bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 4684: Medical providers perceive a lack of trust in the medical system leads to suboptimal esophageal cancer care for African American patients
Authors: Sarwar Sumaiya , Kemp Michael T. , Revels Sha'Shonda L. , Eilender Benjamin M. , Houtschilt Steven R. , Akateh Clifford , Reddy Rishindra M. 
Published: May 2015

Abstract
Background: Although patient outcomes for esophageal cancer have improved, there remains a reduced survivorship among African Americans compared to Caucasians, possibly due to lower use of surgery in African Americans. While various factors contribute to this disparity, we noted a decreased referral of African American patients to thoracic surgeons in our institution. We hypothesized that interviews with medical providers would provide the reasons behind the barriers that hinder the ability of minority patients to receive optimal care for esophageal cancer.
Methods: Providers (n=20) in the Detroit Metro area that treat African Americans with esophageal cancer participated in 30-minute semi-structured interviews to elicit their perspectives regarding barriers and facilitators in their care for this population. The interview inquired into the challenges faced and techniques employed by providers in establishing trust within this population. Interviewed providers included thoracic surgeons, medical oncologists, gastroenterologists, and radiation oncologists.
Results: Most providers suggested that socioeconomic status, not race, was the primary barrier to accessing adequate cancer care. Within the African American population, 80% of providers reported that mistrust was not an issue in their personal experiences in treating minorities with esophageal cancer, but 95% of providers cited mistrust in the medical system as a contributing factor to unfavorable outcomes. Providers who indicated mistrust in the medical system referred to historical instances that may deter African American patients from trusting the medical system. Many also cited techniques for establishing trust including honesty and patient empowerment. Finally, 3 of 20 respondents referred to direct experiences where patient refusal to participate in clinical trials may have contributed to poorer outcomes.
Conclusions: Medical providers believe that mistrust in the medical system is a key barrier for African American patients with esophageal cancer to receive optimal care. Further investigation to elicit patient perspectives should be explored through direct patient surveys. Particular attention should be directed toward how African Americans' trust of the medical community affects the use of surgical treatment for esophageal cancer.
Citation Format: Sumaiya Sarwar, Michael T. Kemp, Sha'Shonda L. Revels, Benjamin M. Eilender, Steven R. Houtschilt, Clifford Akateh, Rishindra M. Reddy. Medical providers perceive a lack of trust in the medical system leads to suboptimal esophageal cancer care for African American patients. [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 4684. doi:10.1158/1538-7445.AM2014-4684
Abstract 4688: Novel prognostic subtype of hepatocellular carcinoma reflecting stem/maturational status of the tumor defined by Gd-EOB-DTPA-enhanced MRI and serum AFP
Authors: Yamashita Taro , Honda Masao , Kaneko Shuichi 
Published: May 2015

Abstract
Survival of patients with hepatocellular carcinoma (HCC) varies on an individually basis, even after surgery for early-stage tumors. Gadolinium ethoxybenzyl diethylenetriamine pentaacetic acid (Gd-EOB-DTPA)-enhanced magnetic resonance imaging (EOB-MRI) has recently been introduced to evaluate hepatic lesions with regard to the activity of the organic anion transporter OATP1B3 as well as vascularity. Here we report that Gd-EOB-DTPA-Enhanced MRI and serum alpha-fetoprotein (AFP) status reflects the stem/maturation status of HCC with distinct biology and prognostic information. Atypical uptake of Gd-EOB-DTPA in the hepatobiliary phase was observed in ∼ 15% of HCCs. This uptake correlated with the low serum alpha-fetoprotein (AFP) levels, maintenance of hepatocyte function with the up-regulation of OATP1B3 and HNF4A, and good prognosis. In contrast, HCC showing reduced Gd-EOB-DTPA uptake with high serum AFP presented poor prognosis with the activation of an oncogene FOXM1. Knockdown of HNF4A in cancer cells, obtained from a surgically resected HCC showing atypical uptake of Gd-EOB-DTPA, resulted in the increase of AFP and FOXM1 and the loss of OATP1B3 expression accompanied with the mesenchymal morphological changes, enhanced cell proliferation and tumorigenesis in vivo. HCC classification based on EOB-MRI and serum AFP level (EOB-AFP classification) predicted overall survival in a retrospective cohort (n = 70), and its prognostic utility was validated in a multi-institution cohort of early-stage HCCs (n = 109). This non-invasive classification system is molecularly based on the stem/maturation status of HCCs and can be incorporated into current staging to improve management algorithms, especially in early stage.
Citation Format: Taro Yamashita, Masao Honda, Shuichi Kaneko. Novel prognostic subtype of hepatocellular carcinoma reflecting stem/maturational status of the tumor defined by Gd-EOB-DTPA-enhanced MRI and serum AFP. [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 4688. doi:10.1158/1538-7445.AM2014-4688
Abstract 4695: Role of KITENIN in malignant gliomas in relation to tumor invasiveness
Authors: Lee Kyung-Hwa , Moon Kyung-Sub , Ahn Eun-Jeong , Oh Se-Jeong , Cho Sang-Hee , Lee Jae-Hyuk , Jung Shin , Kim Kyung Keun 
Published: May 2015

Abstract
Background: KAI1 C-terminal interacting tetraspanin (KITENIN) has been reported to promote tumor invasion and metastasis in various cancers. The aim of this study was to investigate the effect of KITENIN on biological behaviors in human gliomas and in mouse glioma models.
Methods: KITENIN expression was examined using western blot, qRT-PCR and immunohistochemistry on human samples. KITENIN expression rate was compared in each histological grade, and survival rates were analyzed. Tumor invasiveness was investigated both in vitro and in vivo using stable cell lines after KITENIN-overexpression (GL261) and knock down (U251).
Results: Expression of KITENIN tended to be stronger in high-grade gliomas than in low-grade gliomas by western blot & qRT-PCR on frozen human tumor samples and by immunohistochemistry on paraffin-embedded tissues as well. Proportions of strong KITENIN expression were 16.7%, 21.4%, 33.3%, and 56.8%, respectively, from grade I through IV (p=0.001). However, survival analysis using the Kaplan-Meier method did not reveal statistically significant difference between the high KITENIN expression group and the low expression group in terms of overall survival and progression free survival (p=0.55 and 0.807, respectively). In vitro assays revealed that genetic modulation of KITENIN was significantly related with tumor cell invasion & migration. Up-regulated KITENIN expression significantly affected the survival rate possibly due to increased invasiveness in orthotopic mouse glioma models.
Conclusion: Strong KITENIN expression was more likely to be observed in high-grade gliomas and its up-regulation was associated with increased invasiveness supported by shorter survival rates in orthotopic mouse glioma models.
Citation Format: Kyung-Hwa Lee, Kyung-Sub Moon, Eun-Jeong Ahn, Se-Jeong Oh, Sang-Hee Cho, Jae-Hyuk Lee, Shin Jung, Kyung Keun Kim. Role of KITENIN in malignant gliomas in relation to tumor invasiveness. [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 4695. doi:10.1158/1538-7445.AM2014-4695
Abstract 4701: Acquisition of Oct-4 upregulation transactivates MDR1 and is associated with increased tumor recurrence in bladder cancer
Authors: Lu Chia-Sing , Shiau Ai-Li , Shieh Gia-Shing , Su Bing-Hua , Su Wu-Chou , Yang Wen-Horng , Wu Chao-Liang 
Published: May 2015

Abstract
Platinum-based drug like cisplatin is the standard first-line drug to treat patients with bladder cancer. However, tumors may recur and develop into multiple-drug resistant characteristics. The acquisition of resistance to conventional chemotherapy is a challenge in the treatment of bladder cancer relapse. Cancer stem cell (CSC) hypothesis has been an attractive theory. CSCs can resist therapeutic assaults, giving rise to multiple drug resistance and promotion of tumor relapse and metastasis. It has been shown that the fraction of cancer cells expressing MDR1 that functions as an energy-dependent drug efflux pump may be associated with Oct-4 expression. We have demonstrated that Oct-4 expression in bladder cancer predicts tumor progression. In the present study, we proposed that Oct-4 expression in bladder cancer increases MDR1 gene expression and thereby results in multiple drug resistance. We found a positive correlation between Oct-4 and MDR1 expression levels in clinical samples of bladder cancer. Furthermore, overexpression of Oct-4 increased MDR1 expression, which resulted in poor response to cisplatin in human bladder transitional cell carcinoma cells. Conversely, knockdown of Oct-4 reduced MDR1 expression and rendered cells hypersensitive to cisplatin. We also verified that Oct-4 transactivated the MDR1 gene promoter by binding to the Oct-4 response element (ORE). More importantly, Oct-4 and MDR1 gene expression could be induced by treatment with cisplatin, suggesting that Oct-4 is a member of the MDR1 enhanceosome. Our data can explain, in part, the high recurrence rate and drug resistance of bladder cancer. For clinical implication, we demonstrated that reduction of Oct-4 expression by all-trans retinoic acid, a derivative of vitamin A, improved sensitivity of bladder cancer cells to gemcitabine and cisplatin. In addition, we found that high expression levels of Oct-4 and MDR1 were associated with high tumor recurrence. Taken together, our results provide evidence that Oct-4 plays an important role in cisplatin-acquired resistance in bladder cancer. They also implicate Oct-4 as a therapeutic target.
Note: This abstract was not presented at the meeting.
Citation Format: Chia-Sing Lu, Ai-Li Shiau, Gia-Shing Shieh, Bing-Hua Su, Wu-Chou Su, Wen-Horng Yang, Chao-Liang Wu. Acquisition of Oct-4 upregulation transactivates MDR1 and is associated with increased tumor recurrence in bladder cancer. [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 4701. doi:10.1158/1538-7445.AM2014-4701
Abstract 4702: Caveolin-1 confers a multi-modality therapy resistance phenotype in pancreatic cancer cells
Authors: Chatterjee Moumita , Williams Terence M. 
Published: May 2015

Abstract
Caveolin-1 (Cav-1) is a 21kDa protein found in 50-100nm omega-shaped invaginations of the plasma membrane known as caveolae. It has been implicated in the processes of oncogenic cell transformation, tumorigenesis and metastasis. Cav-1 is upregulated in pancreatic cancer and has been shown to be correlated with poor prognosis. We hypothesized that Cav-1 promotes resistance to chemotherapy and radiation, and that downregulation may lead to sensitization to radiation and/or chemotherapy. We found that radiation and chemotherapy up-regulate Cav-1 expression, and that downregulating Cav-1 in multiple pancreatic cancer cell lines by small interfering RNA induces sensitization to chemotherapeutics such as gemcitabine and 5-fluorouracil. Furthermore, genetic knockdown causes reduction in tumor cell proliferation and colony formation. Knockdown of caveolin-1 also led to radiosensitization of tumor cells and resulted in delayed DNA repair as demonstrated by delayed pH2.AX foci resolution, increased mitotic catastrophe, as well as decreased formation of BRCA1 and DNAPK-cs foci in the nuclei of these cells. Furthermore, Cav-1 loss promoted cleavage of Caspase-9 and PARP after treatment with gemcitabine. These results indicate that knocking down Cav-1 in pancreatic cancer cells sensitizes them to radiation with delayed DNA damage repair and also to chemotherapeutics with the onset of apoptosis. In vivo, stable knockdown of Cav-1 attenuated the rate of tumor growth significantly compared to control tumors in subcutaneous xenograft pancreatic tumors. In summary we conclude that Cav-1 is responsible in promoting resistance to radiation and chemotherapy in pancreatic cancer cells and that downregulation of this protein leads to improved therapeutic response. Thus, it is possible that caveolin-1 may serve as a prognostic predictive biomarker in pancreatic cancer patients for response to radiation and chemotherapy.
Citation Format: Moumita Chatterjee, Terence M. Williams. Caveolin-1 confers a multi-modality therapy resistance phenotype in pancreatic cancer cells. [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 4702. doi:10.1158/1538-7445.AM2014-4702
Abstract 4709: ERK1/2 regulates hepatocellular carcinoma through proinflammatory homeobox gene, ISX
Authors: Wang Shen-Nien , Hsu Shih-Hsien 
Published: May 2015

Abstract
Intestine-specific homeobox (ISX), a newly identified proto-oncogene, regulated cell proliferation and drives hepatocellular carcinoma (HCC) formation but the underlying mechanisms linking gene expression and tumor formation remain obscure. In this study, we compared the expression of MAPK (ERK1/2), E2F1 and homeobox gene ISX in 190 paired specimens of HCC and adjacent normal tissues, and also in paired specimens from 11 non-HCC patients. In pathological analysis, ERK1/2 and E2F1 , as ISX expression, exhibited a tumor-specific expression pattern and a high correlation to patient survival time, tumor size, tumor number and progression stage. Enforced expression of ERK1/2 translocated cytoplasm ISX into nucleus and increased cell proliferation by which increased downstream E2F1 expression in hepatoma cells through ISX induction. In contrast, dominant negative ERK1/2 and shRNA-mediated attenuation of ERK1/2 in hepatoma cells decreased nucleus translocation, cell proliferation and malignant transformation in vitro and in vivo. A high positive correlation existed in human hepatoma tumors between ISX and ERK1/2 expression. Together, our results highlight ERK1/2 as an important regulator of ISX in hepatoma progression with significant potential as a prognostic and therapeutic target in HCC.
Citation Format: Shen-Nien Wang, Shih-Hsien Hsu. ERK1/2 regulates hepatocellular carcinoma through proinflammatory homeobox gene, ISX. [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 4709. doi:10.1158/1538-7445.AM2014-4709
Abstract 4712: Personalized ovarian cancer surveillance and detection of a therapeutic drug target in circulating tumor DNA
Authors: Martignetti John A. , Camacho-Vanegas Olga , Priedigkeit Nolan , Camacho-Vanegas Catalina , Pereira Elena , Lin Li , Losic Bojan , Shah hardik , Liao Jun , Ma Jian , Lahiri Pratik , Chee Mark , Schadt Eric , Dottino Peter 
Published: May 2015

Abstract
Retrospective studies have demonstrated that nearly 50% of ovarian cancer patients with normal CA125 levels have persistent disease; however, prospectively distinguishing between patients is currently impossible. Here we demonstrate that for one patient, with the first reported FGFR2 fusion transcript in ovarian cancer, circulating tumor DNA (ctDNA) is a more sensitive and specific biomarker than CA125 and it can also inform on a candidate therapeutic. Over a four year period, during which the patient underwent primary debulking surgery and chemotherapy, tumor recurrences and multiple chemotherapeutic regimens, blood samples were longitudinally-collected and stored. Whereas post-surgical CA125 levels were elevated only three times over 28 measurements, the FGFR2 fusion ctDNA biomarker was readily detectable by qtRT-PCR in all of these same blood samples and in the tumor recurrences. Given the persistence of the FGFR2 fusion, we treated tumor cells derived from this patient and other with the FGFR2 inhibitor BGJ398. Only tumor cells derived from this patient were sensitive to FGFR2 inhbitor treatment. Using the same overall approach, ctDNA is demonstrated in other patients and the results compared to CA125. Taken together, we demonstrate that a relatively inexpensive, PCR-based ctDNA surveillance assay can outperform CA125 in identifying occult disease. To our knowledge, this use of a personalized biomarker represents the first example in ovarian cancer demonstrating the presence of continuous occult disease in the face of negative clinical, radiologic and biochemical examination. Moreover, the recent identification of FGFR fusions in other solid cancers suggests a broader application of this strategy beyond ovarian cancer.
Citation Format: John A. Martignetti, Olga Camacho-Vanegas, Nolan Priedigkeit, Catalina Camacho-Vanegas, Elena Pereira, Li Lin, Bojan Losic, hardik Shah, Jun Liao, Jian Ma, Pratik Lahiri, Mark Chee, Eric Schadt, Peter Dottino. Personalized ovarian cancer surveillance and detection of a therapeutic drug target in circulating tumor DNA. [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 4712. doi:10.1158/1538-7445.AM2014-4712
Abstract 4716: Discovery of biomarkers from highly enriched prostate cancer microparticles for prognostication of prostate cancer
Authors: Biggs Colleen N. , Guo Quiquan , Yang Jun , Chambers Ann F. , Chin Joseph L. , Power Nicholas , Leong Hon S. 
Published: May 2015

Abstract
Prostate cancer microparticles (PCMPs) are essentially fragments of tumor cells that are present in various bodily fluids such as plasma and urine. By using nanoscale flow cytometry, multiple biomarkers can be assessed on PCMPs in patient plasma, a convenient “fluid biopsy” for prostate cancer (PCa). Discovering biomarkers specific for metastatic PCMPs would establish a non-invasive fluid biopsy for detecting the earliest onset of metastatic disease for patients post-prostatectomy. Discovery of biomarkers specific to Gleason score 6 (3+3) and 8 (4+4) lesions that are decorated on the surface of PCMPs would help establish a non-invasvie fluid biopsy for tumor upstaging (i.e., Gleason 6 to 7) of patients placed on active surveillance who have deferred prostatectomy. We hypothesize that biomarkers specific for metastatic PCMPs or Gleason Score-specific PCMPs can only be discovered via proteomics analysis on highly purified PCMPs from plasmas which have minimal levels of non-target microparticles and plasma proteins. To do this, plasmas were incubated with biotinylated anti-PSMA mAb and PSMA+ve microparticles were isolated from plasma by using a magnetic column after several purification runs. Eluted samples were then submitted to nanoscale flow cytometry in which elution fractions that exhibited minimal non-target microparticle concentrations (&lt;1000 events/uL) were submitted to proteomics analysis. PCMPs from plasma samples representing localized (N=7, lymph node negative, PSA&gt;5 ng/mL, Gleason Score 3+3) and metastatic (N=7, confirmed bone metastases, PSA&gt;10 ng/mL, Gleason 4+4) were isolated, evaluated and submitted for iTRAQ labeling, high pH reversed phase fractionation and LC-MS/MS analysis. All data was analyzed using Proteome Discoverer 1.3 and MASCOT v2.3 software. Mass spectometry analysis revealed 8 proteins significantly upregulated and 5 proteins downregulated in the majority of metastatic plasma samples compared to localized plasma samples. Data was normalized to albumin levels by western blot and mass spectrometry. Based on these results, we have identified 8 proteins that may be specific for a subpopulation of PCMPs from metastatic PCa patients. Out of these, 6 may be candidates for flow cytometry because they are membrane-bound or are cytoskeletal elements potentially exposed to the extracellular space (CLIC1, PVR, YWHAE, KRT16, K1C10, KRT2).
Citation Format: Colleen N. Biggs, Quiquan Guo, Jun Yang, Ann F. Chambers, Joseph L. Chin, Nicholas Power, Hon S. Leong. Discovery of biomarkers from highly enriched prostate cancer microparticles for prognostication of prostate cancer. [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 4716. doi:10.1158/1538-7445.AM2014-4716
Abstract 4723: Prognostic significance of EGFR expression in localized gastric cancer
Authors: Park Ji Soo , Kim Hyo Song , Bae Yoon Sung , Noh Sung Hoon , Kim Hyunki 
Published: May 2015

Abstract
Background: The role of epidermal growth factor receptor (EGFR) expression as predictive or prognostic biomarker in gastric cancer is still in controversy. The aim of this study is to find prognostic role of tumor EGFR expression in gastric cancer patients after curative resection.
Methods: From January 2000 to September 2003, gastric cancer patients who received curative gastrectomy were included in this study. We retrospectively collected clinical characteristics and survival data of the patients, and analyzed EGFR expression on tissue microarrays from formalin-fixed paraffin-embedded specimens of primary tumor tissues by immunochemical staining (IHC). EGFR expression was scored to 0, 1+, 2+ or 3+ based on intensity of reactivity.
Results: Of total 937 patients, 295 (31.5%) patients, 101 (10.8%) patients and 36 (3.8%) patients showed EGFR 1+, 2+, and 3+ expression by IHC, respectively. EGFR overexpression (2+/3+) is more frequently found in intestinal type than diffuse or mixed type (24.2% vs. 5.1%, P&lt;0.001). In stage III disease according to AJCC 7th edition, unlike other stages, the patients with EGFR overexpression (2+/3+) had longer disease free survival (hazard ratio [HR], 0.639; 95% confidence interval [CI], 0.434-0.938; P=0.022) and longer overall survival (HR, 0.630; 95% CI, 0.445-0.890, P=0.009) than other patients in univariate analysis. Additionally, in 279 patients who had stage III gastric cancer with diffuse type histology and received 5-fluorouracil (5-FU) based adjuvant chemotherapy, EGFR overexpression was favorable prognostic marker for overall survival (HR, 0.365; 95% CI, 0.161-0.827; P=0.016) in multivariate analysis, while old age and lymphovascular invasion were poor prognostic factors.
Conclusion: EGFR overexpression was potentially favorable prognostic biomarker for stage III gastric cancer, especially in the patients who received 5-FU based adjuvant chemotherapy.
Citation Format: Ji Soo Park, Hyo Song Kim, Yoon Sung Bae, Sung Hoon Noh, Hyunki Kim. Prognostic significance of EGFR expression in localized gastric cancer. [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 4723. doi:10.1158/1538-7445.AM2014-4723