bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract A130: Spatial and temporal patterns in female breast carcinoma incidence in Pennsylvania, 1985–2004
Authors: Han Yueh-Ying , Talbott Evelyn , Donovan Maryann 
Published: May 2012

Abstract
Objective: The assessment of spatial and temporal trends in breast carcinoma incidence can signal changes in ascertainment, changes in risk, and possibly point to changes in underlying risk factors. It is important to develop geographic maps to identify hot spots where cancer rates, by race and by histologic type, are elevated to better appreciate changes in cancer risk.
Methods: Incidence data for breast carcinoma, 1985–2004, was requested from the Pennsylvania Cancer Registry (PCR). Joinpoint regression model was applied to characterize age-, race- and histologic type-specific breast tumor incidence time trends in Pennsylvania (PA). Geographic Information System methods and spatial analysis is also being applied to these data to detect spatial clusters of diagnosed breast carcinoma in PA.
Results: Among whites, age-adjusted incidence for ductal carcinoma in situ (DCIS) increased significantly from 1985 to 1999 and incidence for lobular carcinoma in situ (LCIS) slightly increased from 1994 to 2004, although this increase was not significant. Among blacks, age-adjusted incidence for DCIS and LCIS increased significantly over the entire study period. Age-adjusted incidence for malignant breast carcinoma slightly decreased from 1997–2004 among blacks but more recently since 2001 has shown a sharp decrease among whites (annual percent change = −3.0). Between 1985 to 2004, for women under age of 40, age-adjusted incidence of breast carcinoma in situ (DCIS, LCIS, mixed) significantly increased 4.5% and 10.0% annually for whites and blacks, respectively. Incidence for malignant breast carcinoma slightly decreased over the study period.
To better define invasive breast cancer risk in PA, spatial clustering analysis performed to identify county-specific changes in malignant breast carcinoma incidence. This analysis showed significant spatial clustering in Pennsylvania (P=0.024) and the region of increased invasive breast cancer was clustered in seven southeastern counties.
Conclusion: Incidence for breast carcinoma in situ increased significantly among women in PA. An increase in invasive breast cancer was identified in seven southeastern counties. Factors responsible for the state-wide increase in breast carcinoma in situ and the elevated invasive breast cancer incidence in southeastern Pennsylvania should be carefully assessed.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):A130.
Abstract A131: Antacid use and risk of larynx cancer in the NIH-AARP Diet and Health Study
Authors: Abnet Christian C. , Freedman Neal D. , Hollenbeck Albert , Schatzkin Arthur 
Published: May 2012

Abstract
Antacids are used to treat heartburn and their use serves as a proxy indicator of gastroesophageal reflux disease. We tested the association between self-reported antacid use and risk of laryngeal squamous cell carcinoma (N=240) in a prospective cohort study using Cox proportional hazards models to estimate hazard ratios (HR) and 95% confidence intervals (95%CI) adjusted for potential confounders. We also estimate the risks for esophageal squamous cell carcinoma, and esophageal and gastric cardia adenocarcinomas for comparison. Antacid use showed significant associations with risk of esophageal and gastric cardia adenocarcinomas, 2.34 (1.79–3.06) and 1.45 (1.06–1.98) respectively, but not esophageal squamous cell carcinoma 0.99 (0.65–1.49). For laryngeal squamous cell carcinoma we found significantly increased risk 1.32 (1.01–1.72). In sex and smoking-status stratified models for the larynx, we saw a stronger association in men that had never smoked tobacco, 13.52 (2.89–63.22), compared to ever smokers, 1.20 (0.89–1.63). The small number of women with larynx cancer precluded stratified models. Our study suggests that gastroesophageal reflux may increase the risk of laryngeal squamous cell carcinoma.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):A131.
Abstract A132: A descriptive study on the factors affecting mortality and disease-free survival among triple-negative breast cancer patients
Authors: Ong Kian Koc Jean Bernadette U. , Desai Ajit , Pomerantz Sherry , Kathy Pincus 
Published: May 2012

Abstract
Introduction: Triple-negative breast cancer patients have a worse prognosis as compared to other subtypes of breast cancer. Patients are usually diagnosed at a younger age. Tumor size is usually larger with poorly differentiated histology and possible visceral metastasis. Several studies have been published on the risk factors for developing triple negative breast cancer. On the other hand, factors predicting mortality after diagnosis among triple negative breast cancer patients is still lacking.
Objectives: The study aimed to describe the population of triple negative breast cancer patients diagnosed at Albert Einstein Medical Center from 2003–2007. Demographic data, risk factors and treatment interventions in this population were gathered. The measured outcomes were mortality and disease free survival.
Methods: This study was a retrospective review of women diagnosed with triple negative breast cancer at the Albert Einstein Healthcare Network Cancer Center in 2003–2007. Patients diagnosed with cancer metastasized to the breast and causes of death other than from complications of cancer were excluded from the study.
Statistical Analysis: Descriptive statistics and frequency distribution were used to categorize the characteristics of the subjects. Chi-square test was used for bivariate analysis. Logistic regression was used for multivariate analysis.
Results: A total of 214 patients were diagnosed with triple negative breast cancer from 2003–2007. 114 (53%) were African Americans, 84 (39%) were Caucasians and 16 (7%) belonged to other racial groups. The mean age of diagnosis was 56.6 (SD 15.9) years old. At the end of the four year period, 48 (22.4%) of the 214 patients died. Using chi square test and logistic regression, patients who underwent chemotherapy were less likely to die (95% CI 0.14 – 0.83, p 0.02, OR 0.35). The patients with tumor size more than 2 cm or had history of ischemic heart disease had increased mortality (95% CI 1.36 – 8.04, p 0.01, OR 3.3 and 95% CI 1.29 – 49, p 0.03, respectively). Chemotherapy was significantly associated with disease free survival (95% CI 1.49 – 18.65, p 0.01, OR 5.27). There was no significant association between mortality or disease free survival to age and race.
Conclusion: Early diagnosis and screening significantly affects treatment and survival outcome. Prompt chemotherapy may contribute to a patient's survival and disease free status. Tumor size more than 2 cms and the presence of ischemic heart disease were significant predictors of mortality outcome whereas age and race were not found to be associated with mortality or disease free survival.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):A132.
Abstract A139: Effects of simvastatin and of a cyclic nonapeptide derived from alpha fetoprotein on the proliferation of ERα-positive mammary tumor cells in culture
Authors: Torres Cristian G. , Sierralta Walter Daniel 
Published: May 2012

Abstract
Introduction: Estradiol (E2) stimulate the progression of many mammary tumors, including those of dogs, by association to estrogen receptors (ER). We have recently reported on the effects of E2 and of an AFP-derived cyclized peptide (cP) on the proliferation of cancer cells from different mammalian species demonstrating that, in ER-positive cells, estradiol increased cell proliferation and the phosphorylation of ERK 1/2; these effects were effectively inhibited by the presence of cP in the culture medium. It has been reported that statins restrain the proliferation in culture of mammary tumor cells. We report here on the effects of statins and cP on the estrogen-stimulated proliferation of mammary tumor cells.
Aims: Evaluate the proliferation on mammary tumor cells after exposure to E2, without / with cP and simvastatin; comparison with the effect of ICI 182,780 (ICI).
Methods: MCF7 cells grown in DMEM F12 containing ITS (insulin, transferrin, selenium), 1% charcoal/dextran-twice-treated calf serum, 3% hydroxyethilated starch (HAES) and antibiotics were incubated of estradiol in the absence and presence of cP and various concentrations of simvastatin. Cell proliferation measurement and the assessment of viability (trypan blue) was done by haemocytometry.
Results and Conclusions: The proliferation of control (unstimulated) MCF7 cells, was not affected by the presence of either simvastatin or cP in the culture medium. The addition of 2nM E2 significantly increased the proliferation rate of the cells. The effect was reduced by cP to basal values, i.e. to the same extent than the specific antagonist ICI does. At the concentrations used, simvastatin had no effect on the proliferation of MCF7 cells stimulated with estradiol. We suggest that the effects of cP on the proliferation of estradiol-stimulated MCF7 cells are probably not related with a prenylation of ER.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):A139.
Abstract A140: Chemoprevention of familial adenomatous polyposis by a flexible-heteroarotinoid (Flex-Het), SHetA2, in APCMin mice
Authors: Guruswamy Suresh , Benbrook Doris , Zhang Yuting , Qian Li , Mohammed Altaf , Rao Chinthalapally V. 
Published: May 2012

Abstract
Colorectal cancer is the second most common cancer in the western world with 1 million new cases worldwide each year. Flexible Heteroarotinoids (Flex-Hets) are a promising new class of anticancer compounds that regulate cell cycle progression, differentiation and apoptosis, as well as xenograft tumor growth and angiogenesis in many cancer types. The lead Flex-Het, Sulfur heteroarotinoid A2 (SHetA2), prevents DMBA-induced transformation in endometrial organotypic cultures in vitro and is currently in preclinical testing in the NCI RAPID program. In this study, the potential in vivo chemopreventive effects of SHetA2 were evaluated in APCmin/+ mice. Six-week old APCmin/+ mice were assigned to three different treatment groups with normalized distributions of males and females. Drug was dissolved in corn oil (0 - placebo, 30 mg/kg SHetA2, 60 mg/kg SHetA2) and administered by gavage five days per week for 12 weeks. There was no statistically significant difference in body weight between any of the treatment groups and controls. All mice were killed and the total number and size of tumors along the entire length of the intestine and colon were visually counted using a magnified lens. SHetA2-treated groups exhibited dramatic reductions in the total number of intestinal tumors at both doses (SHetA2 30 mg/kg - 60%, SHetA2 60 mg/kg - 54%, P&lt;0.0001). On average, mice developed about 50 tumors per animal in the small intestine of the control, whereas there were only 20 tumors (SHetA2 30 mg/kg) and 23 tumors (SHetA2 60 mg/kg) in the treatment groups. Neither of the SHetA2 doses administered caused intestinal ulceration or acute toxicity. Both doses reduced the numbers of large (&gt;2 mm), medium (1–2 mm) and small (&lt;1 mm) adenomas. When data were analyzed for colon alone, the mean number of tumors per mouse was 2 in the control group, 0.3 with 30 mg/kg SHetA2, and 0.75 with 60 mg/kg SHetA2. Colon tumor incidences were 70%, 30% and 40% for control, 30 mg/kg SHetA2 and 60 mg/kg SHetA2, respectively. Although SHetA2 at both 30 mg/kg and 60 mg/kg appeared to cause a parallel trend in inhibiting tumor growth, 60 mg/kg concentration did not show greater inhibition than 30 mg/kg. Results from this study, for the first time, indicate that the Flex-Het, SHetA2, significantly decreases small intestinal and colon tumor formation. Currently, work is in progress to study the molecular and cellular activities involved in SHetA2 chemoprevention activity. (Supported by Kerley-cade chair endowment, R01-102947 and R01-CA-106713)
Citation Information: Cancer Prev Res 2010;3(1 Suppl):A140.
Abstract A147: Curcumin modulates gene expression profile and delays tumor progression of prostate cancer
Authors: Killian Peter H. , Kronski Emanuel , Mirisola Valentina , Pfeffer Ulrich , Nerlich Andreas G. , Bachmeier Beatrice E. 
Published: May 2012

Abstract
Curcumin is a polyphenol, derived from the plant Curcuma longa that has promising anticancer properties in breast, colon, pancreas and some other cancer types. We recently demonstrated that the metastatic potential of breast cancer cells is strongly reduced upon treatment with Curcumin in a murine model of hematogenous metastasis: 68% of the mice treated had no or few metastases as opposed to 17% of the untreated mice.
In order to elucidate its anti-tumoral effects in prostate cancer, we used three human prostate cancer cell lines of clear defined and graduated tumorigenicity (LnCaP&lt;DU145&gt;PC3) for our studies. In a first approach, we intended to obtain a complete picture of Curcumin-responsive genes and therefore we performed gene expression profiling (GeneChip Arrays Affymetrix) of Curcumin-treated cells versus non-treated cells followed by statistical analysis. Thereby we found 71 genes whose expression was significantly altered among which 8 genes were down-regulated. Treatment of prostate cancer cells with Curcumin reduced tumor cell proliferation (BrdU assay) and invasion (Matrigel assay) in a time and dose dependent manner. Furthermore expression of matrix-degrading enzymes (MMPs) which is a prerequisite for matrix degradation was significantly down-regulated on transcript as well as on protein level.
The underlying regulation mechanism involves the survival associated NFγB signaling pathway: Fluorescent translocation assays clearly demonstrated that Curcumin inhibits p65 translocation into the nucleus of the tumor cells, which in consequence leads to diminished transcription and expression of tumor progression related genes and gene products resulting in the induction of apoptosis.
Taken together, these features make Curcumin a promising drug for cancer chemoprevention and antitumor therapy of prostate cancer.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):A147.
Abstract A26: CEA and CA 19-9 as biomarkers for prevention of gall bladder cancer
Authors: Kapoor Vinay K. , Agrawal Vinita , Goel Amit , Krishnani Narendra , Pandey Rakesh , Agrawal Suraksha 
Published: May 2012

Abstract
Objective: Gall bladder cancer (GBC) is the commonest biliary tract cancer worldwide. It is the commonest gastro-intestinal cancer in women in northern India; it is common in Native American Indian people also. GBC is usually associated with gall stones (GS) and chronic cholecystitis (CC); xantho-granulomatous cholecystitis (XGC) is a variant of CC. Most patients with GBC are diagnosed at an advanced stage and overall prognosis is poor. Prophylactic cholecystectomy in patients with asymptomatic GS can prevent GBC, but it can not be advised in everyone with GS. There is a need to identify some bio-markers for early diagnosis and prevention GBC.
Materials and Methods: We evaluated the immuno-histo-chemical (IHC) expression of carcino-embryonic antigen (CEA) and carbohydrate antigen (CA) 19-9 in histo-pathologically confirmed GBC (n=51), CC (n=68), XGC (n=42) and normal GBs removed during operations on bile duct, liver and pancreas (n=10). IHC was performed using mouse monoclonal primary antibodies for CEA (Clone II-7, 1:100, Dako) and CA 19.9 (Clone 116-NS-19-9, 1:100, Dako) using labeled Streptavidin Biotin Peroxidase method. Intensity of staining was recorded as absent (0), mild (1), moderate (2) and intense (3) while the percentage of nuclei stained were scored as absent/&lt;5% (0), &gt;5 &lt;10% (1), 10–50% (2) and &gt;50% (3). The total score was calculated by adding the intensity score and the percentage score and ranged from 0–6. A score of ≥3 was considered as positive.
Results: CEA expression was present in 42/51 (82%) of GBC - it was apical in 13, focal cytoplasmic in 15 and diffuse cytoplasmic in 14 cases. CEA expression was seen in 18/68 (27%) of CC - it was apical in all 18 with focal cytoplasmic in 9. CEA expression was seen in 4/42 (10%) of XGC - it was apical in all 4; many cases with XGC, however, did not have epithelium. All 10 normal GBs showed apical CEA expression. Diffuse cytoplasmic staining of CEA was seen in only GBC and was not seen in CC, XGC and normal GBs. CA 19-9 expression was seen in 38/51 (75%) of GBC - all cytoplasmic; all 13 CA19-9 negative GBCs were high grade on histopathology. All CC, XGC and normal GBs showed apical and diffuse cytoplasmic positivity for CA 19-9.
Conclusion: Tumor markers such as CEA and CA 19-9 can be used to screen patients with asymptomatic GS to identify a sub-group with higher risk to develop GBC who can then be offered prophylactic cholecystectomy for secondary prevention of GBC.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):A26.
Abstract A33: Expression of markers of inflammation and angiogenesis in preneoplastic lesions and colon cancer progression
Authors: Cammarota Rosaria , Bertolini Valentina , Pennesi Giuseppina , Bucci Eraldo O. , Garlanda Cecilia , Barberis Massimo C. , Sessa Fausto , Noonan Douglas M. , Albini Adriana 
Published: May 2012

Abstract
Colorectal cancer (CRC) was the first solid tumor to be successfully targeted with anti-angiogenic therapy in the clinic. Tumor angiogenesis is critical for cancer progression in that it permits expansion of the tumor mass and fosters malignant dissemination. Angiogenesis is a multistep process involving endothelial cells as well as numerous stromal components within the tumor microenvironment that also represent potential therapeutic targets. Inflammation dependent-angiogenesis is increasingly recognised as a central force in tumor growth and progression, while use of anti-inflammatory drugs has been found to reduce incidence of CRC carcinoma potentially through repression of tumor angiogenesis. We investigated the link between inflammatory angiogenesis and colorectal cancer in archival tissues across a range of pathologies that represent diverse steps in the progression of CRC: 16 cases of ulcerative colitis (URC), 16 adenocarcinomas developed from pre-existing tubular or tubulo-villous adenomas, 33 tubular or tubulo-villous adenomas with low grade dysplasia, and 33 infiltrating adenocarcinomas. Immunohistochemical analysis was performed with antibodies targeting markers of endothelial cells (CD31), macrophages (CD-68), neutrophils (CD15), growth factors (HGF), cytokines (IL-6) and up-stream receptors (TLR4). Epithelial, interstitial and endothelial/vascular compartments were chosen for analysis. Staining for (HGF) showed a rapid drop from healthy to pathological conditions, but did not show changes in staining intensity with the different stages of CRC progression. In contrast, the markers for vascularization (CD31) inflammatory cells (CD68, CD15) and inflammation (IL-6 and TLR4) increased in staining intensity as a function of tumor progression as determined by histopathology. IL-6 and TLR4 staining appear to correlate with event-free survival. These data suggest that inflammation increases along with tumor progression, and staining for CD68, CD15, IL-6, and CD31 appear to act as early tumor markers that increase with tumor progression, from precursor entities to invasive CRC. Increased TLR-4 and IL-6 was also found in tumor tissues derived from animals lacking Tir-8, an interleukin-1/Toll-like receptor family member highly expressed in the intestinal mucosa, in the azoxymethane and dextran sulfate sodium salt (DSS) model of CRC, confirming that these markers of inflammatory events are associated with colorectal tumor progression.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):A33.
Abstract A36: Bracken fern carcinogen causes cancer in humans
Authors: Shahin Mahmood 
Published: May 2012

Abstract
Bracken fern (genus Pteridium) is the only plant known to cause cancer naturally in animals. In addition to the well recognised syndromes of thiamine deficiency, acute haemorrhage associated with myeloid aplasia and blindness due to retinal degeneration, it causes neoplasia of urinary bladder and in some circumstances oesophagus origin. In addition, it has been shown to cause neoplasia in a wide range of tissues in many experimental species. The major carcinogen has been shown to be ptaquiloside (PT), a norsesquiterpene glucoside that can be present in bracken in extraordinary concentrations, up to 13000 ppm. The highest concentrations were found in the crosiers and young fronds. The mutagenicity, clastogenicity, tetratogenicity and carcinogenicity of PT have been convincingly demonstrated. Under alkaline conditions the loss of the glucose give rise to the formation of a dienone intermediate which possess a highly reactive cyclopropyl ring capable of reacting with cellular macromolecules. Pt has been shown to alkylate DNA at N3 of adenines in the minor groove, preferentially in 5′-TAG and 3′-A in 5′-AA-3′ sequences. It also alkylates N7 guanines in the major groove occurring in 5′-TG sequences. It is believed that these alkylation lead to mismatch repair and subsequent mutations in particular proto-oncogene. Recently a rat model of carcinogenesis has been established using intravenously administrated PT. Some epidemiological evidence has indicated higher risk of cancer in people who consume bracken fern crosiers, people who consume milk of cows feeding on bracken and those live in bracken-infested areas. PT has been found in the milk of cows fed on bracken fern experimentally and the milk of bracken fed cows has been shown to cancer in rats. PT carcinogenesis presents an excellent model of environmental carcinogenesis. More recently it has been found that immunosuppressive effects of bracken fern (P. aquilinum) and that many of the functions that were modulated could contribute to the increased risk of cancer formation in exposed hosts.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):A36.
Abstract A44: Role of HLA-G 14bp insertion deletion in cancer susceptibility and progression
Authors: Abbas Ata , Hussain Syed Rizwan , Naqvi Hena , Fatima Rabab , Babu Sunil G. , Singh Pradyumn , Mahdi Farzana 
Published: May 2012

Abstract
Human leukocyte antigen -G (HLA-G) is an immunosuppressive protein with multiple functions. The 14bp insertion / deletion in exon 8 of HLA-G gene have been shown to play an important role in HLA-G mRNA stability as well as expression level; and can be correlated with its immunosuppressive function. The role of HLA-G in various cancers has already been demonstrated. Cancerous cells start expressing HLA-G which in turn provides a shield for various immune responses. In the present study we have tested the possibility of the role of 14bp insertion / deletion polymorphism of HLA-G in cancer progression and susceptibility. We have genotyped 59 cancer samples (26 benign and 33 malignant) and 79 matched controls for 14bp polymorphism of HLA-G. Data showed increase of +14bp/−14bp and −14bp/−14bp genotype with both benign and malignant cancer. We observed significantly higher frequency of +14bp/+14bp genotype in control (p=0.01). This is consistent with both benign and malignant tumors as well as cancer types showing possibility of protective effect of +14bp/+14bp genotype in various cancers. However, further studies will be required with large sample size to test this hypothesis. The +14bp/−14bp and −14bp/−14bp genotypes have already been showed to be associated with higher expression of HLA-G and its mRNA stability and might be providing favorable micro-environment for cancer progression. There is no published work till date showing the role of HLA-G 14bp polymorphism in various cancers. These preliminary data showed that HLA-G 14-bp genotypes might be playing an important role in pathogenesis of various cancers.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):A44.