bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract B70: Perception of contraceptive use among black people infected with prostate cancer in high risk urban poor population in Africa
Authors: Odor King Odor 
Published: October 2015

Abstract
Prostate cancer is a growing public health challenge in Africa, the pandemic affects every individual including healthy person especially the black people. To combat sexually transmitted infections among prostate cancer infected black people, contraceptive-use is effective measure to interrupt any transmission. However, perception of black people about contraceptive usefulness has been limited to research. This study therefore examined prostate cancer among black population in Africa
The study was cross-sectional in design. A multi-stage-stratified-random-sampling technique were adopted to select 400 adults aged 25years and above in Nigeria. A pre-tested questionnaire developed from results of 10 focus-group-discussions (FGD) was used to collect information. FGD and questionnaire data were analyzed thematically and descriptively using chi-square statistics respectively.
Twenty-five percent of the participants who were sexually active, one year preceding the study had multiple premarital-sex. Among the subgroup that had multiple premarital-sex, only few (6.8%) used a contraception in the episode. More males (5.3%) than females (1.5%) used contraception in last premarital-sex (p&lt;0.5). Non-contraceptive use was due to confidence in traditional herbs perceived to prevent prostate cancer. Similarly, FGD participants were unanimous in their opinion visiting tradomedicine dealers and the believe (10.3%) herbs/concussion-use could prevent prostate cancer.
Risky sexual engagement among black people could be a distortion to prostate cancer reduction, because safe sex practices among this population was unimportant based on perception. In order to mitigate prostate cancer in Africa, information on safe-sex practices among young people are needed to address this misconception.
Note: This abstract was not presented at the conference.
Citation Format: King Odor Odor. Perception of contraceptive use among black people infected with prostate cancer in high risk urban poor population in Africa. [abstract]. In: Proceedings of the Seventh AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 9-12, 2014; San Antonio, TX. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2015;24(10 Suppl):Abstract nr B70.
Abstract B89: The significance of Vitamin D deficiency and anaerobes in prostate cancer
Authors: Oliver Tim , Blackburn Lucy , Chinegwundoh Frank 
Published: October 2015

Abstract
Objective: Long-term sun exposure estimates correlate with risk of PC possibly due to long-term Vitamin D deficiency diminishing macrophage function allowing persistence of low grade pathogens causing chronic inflammation leading to Proliferative Inflammatory Atrophy and then cancer. Recently infection with two low grade pathogenic organisms, teenage acne associated Vitamin D sensitive anaerobic bacterium Propionibacterium.acnes (PA) and protozoan Trichomonas vaginalis (TA), have been notable exceptions. This presentation reports a systematic review of reports on anaerobes, circumcision and the association of sun exposure in causation of PC and considers how these observations could contributing to increased PC in Africa
Methods: Pubmed searches using terms prostate or prostatic, sunshine or UVB or Vitamin D and acne or PA or TA were performed
Results: Two systematic reviews of PC and Vitamin D failed to produce a consistent association. 4/4 studies of index of long-term sun exposure involving 1568 patients and 9/12 geographic studies demonstrated that high UVB exposure reduced PC risk. 4/5 publications on PA and PC and 2/3 publications on TV and PC showed consistent increase risk of PC associated with infection. Ten studies involving 5681 patients demonstrated significant reduction of PC in circumcised individuals (OR 0.87), including one in African American Men showing lower incidence of circumcision possibly contributing to their higher frequency
Conclusion: Reduced long-term Vitamin D mediated non-specific macrophage surveillance against low-grade pathogenic anaerobes could explain these associations with PC and increasing urbanisation could be a factor in the health inequality as measured by prostate cancer incidence in African-American men.
Citation Format: Tim Oliver, Lucy Blackburn, Frank Chinegwundoh. The significance of Vitamin D deficiency and anaerobes in prostate cancer. [abstract]. In: Proceedings of the Seventh AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 9-12, 2014; San Antonio, TX. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2015;24(10 Suppl):Abstract nr B89.
Abstract IA17: The Cdk4/E2F pathway drives centrosome amplification and chromosome instability in breast cancer cells
Authors: Saavedra Harold I. 
Published: October 2015

Abstract
Chromosome instability (CIN) instigates various malignant phenotypes, including deregulated proliferation, apoptosis and invasion to initiate and sustain carcinogenesis. A major source of CIN in cancer is centrosome amplification (CA), defined as the acquisition of abnormal number of centrosomes (3 or more) that may result in defective mitosis, chromosome missegregation and aneuploidy. CA is present in pre-malignant breast lesions and high percentages of CA correlate with metastasis to the lymph nodes. CA may facilitate breast tumorigenesis, albeit this hypothesis has to be tested. Our laboratory found that CA and binucleation, intermediates to tetraploidy, are more likely to occur in Her2+ER-PR- (Her2+) breast cancers, while triple-negative (TN or Her2-ER-PR-) display other forms of CIN, such as micronuclei, defined as missegregated whole or fragmented chromosomes. The Her2 and TN subtypes differ from good-prognosis breast cancers such as luminal in that they accumulate high frequencies of CIN. Even though all breast cancer patients respond similarly to radiation therapy, Her2+ and TN patients are more likely to recur. Our laboratory searches for sources of CA and CIN in breast tumors and found that CA and CIN are suppressed by silencing of Cdk4 and the E2F activators. We have shown that silencing of CDK4 radiosensitizes TN and Her2+ breast cancer cells by activating intrinsic apoptotic pathways. We propose that inhibiting the cell and centrosome machinery would represent future treatment modalities for breast cancer.
Citation Format: Harold I. Saavedra. The Cdk4/E2F pathway drives centrosome amplification and chromosome instability in breast cancer cells. [abstract]. In: Proceedings of the Seventh AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 9-12, 2014; San Antonio, TX. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2015;24(10 Suppl):Abstract nr IA17.
Abstract IA27: The changing landscape of U.S. cancer survivorship
Authors: Ramirez Amelie G. 
Published: October 2015

Abstract
More people are surviving cancer than ever, with nearly 14.5 million cancer survivors currently living in the United States, according to federal statistics. That number is expected to reach 19 million by 2024, largely due to increases in cancer diagnoses in an aging population and advances in cancer treatment and early detection. In 2005, the Institute of Medicine released From Cancer Patient to Cancer Survivor: Lost in Translation, a landmark report that highlighted a lack of best practices in caring for survivors. Since that report, several initiatives have been implemented to address the needs of the growing survivor population. However, the cancer survivorship experience isn't the same in all populations. Within medically underserved racial/ethnic populations there are several factors that impact the survivorship experience and quality of life during the survivor period. This presentation will serve as an introduction into the survivorship experiences of different racial/ethnic groups as well as some of the challenges around measuring health related quality of life within these groups.
Citation Format: Amelie G. Ramirez. The changing landscape of U.S. cancer survivorship. [abstract]. In: Proceedings of the Seventh AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 9-12, 2014; San Antonio, TX. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2015;24(10 Suppl):Abstract nr IA27.
Abstract A07: Decline in the growth of murine T-cell lymphoma via modulation of PI3K signaling pathway: Key role of quercetin and PI-103
Authors: Maurya Akhilendra Kumar , Vinayak Manjula 
Published: October 2015

Abstract
Deregulation in cell proliferation, oxidative status, antiapoptosis and survival are involved in development of cancer. The cellular signaling cascades mediated by Phosphatidylinositol 3-kinase (PI3K) with their ability to stimulate cell proliferation and suppress apoptosis, has been considered to play key role in tumor initiation, promotion, and progression. Therefore, use of inhibitors or antioxidants like natural flavonoids could be promising strategy to target PI3K pathway for suppression of carcinogenic process. The present study was aimed to investigate the anti-cancer activity of quercetin, a natural flavonoid and PI-103, a synthetic inhibitor in transplantable murine T-cell lymphoma. Cytotoxicity, apoptotic potential, cell survival, cell proliferation as well as antioxidant defense are evaluated in ascite cells of murine T-cell lymphoma in vivo and in primary culture. Significant decline in level of AKT1, PKCα, COX 2 as well as regulatory domain of PI3K (p85α), AKT1 and Bad, suggested implication of quercetin in regression of lymphoma by down regulation of cell proliferation and survival. Improvement of active PKCδ, p53, active caspase 3, 9 and cleaved PARP supported its cell apoptotic mechanism in cancer prevention. Additionally, decreased ROS level and LDH A activity contributes to reduced survival of cancer cells. Inhibition of p110α by PI-103 resulted in suppression of phospho-AKT and p85α level in primary culture. Modulation of various molecular targets including PI3K/AKT signaling by quercetin and PI-103 in vitro and in vivo tumor models suggests the importance and contribution of antioxidant quercetin in the prevention of cancer.
Citation Format: Akhilendra Kumar Maurya, Manjula Vinayak. Decline in the growth of murine T-cell lymphoma via modulation of PI3K signaling pathway: Key role of quercetin and PI-103. [abstract]. In: Proceedings of the AACR Special Conference: Targeting the PI3K-mTOR Network in Cancer; Sep 14-17, 2014; Philadelphia, PA. Philadelphia (PA): AACR; Mol Cancer Ther 2015;14(7 Suppl):Abstract nr A07.
Abstract A11: Crosstalk between mTORC1 and estrogen receptor in breast cancer
Authors: Alayev Anya , Salamon Rachel S. , Holz Marina K. 
Published: October 2015

Abstract
Approximately two thirds of all breast cancer cases are estrogen receptor (ER) positive, which underscores the dependence of cancer cells on estrogen for growth and survival. However, resistance to endocrine therapy develops in most cases. mTORC1 (the mechanistic target of rapamycin complex 1) is a critical node of estrogen signaling in the cell, however the mechanism of estrogen activation of mTORC1 is not well understood. We have previously demonstrated that mTORC1 promotes growth factor-mediated ER activation by phosphorylating ERα on Ser167. This phosphorylation, which is mediated by the mTORC1 effector kinase S6K1, is important for ERα dimerization, DNA binding and transcriptional activity, is associated with endocrine resistance and correlates with therapy response. Moreover, ERα promotes expression of S6K1, generating a feed-forward positive activation loop. Our current efforts are focused on fully understanding the nature and mechanism of the relationship between mTORC1 and estrogen pathways. Our data indicate that mTOR, raptor and ER form a complex whereby ER directly interacts with raptor. Moreover, this interaction is stimulated by estrogen as seen by co-immunoprecipitation analysis. We additionally found that ER and raptor co-localize to the nucleus upon estrogen stimulation, where they interact as detected by both immunofluorescence and cellular fractionation experiments. Our current efforts are focused on understanding the role of this interaction and the mechanism of estrogen mediated localization of raptor to the nucleus. We are also investigating the role of raptor and estrogen receptor interaction in endocrine therapy treatment and resistance.
Citation Format: Anya Alayev, Rachel S. Salamon, Marina K. Holz. Crosstalk between mTORC1 and estrogen receptor in breast cancer. [abstract]. In: Proceedings of the AACR Special Conference: Targeting the PI3K-mTOR Network in Cancer; Sep 14-17, 2014; Philadelphia, PA. Philadelphia (PA): AACR; Mol Cancer Ther 2015;14(7 Suppl):Abstract nr A11.
Abstract A25: Effect of Rab25 on Akt1 phosphorylation
Authors: Buyru Nur , Seven Didem , Dogan Soydan , Koseoglu Hikmet , Karaman Emin 
Published: October 2015

Abstract
Head and neck squamous cell carcinoma (HNSCC) is a heterogeneous disease and despite therapeutic improvements and reconstructive modalities, the overall survival rate remains relatively poor. Although, tobacco and alcohol consumption are recognized as critical risk factors, genetic and epigenetics factors and viral infections also contribute to the progression of HNSCC. Several studies have assessed the status of known oncogenes and tumor suppressor genes to identify novel genomic events in HNSCC.
Rab25 belongs to the Rab family of small GTPases. Rab25 has been described in conflicting previous studies as a promoter or suppressor of cancer. More recently, Zhang et al. reported that overexpression of Rab25 contributes to metastasis through activation of the Akt/GSK-3β/Snail pathway signaling in bladder cancer, which act as molecular switches that belong to the Ras protein superfamily and regulate vesicle trafficking in eucaryotic cells.
The phosphotidylinositol 3-Kinase (PI3K) signaling pathway plays a critical role in cellular growth, proliferation and survival. Signaling through this pathway is commonly upregulated during tumorigenesis. Akt/PKB is a Ser/Thr kinase and the central member of the PI3K/Akt signaling pathway. It is activated by phosphorylation and subsequently phosphorylates diverse growth –controlling effectors and regulates the synthesis, stability and subcellular localization of cell cycle regulators.
In this study, we investigated the phosphorylation of Akt1 and whether it occurs under the effect of Rab25 expression in HNSCC.
For this purpose we analyzed the Rab25 protein by Western Blot in 57 HNSCC tumors and corresponding non-cancerous tissue samples. To detect the effect of the Rab25 protein on Akt1 activation we also analyzed the amount of total Akt1 and phosphorylated Akt1 in the same tissue samples. Our results indicate that Rab25 is down-regulated in 56.2% of the HNSCC tumor samples compared to their normal counterparts. On the other hand, the change in Akt1 phosphorylation was in the same direction with Rab25 protein expression (p: 0.04)
Citation Format: Nur Buyru, Didem Seven, Soydan Dogan, Hikmet Koseoglu, Emin Karaman. Effect of Rab25 on Akt1 phosphorylation. [abstract]. In: Proceedings of the AACR Special Conference: Targeting the PI3K-mTOR Network in Cancer; Sep 14-17, 2014; Philadelphia, PA. Philadelphia (PA): AACR; Mol Cancer Ther 2015;14(7 Suppl):Abstract nr A25.
Abstract A32: Cell dormancy and tumorigenicity due to PTEN loss
Authors: Thompson Keyata N. , Whipple Rebecca A. , Charpentier Monica S. , Boggs Amanda E. , Bhandray Lekhana , Chakrabarti Kristi R. , Martin Stuart S. , Vitolo Michele I. 
Published: October 2015

Abstract
Breast cancer is the most frequent malignancy in women, and although many breast cancers are curable via surgery, approximately one quarter maintain a latent and insidious characteristic of slow growth with early metastasis. The loss of the tumor suppressor PTEN is associated with breast cancer stage, increased lymph node status, and disease-related death, and the high rate of loss in primary tumors suggests a potential role in initiation and/or progression of the disease. However, specific cellular alterations in human breast epithelium controlled by PTEN inactivation, which lead to an increased metastatic phenotype, remain poorly defined. Many breast cancers have an activated PI3K pathway either due to PTEN loss or PI3K mutation, while a large fraction of breast tumors carry oncogenic mutations that cause hyperactivation of the MAPK/ERK cascade (20%–25% ErbB2, 5% KRAS, 2% BRAF, 1% HRAS, 1% NRAS). Using the isogenic non-tumorigenic MCF-10A and MCF-10A PTEN-/- cells, we have determined that PTEN-/- cells persist in mouse xenografts while their isogenic counterparts disappear. Although the PTEN-/- cells form small, 2mm tumors, these cells do not produce large growths. Since the current view of cancer is based on a “multi-hit” hypothesis: human cancers display a multitude of genetic and epigenetic changes, and a number of such alterations are required for the step-wise progression of tumor development, the activation of both signaling pathways may cooperate to promote tumorigenesis. We therefore tested the hypothesis that the activation of the MAPK pathway in a PTEN-negative background promotes tumorgenicity. To determine the cooperativity of PTEN loss and the MAPK pathway, we have expressed activated KRAS(V12) in the MCF-10A PTEN-/- cells. The combination of PTEN loss and KRas(V12) expression resulted large tumors within 4 weeks of injection. Interestingly, we discovered that “one-hit” of either PTEN loss or active Ras leads to a cellular persistence in vivo, a characteristic that may have been previously overlooked in more genetically unstable tumor cells.
Citation Format: Keyata N. Thompson, Rebecca A. Whipple, Monica S. Charpentier, Amanda E. Boggs, Lekhana Bhandray, Kristi R. Chakrabarti, Stuart S. Martin, Michele I. Vitolo. Cell dormancy and tumorigenicity due to PTEN loss. [abstract]. In: Proceedings of the AACR Special Conference: Targeting the PI3K-mTOR Network in Cancer; Sep 14-17, 2014; Philadelphia, PA. Philadelphia (PA): AACR; Mol Cancer Ther 2015;14(7 Suppl):Abstract nr A32.
Abstract A34: GDC-0980, a dual PI3K/mTOR inhibitor, selectively inhibits NF2 mutant malignant mesothelioma (MM) cells and inhibits TOR signaling without activating Akt or ERK
Authors: Zauderer Marjorie G. , Moulik Kamalika , Cooper Jonathan , Krug Lee M. , Giancotti Filippo 
Published: October 2015

Abstract
Purpose: Inactivation of Merlin/NF2 is common, occurring in 45-60% of mesotheliomas. Merlin loss leads to hyperactivation of TOR signaling and dysregulation of this pathway drives tumor development and growth. Cytostatic inhibition of TOR with rapamycin in MM cells has limited impact (Lopez-Lago Mol Cell Biol 2009). Rapamycin releases two major negative feedback loops that restrain Akt-TOR signaling, thereby leading to hyperactivation of both Akt and ERK. Effective growth inhibition likely requires dual inhibition of PI3K and mTOR. We therefore sought to assess the activity of the potent and selective dual PI3K/mTOR inhibitor GDC-0980 in MM cells with respect to cell proliferation and hyperactivation of Akt and ERK.
Experimental Procedures: NF2 mutant cell lines, VAMT and JMN, and NF2 wild type cell lines, H-Meso and 211-H, were cultured in the presence of increasing concentrations of GDC-0980 for 48 hours and subjected to MTT assay. Values were normalized to untreated samples at day 0. Meso 33 and JMN malignant mesothelioma cell lines were treated with increasing doses of GDC-0980 for 2 hours and subjected to immunoblotting for P-S6, P-4E-BP1, P-Akt (S473), P-ERK, and ERK2.
Results: GDC-0980 effectively inhibited proliferation of the NF2 mutant cell lines by 40% but had little or no effect on NF2 wild type cell lines (statistically significant difference at 80 nM with p&lt;0.006). 100 nM GDC-0980 completely suppresses activation of TOR as assessed by phosphorylation of S6 and 4E-BP1 in Meso-33 cells. Higher concentrations were required for these events in JMN cells. However, in both Meso-33 and JMN cells, these effects were not associated with overactivation of Akt or ERK.
Conclusions: GDC-0980 is a potent inhibitor of proliferation in MM cells with NF2 mutations and does not cause hyperactivation of Akt and ERK. Along with our ongoing preclinical work with cell lines and xenograft mouse models, the data from a recent phase I clinical trial with an expansion cohort in mesothelioma (NCT00854152) provide a strong rationale for the development of biomarker-driven clinical trials of GDC-0980 and other PI3K/mTOR inhibitors in mesothelioma.
This work was supported in part by Genentech.
Citation Format: Marjorie G. Zauderer, Kamalika Moulik, Jonathan Cooper, Lee M. Krug, Filippo Giancotti. GDC-0980, a dual PI3K/mTOR inhibitor, selectively inhibits NF2 mutant malignant mesothelioma (MM) cells and inhibits TOR signaling without activating Akt or ERK. [abstract]. In: Proceedings of the AACR Special Conference: Targeting the PI3K-mTOR Network in Cancer; Sep 14-17, 2014; Philadelphia, PA. Philadelphia (PA): AACR; Mol Cancer Ther 2015;14(7 Suppl):Abstract nr A34.
Abstract A48: Crosstalk between ERK2 and Akt1 in tumor cells with constitutive K-RAS activity leads to the limited response to PI3K inhibition
Authors: Toulany Mahmoud , Rodemann H. Peter 
Published: October 2015

Abstract
Constitutive K-RAS activity in K-RAS mutated (K-RASmut) non-small cell lung cancer (NSCLC) cells leads to resistance to EGFR targeting strategies. Analyzing the K-RAS activity status revealed that a constitutive high K-RAS activity is observed not only in K-RASmut NSCLC cells but also in head and neck squamous cell carcinoma (HNSCC) cells presenting K-RAS wild-type (K-RASwt) overexpression. Similar to K-RAS-mutated NSCLC cells, increased K-RAS activity in HNSCC cells overexpressing K-RASwt was associated with the stimulated production of the EGFR ligand amphiregulin and resistance to EGFR tyrosine kinase (EGFR-TK) inhibitors such as erlotinib. Overexpression of mutated K-RAS in HNSCC cells expressing low level of K-RASwt stimulated Akt1 phosphorylation and increased clonogenic activity. Conversely, knockdown of K-RAS in K-RASmut NSCLC cells and in HNSCC cells presenting overexpression of K-RASwt resulted in sensitization to the anti-clonogenic activity of erlotinib. K-RAS activity results in both EGFR-dependent and EGFR-independent Akt1 activity. Short-term treatment (2 h) of cells with EGFR-TK or PI3K inhibitors (erlotinib and PI-103) resulted in repression of Akt1 activation, whereas long-term treatment (24 h) with inhibitors led to reactivation of Akt1 and stimulated clonogenicity. Akt1 re-activation was MAPK-ERK2-dependent and associated with a lack of complete response to anti-clonogenic activity of PI-103. A complete response was observed when PI-103 was combined with MEK inhibitor PD98059. Together, inhibition of clonogenicity in tumor cells presenting constitutive K-RAS activity independent of K-RAS mutational status can be achieved by the combination of PI3K and MAPK inhibitors.
Supported by grants from the Deutsche Forschungsgemeinschaft [Ro527/5-1 and SFB-773-TP B02] and the Federal Ministry of Research and Education(BMBF grants 0258416, 03NUK006D) awarded to HPR as well as GRK 1302/2 (T11) awarded to MT/HPR.
Citation Format: Mahmoud Toulany, H. Peter Rodemann. Crosstalk between ERK2 and Akt1 in tumor cells with constitutive K-RAS activity leads to the limited response to PI3K inhibition. [abstract]. In: Proceedings of the AACR Special Conference: Targeting the PI3K-mTOR Network in Cancer; Sep 14-17, 2014; Philadelphia, PA. Philadelphia (PA): AACR; Mol Cancer Ther 2015;14(7 Suppl):Abstract nr A48.