparities, the causation of which is not well understood. Main hypothesis. We hypothesized that select clinical and/or bio-behavioral risk factors are associated with prostate cancer in African American men. Participants and Methods. 105 African American men aged 34-80 (35 cases and 70 controls) were recruited. Univariable and multivariable logistic regression models were built to test the marginal and joint effects of the variables when predicting the cancer status. Results. In the univariable regression models, PSA (ng/ml; p&lt;.001), smoking (cigarettes/day; p=0.011), diagnosis of benign prostatic hyperplasia (BPH, yes/no; p&lt;.001), diagnosis of prostatitis (yes/no; p&lt;.001) and prostatic intraepithelial neoplasia (PIN, yes/no; p=&lt;.001) were independently associated with the prostate cancer diagnosis. However, only PSA (4.340; (1.484, 12.689)) and diagnosis of BPH (14.248; (1.132, 179.310)) remained significant in the age-adjusted multivariable logistic regression model. Conclusions. Our results suggest that, as expected, PSA levels are associated with prostate cancer in African American men. Interestingly, a history of BPH is also associated with prostate cancer in African American men. Despite the limitation of a small sample size, our data is in agreement to a recent report (Pettaway et al, 2011) in which African Americans with BPH were observed to have a much greater risk of developing prostate cancer than similar Caucasian men, highlighting differences in the biology of prostate cancer between populations. References Curtis A. Pettaway, Lois E. Lamerato, Michael T. Eaddy et al. Benign prostatic hyperplasia: racial differences in treatment patterns and prostate cancer prevalence. BJU International (1 0 8) 1 3 0 2 - 8, 2011
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 3592. doi:1538-7445.AM2012-3592
Abstract 3601: Telomere length assessment in human archival tumor tissues by quantitative PCR method (qTL)
Authors: Wang Hui 
Published: August 2012

Abstract
Telomeres are essential for maintenance of genomic stability. Short telomeres have been associated with genomic instability, and initiation and progression of human cancers. To protect their telomeres, up to 90% of human cancers activate telomerase. Inhibition of telomerase by imetelstat, a specific and potent inhibitor, has resulted in telomere shortening, as well as tumor response in animal models. We propose that tumors with short telomeres may be more responsive to imetelstat than tumors with long telomeres. This hypothesis will be tested by measuring baseline telomere lengths in archival tumors of patients in imetelstat Phase II clinical trials, and correlating tumor telomere length with clinical outcome. In order to accomplish this, a fast, high-throughput qPCR-based method for telomere length measurement in genomic DNA extracted from FFPE tissue sections was developed. Using this assay, telomere repetitive DNA sequences and single-copy gene control were successfully amplified. The assay required very little genomic DNA (1-10ng per PCR reaction). Thus, small tissue sections (20 mm2) could be easily accommodated. Using this technique, we were able to perform the first comparison of relative telomere lengths in 22 human breast cancer samples and 8 human tumor cell lines in matched fresh-frozen and FFPE samples. Telomere lengths measured in FFPE samples by the qPCR method strongly correlated with the telomere lengths measured by TRF in matched fresh-frozen samples. Therefore, our method provides a useful tool for assessment of telomere length as a potential predictive biomarker of responsiveness to telomerase inhibition in clinical archival tumor tissue.
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 3601. doi:1538-7445.AM2012-3601
Abstract 3606: Dynamic expression of pepsinogen I in gastric diseases sequence and relationship with Helicobacter pylori infection
Authors: Li Ping , Sun Liping , Yuan Yuan 
Published: August 2012

Abstract
Serum PG I and PG I /PGII levels seemed to be related to the functional changes in the stomach, and their use as ‘serological biopsy’ in gastric cancer and precancerous diseases has been reported over 20 years. But the dynamic expression of pepsinogen I in situ of gastric mucosa and the value to detect gastric cancer and precancerous diseases, relative to the serum pepsinogen I is still unclear. Helicobacter pylori is a gram-negative bacterium that colonizes the stomach. More than 50% of the adult population are infected with H. pylori worldwide. Numerous studies have reported that healthy volunteers and gastric ulcer patients with H pylori infection have increased serum pepsinogen I levels which decrease after H pylori eradication. The evidence whether expression of pepesinogen I in situ affected by H pylori infection is not available. We thus conducted this study to investigate the dynamic expression of pepsinogen I in superficial gastritis, atrophic gastritis, gastric cancer and also H.pylori-associated gastric lesions and evaluate the application value of pepsinogen I in classifying gastric cancer and its precancerous diseases, and also the influence of H pylori on pepsinogen I expression. The expression of pepsinogen I was determined by immunohistochemistry method in 185 cases with mucosa taken from gastric corpus as well as from antrum. H.pylori infection was determined by histological examination and ELISA. Serum pepsinogen I and II were determined by ELISA. We found that Pepsinogen I was only expressed in the gastric corpus. There were 185 cases from gastric corpus and the positive rate of pepsinogen I expression in superficial gastritis, atrophic gastritis and gastric cancer decreased significantly in sequence (P&lt;0.05;100% vs. 83.3%vs0.0%), and the over-expression rate also decreased along with the sequence: normal, superficial gastritis, atrophic gastritis and gastric cancer (p&lt;0.05; 93.3%vs72.9% vs22.2vs0.0%). The over-expression rate of pepsinogen I in superficial gastritis with H pylori infection was higher than that without H pylori infection (P=0.035; β2 = 4.46).The serum expression of Pepsinogen I had no statistical difference (P&gt;0.05) and the ratio of sPGA to sPGC decreased along with the above groups. (P&lt;0.05). In conclusion, expression of PGI in situ has positive correlation with the degree of malignancy of gastric mucosa. and it is good biomarker for the diagnosis of gastric cancer and precancerous diseases. Also, The expression of PGI has positive correlation with H.pylori infection, and maybe is an important part in the H pylori- related damage or a good marker for screening H.pylori infection.
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 3606. doi:1538-7445.AM2012-3606
Abstract 3612: Detection and quantification of tumor-derived microparticles in a murine orthotopic tumor progression model
Authors: Korman Abraham , Green Lisa , White Sandy , Burch John , Clutinger Catherine , Li Li , Neubauer Blake L. , Landschulz Katherine T. 
Published: August 2012

Abstract
Approximately 85% of newly identified pancreatic cancer patients are estimated to die within one year of diagnosis. This poor prognosis is attributable in part to inadequate early detection methods, with the presence of pancreatic cancer often becoming evident only upon metastasis. Development of non-invasive early detection technologies that permit earlier initiation of treatment might increase the likelihood of patient survival. Our research centered on the task of developing a method for the detection of tumor-derived microparticles (MPs) using a murine orthotopic pancreatic tumor model. MPs are 100nm to 1.5µm membrane blebs released from cells via budding upon cell activation or during apoptosis which then circulate in the bloodstream. Cell-derived MPs retain characteristics, including cell surface antigens, of their parent cells. These antigens serve as cellular “fingerprints” of MP origin. In this way, the presence of cell-specific (e.g. tumor-specific) MPs signals the presence of a tumor, and therefore, serves as a biomarker of disease. The Mia-Paca-2 human pancreatic cell line expresses the cell surface tumor marker MUC-1 and this model has been widely used as a murine xenograft model to evaluate experimental therapeutics. In a novel orthotopic model of tumor growth, 5x106 Mia-Paca-2 cells were injected directly into the pancreas of athymic nude mice, while control mice were sham-injected. Treated and control mice groups of mice were sacrificed every two weeks for 8 weeks, at which points, each pancreas was weighed, tumor weight calculated, and blood drawn. Blood-derived MUC-1 expressing MPs were enriched from a subset of Mia-Paca-2-injected mice representing treatment and compared by flow cytometry with MPs enriched from control mice. Our findings suggested a correlation between tumor size and the concentration of detected MPs in early time-points following injection of tumor cells. This relationship changed with advanced tumor progression, where a significant drop in detectable MPs was observed. These preliminary findings support the contention that measurement of circulating tumor-derived MPs may be used for the early detection of pancreatic cancer. While sensitivity remains to be confirmed and further characterization is needed, this potentially translational method is non-invasive and compatible with multiple, longitudinal measurements. Further work will be needed to elucidate the relationship between MPs generation and tumor growth, and the relationship between MPs and metastatic tumor progression.
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 3612. doi:1538-7445.AM2012-3612
Abstract 3616: Validation and fitness testing of a quantitative immunoassay for HIF1α in biopsy specimens
Authors: Park Sook Ryun , Kinders Robert J. , Khin Sonny , Hollingshead Melinda , Parchment Ralph E. , Tomaszewski Joseph E. , Doroshow James H. 
Published: August 2012

Abstract
HIF1α is an important marker of hypoxia in human tumors that is altered in a number of cancers, but a reproducible method to determine changes in HIF1α protein expression in human tumor biopsy specimens has not been available. While HIF1α is being used as a pharmacodynamic marker in clinical trials in the NCI (CTEP# 8610, 8856, 8880), an important limitation in measuring the change in HIF1α induced by cancer therapeutic agents is the lability of the protein, in the presence of oxygen, upon collection of the sample. We have devised a method of specimen collection, handling, and extraction that preserves and stabilizes HIF1α levels in tumor biopsies. Degassed collection buffer yielded a significant increase of recovered HIF1α levels compared to the standard method of flash-freezing. The addition of 2-hydroxyglutarate, an inhibitor of prolyl hydroxylase domain enzyme that is involved in the degradation pathway of HIF1α under normoxic conditions, to the collection buffer showed a trend for improved yield of the HIF1α recovery. Sonication and homogenization with ceramic beads were superior to homogenization with metallic beads or tissue grinding. Employing this specimen-handling method allowed validation of a two-site immunoassay for HIF1α quantitation in solid-tissue extracts generated from tumor biopsies. Intra-assay variability was less than 10%, and inter-assay variability was less than 20%. Accuracy, assessed by spike recovery, was 99 +/− 7%. HIF1α readings declined linearly with decreasing sample load over a range of 1 to 10 µg protein per well. Fitness for purpose was demonstrated by quantifying a reduction in HIF1α protein levels following topotecan or indenoisoquinoline NSC 743400 treatment in an A375 xenograft model, followed by assessment of other xenograft models. HIF1α was also demonstrated to be upregulated under low oxygen tension culture conditions in DU145 human prostate cancer cells. Funded by NCI Contract No. HHSN261200800001E.
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 3616. doi:1538-7445.AM2012-3616
Abstract 3618: Rapid and quantitative lateral flow point-of-care Therapeutic Drug Monitoring (TDM) assays for LH and FSH
Authors: Hwang Larn , Hsiao Chao , Motamed Kouros , Trieu Vuong 
Published: August 2012

Abstract
Introduction: Hormone manipulation therapies, such as long-acting gonadotropin-releasing hormone (GnRH) agonists, are used in the treatment of estrogen-dependent forms of breast cancer, as well as prostate cancer, because down-regulation of Luteinizing Hormone (LH) and Follicle Stimulating Hormone (FSH) leads to a decline in hormonal support to the ovary and testis. Effectiveness of hormone manipulation therapies can be monitored by quantitation of LH and/or FSH. Methods & Results: Traditionally, these hormones are measured by ELISA assays that require blood to be drawn at either a doctor's office or a diagnostic laboratory. Here, we describe the development of rapid point-of-care tests for detection of these hormones that are quantitative and applicable to plasma, serum, as well as urine. These assays exhibit dynamic ranges of 17-170 mIU/ml for LH and 0.01-10 IU/ml for FSH. They exhibit linear correlation between nominal and actual values, with correlation coefficients greater than 0.95. They comply with FDA guidance for bioanalytical assays. And they utilize cassettes that are read using an optical reader with radio-frequency identification (RFID) capability, and the data can be printed out or stored on the reader for uploading onto the hospital database. The reader utilizes confocal optics with a low distance-to-target ratio. The reflectometric measurement is converted to activity units, using an established calibration curve embedded in the RFID. The cassettes are made to be stable for up to 72 hours and can be shipped to a central lab or doctor's office for quantitation if the patient does not have access to the reader. Conclusion: Rapid and quantitative point-of-care tests (POCTs) for LH and FSH have been developed for field deployment directly at home, and the cassettes can be read directly by the patient or can be shipped to the central lab/doctor's office for reading. As TDM, these tests should allow for more effective dosing of the patients and thereby improving effectiveness of hormone manipulation therapy. The tests are also patient-centric, inviting better compliance and patient participation in personalizing his/her treatment. The simplicity of the assays would allow for their deployment in underdeveloped regions lacking access to central laboratories with specialized and expensive equipments. Clinical studies are ongoing to evaluate the usefulness of these assays.
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 3618. doi:1538-7445.AM2012-3618