bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 656: Clinical profiles predict early non-adherence to adjuvant endocrine treatment in a prospective breast cancer cohort
Authors: Markkula Andrea , Hietala Maria , Henningson Maria , Ingvar Christian , Rose Carsten , Jernström Helena C. 
Published: August 2012

Abstract
Non-adherence to adjuvant endocrine breast cancer treatment adversely affects disease-free and overall survival. Clinical predictors of non-adherence may allow for specific interventions to reduce non-adherence and improve survival. The aim was to investigate whether clinical characteristics predict non-adherence. Clinical characteristics and information on adherence were obtained from 417 breast cancer patients in a population-based prospective cohort from southern Sweden using patient charts, pathology reports, and questionnaires filled out at the 1- and 2-year follow-up visits. A BMI&lt;25, preoperative current smoking, and drinking alcohol less often than twice a month predicted non-adherence at the 1-year (OR 6.43, 3.12-13.24) and the 2-year visits (OR 4.91, 2.33-10.36) in patients with at least two of these clinical characteristics. When low histological grade (I) was added to the model, having at least two of these four clinical characteristics predicted non-adherence at the 1-year (OR 5.84, 2.73-12.51) and the 2-year visits (OR 5.66, 2.54-12.63) and identified &gt;72% of the non-adherent patients. Thirteen non-adherent patients declined treatment and were never prescribed endocrine treatment. In conclusion, two clinical profiles predicted early non-adherence and may be clinically useful if validated in an independent cohort.
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 656. doi:1538-7445.AM2012-656
Abstract 657: Perinatal factors and breast cancer risk: The CECILE study
Authors: Menegaux Florence , Anger Antoinette , Truong Therese , Guenel Pascal 
Published: August 2012

Abstract
Objectives: Perinatal period and adolescence are key periods of breast cancer development with increased susceptibility to carcinogens. A high level of endogenous estrogens in utero was suggested as a possible risk factor for breast cancer in daughters. We investigated the role of perinatal factors in breast cancer in the CECILE study, a population-based case-control study. Methods: The CECILE study was conducted in two French départements (Côte d'Or, Ille-et-Vilaine) between 2005 and 2008. A total of 1232 incident breast cancer cases and 1317 population age-matched controls were included. An in-person interview was conducted using a standardized questionnaire to obtain information on recognized or suspected risk factors for breast cancer. A self-administered questionnaire was used to obtain information on perinatal factors and was returned by mail by 871 cases (71%) and 915 controls (69%). The perinatal questionnaire included information on parental characteristics (maternal and paternal age, maternal smoking status, hypertension or pre-eclampsia during pregnancy, exposure to diethylstilboestrol) and women’ birth characteristics (birth weight, length at birth, preterm birth, birth order and having been breast-fed). Analyses were conducted using unconditional logistic regression adjusting for age and recognized risk factors for breast cancer. Results: With the exception of maternal smoking (OR=0.57 [0.38-0.85]), there was no association between breast cancer risk and the other parental characteristics. We observed a J-shaped association between birth weight and breast cancer risk, with an OR of 1.54 [1.15-2.06] in women whose birth weight was 3500 grams or more as compared with women whose birth weight was 2500 to 3499 grams. We also observed an increased risk of breast cancer with an increase of birth order (OR=1.12 [0.91-1.37] for birth order 2 to 4; OR=1.42 [1.02-1.99] for birth order [[Unsupported Character - [[Unsupported Character - &#61619;]]]] 5, p trend=0.04). No association were observed for women who have been breast-fed, for length at birth or preterm birth. Conclusion: Our results support the hypothesized association between intrauterine estrogens exposure and risk of breast cancer in daughters.
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 657. doi:1538-7445.AM2012-657
Abstract 66: Inhibition of glioma cell proliferation and tumor development by Sox21
Authors: Caglayan Demet , Kastemar Marianne , Westermark Bengt , Ferletta Maria 
Published: August 2012

Abstract
Sox2 and Sox21 are two transcription factors important for the developing, as well as the adult, CNS, and they are often co-expressed. Sox2 is an embryonic stem cell marker, whereas ectopic forced expression of Sox21 has been shown to induce differentiation in embryonic stem cells. Further, Sox2 is important for maintenance of neural stem cells whereas Sox21 is important for neurogenesis. These two transcriptionfactors are thus in opposite relation to each other and it is believed that a proper balance between them is needed to regulate target genes. Sox2 is highly expressed in brain tumors and up to 97% of GBM samples express Sox2. While the expression of Sox2 has been shown in GBM, in primary glioma cells and established glioma cell lines, less is known about Sox21 in glioma. We have previously shown that Sox2 and Sox21 are co-expressed in adult and childhood brain tumors and are in a functional relationship in glioma cells. Sox2 keeps glioma cells in a proliferative state whereas over expression of Sox21 reduces Sox2 expression and decreases cell proliferation with an increased tendency of apoptosis and differentiation of the glioma cells. We have now further elucidated this effect in vivo by injecting established inducible-Sox21 glioma cell lines subcutaneously into the flank and orthotopically into the brain of SCID mice. Regardless of the injection site, increased Sox21 expression in these tumors reduces tumor growth. The tumors from treated mice were significantly smaller in size and there is a significant increase in survival time. This effect was dependent on the time of Sox21 induction, where an earlier turn on gives even smaller tumors. Total depletion of Sox2 was not achieved despite forced Sox21 expression. Further we show that Sox2 deficiency leads to an inability to form tumors. With its dual effect, the ability to decrease Sox2 expression and the ability to aberrantly differentiate tumor cells, Sox21 becomes a very important factor for future research around therapeutic possibilities in GBM.
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 66. doi:1538-7445.AM2012-66
Abstract 664: Menthol cigarettes in relation to breast cancer incidence in African American women
Authors: Bethea Traci N. , Rosenberg Lynn , Boggs Deborah A. , Palmer Julie R. 
Published: August 2012

Abstract
The Tobacco Products Scientific Advisory Committee has found that smokers of menthol cigarettes have an earlier age at smoking initiation, less success in smoking cessation, and are more likely to be African American than smokers of non-menthol cigarettes. However, whether menthol cigarettes are associated with higher cancer risk relative to non-menthol cigarettes is unclear. Recent studies of smoking and breast cancer suggest that long-term smoking may associated with a small increase in risk, but no data are available on type of cigarette. We assessed the relative effects of menthol and non-menthol cigarettes on incidence of breast cancer in a large prospective cohort of African American women. The Black Women's Health Study has followed approximately 59,000 women with biennial questionnaires since enrollment in 1995. Beginning in 2003, data has been collected on whether cigarettes smoked were menthol or non-menthol; menthol cigarettes were reported by 64.7% of smokers who provided information. During follow-up from 2003 through 2010, 739 incident breast cancer cases occurred. In proportional hazard models that controlled for age and numerous breast cancer risk factors, hazard ratios (HR) were computed for categories of pack-years of smoking of the two types of cigarettes relative to a reference group of never-smokers who reported no regular exposure to second-hand smoke. The HR for β20 pack-years of smoking non-menthol cigarettes was 1.70 (95% confidence interval (CI) 1.04-2.76); for β20 pack-years of smoking menthol cigarettes, the HR was 1.14 (95% CI, 0.72-1.82). Our findings suggest that, to the extent that higher pack-years of smoking may be associated with breast cancer, smoking menthol cigarettes is not more harmful than smoking non-menthol cigarettes.
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 664. doi:1538-7445.AM2012-664
Abstract 673: Obesity, weight gain, physical activity and polymorphism in mTOR pathway and risk of renal cell carcinoma
Authors: Shu Xiang , Lin Jie , Wood Christopher G. , Tannir Nizar M. , Wu Xifeng 
Published: August 2012

Abstract
Background: The role of obesity, physical activity and weight gain in renal cell carcinoma (RCC) has not been well understood. Given the crucial role of PI3K-AKT-mTOR pathway (or mTOR pathway) plays in metabolism, cell growth and tumorigenesis, it is important to evaluate the joint effect of genetic variants in this pathway and energy balance risk factors for RCC. Methods: In this case-control study, 577 Caucasian cases and 593 Caucasian healthy controls were included in the analyses. Cases and controls were frequency-matched by age (±5 years), gender and county of residence. Epidemiological data were collected via in-person interview. Genotyping data of 157 SNPs was extracted from previous GWAS which has been done using Illumina HumanHap660K/610K BeadChips in the laboratory. Unconditional logistic regression was used to calculate odds ratios and their 95% confidence interval (CI). Results: Obesity at age 20, age 40 and 3 years prior to the diagnosis or recruitment were each significantly associated with increased RCC risk. Moderate (10.1-25 lbs) and massive weight gains (&gt;25 lbs) from age 20 to 40 increased RCC risk by 46% (95%CI: 1.16-2.34) and 62% (95%CI: 1.10-2.39), respectively. Low physical activity was associated with 4.08-fold (95%CI: 2.92-5.70) of increased RCC risk. Three SNPs had significant association and their cumulative effect had increased the risk up to 85% (OR: 1.85, 95%CI: 1.28-2.68). When considering multiple risk factors, subjects who were overweight or obese, experienced weight gain during adulthood (&gt;10 lbs), had history of hypertension and unfavorable genotypes in mTOR pathway had 12.84-fold increased risk (95%CI: 5.08-32.46) of RCC. Conclusion: Our results provided strong evidence that energy balance risk factors and genetic variants in mTOR pathway could jointly influence the susceptibility to RCC. Our findings have implications on RCC prevention if confirmed in future independent studies.
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 673. doi:1538-7445.AM2012-673
Abstract 695: Significant loss of nuclear expression of Actinin-4 in metastatic breast carcinoma and lymph nodes: A novel biomarker for metastatic breast carcinoma
Authors: Chen Cui P. , Herrmann Marille , Akoa Achille , Alper Özgül M. , Alper Özge 
Published: August 2012

Abstract
Background: Actinin-4 is an actin cross-linked protein. The expression and subcellular distribution of actinin-4 (ACTN4) has been associated with multiple roles in tumorigenicity and cancer metastasis. In the present study, we developed a novel antibody against human actinin-4 and investigated the clinical utility of actinin-4 as a biomarker in metastatic breast cancer. Methods and findings: We generated a novel monoclonal antibody (AB-Actinin-4) using hybridoma technology and native ACTN4 protein as an immunogen. The antibody specifically recognized both native and denatured human Actinin-4 protein and displayed high affinity as assessed by ELISA, immunohistochemistry assay, western blot and flow cytometry. Using this antibody and ELISA as well as immunohistochemical techniques, we examined plasma levels and tissue expression of actinin-4 in healthy controls’ and breast cancer patients’ samples. 50 plasma samples from healthy controls and breast cancer patients were analyzed for the presence of soluble actinin-4. ELISA results showed significantly decreased actinin-4 levels in plasma samples from patients with breast carcinomas compared to healthy control plasma. A total of 156 cases, including 70 normal, 36 non-metastatic breast carcinoma, 50 breast carcinoma tissues with regional metastasis, and 50 matched metastatic lymph nodes were examined. The immunoreactivity of actinin-4 was located mainly in nucleus and cytoplasm of cells. To assess the difference between groups, the staining intensity and intracellular distribution were compared and the intensity in nucleus and cytoplasm was separately scored as 0, 1+, 2+ and 3+. Grades 0 and 1+ were defined as negative and 2+ and 3+ as positive. Significant differences between the groups were found in nuclear staining. 92% of normal and 89% of non-metastatic breast carcinoma samples displayed positive nuclear staining. In contrast, only 29% of metastatic lymph nodes and 51% of metastatic breast cancer tissues showed strong nuclear staining. Conclusion: Actinin-4 demonstrated significantly decreased expression in plasma from breast cancer patients. Metastasis leads to significant loss of the nuclear expression of Actinin-4 in breast cancer tissues, in comparison to normal and non-metastatic breast carcinoma tissues. Our data suggests that Actinin-4 might have significant impact in breast cancer metastasis. Actinin-4 may serve as a reliable biomarker for the diagnosis and prognosis of metastatic breast cancer as well as could be a therapeutic target.
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 695. doi:1538-7445.AM2012-695
Abstract 697: Clinical and prognostic comparison between triple-negative and non-triple-negative breast cancer
Authors: Ding Shian-Ling , Lee I , Cheng Chun-Wen , Lin Yu Hsin , Chang Jia-Ming , Shen Chen-Yang 
Published: August 2012

Abstract
Aim: The triple-negative breast cancer (TNBC) subtype is characterized by the lack of expression of estrogen and progesterone receptors (ER/PR) and Her2/neu protein. The present study aimed to evaluate the five-year survival rates and clinico-pathological characteristics of patients with TNBCs and those with non-TNBCs in Taiwan. Methods: This study was conducted on 313 ethnic Chinese women with primary breast cancer using tissue microarrays to perform a standardized immunohistochemical analysis. Results: Of the 313 patients, 10.5% had the TNBC phenotype. The median age of the TNBC patients was lower than that of the non-TNBC patients (47 vs. 59 years). One of the more striking differences between the TNBC and non-TNBC women was tumor differentiation, with 29.6% of the non-TNBC group having a poorly differentiated tumor compared to 45.5% of the TNBC group (p=0.01). Cox proportional hazards model results showed that (a) ER, PR, or Her2/neu status was not associated with survival rate in early-stage patients and (b) ER negativity (p = 0.03, HR = 3.4) and Her2/neu negativity (p = 0.04, HR= 4.4) were two independent predictors of the five-year survival rate in advanced-stage (stage III-IV) women. Conclusion: The TNBC phenotype represents a specific molecular profile. However, it does not always lead to worse survival, especially in women with early breast cancer.
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 697. doi:1538-7445.AM2012-697
Abstract 707: CD133 is a useful surrogate marker to predict chemosensitivity of neoadjuvant chemotherapy for breast cancer
Authors: Aomatsu Naoki , Yashiro Masakazu , Kashiwagi Shinichiro , Morisaki Tamami , Fukuoka Tatsunari , Hirakawa Tosiki , Hasegawa Tsuyoshi , Matsuoka Junko , Takashima Tsutomu , Kawajiri Hidemi , Onoda Naoyoshi , Ishikawa Tetsuro , Hirakawa Kosei 
Published: August 2012

Abstract
Background:Current studies have demonstrated that neoadjuvant chemotherapy (NAC) improves survival outcomes and increases the chance for breast conservation when applied preoperatively. However, no reliable maker to predict chemosensitivity of NAC is not available. CD133 has been considered as a cancer stem cells (CSCs) marker in many kinds of tumors such as breast cancer, colorectal cancer and brain cancer. The aim of this study was to evaluate the value of CD133 as a surrogate maker to predict chemosensitivity of NAC for breast cancer. Experimental Design: A total of 102 patients with breast cancer of stage II and III, as evaluated by core needle biopsy and ultrasonography, was treated with NAC. Expressions of CD133, estrogen receptor, progesterone receptor, and HER2 were assessed by immunohistochemistry. Results: The clinical complete response (CR) rate of all patients was 18% (18/102), partial response (PR) was 61% (62/102), no change (NC) was 20% (20/102), and progressive disease (PD) was 2% (2 /102). The response rate (RR) was 78% (80/102). The pathological complete response rate (pCR) was 29%. The pCR rate and pathological response of CD133-positive cases was significantly lower than that of CD133-negative cases. The recurrence rate of CD133-positive cases was significantly higher than that of CD133-negative cases. CD133 expression showed a poor disease free survival and overall survival time. A multivariate logistic regression analysis showed that CD133 expression was an independent prognostic factor in breast cancers treated with NAC. Conclusion: CD133 is a useful surrogate maker to predict chemosensitivity of NAC chemotherapy for breast cancer.
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 707. doi:1538-7445.AM2012-707
Abstract 71: Mutational analysis for IDH1 and IDH2 in pediatric leukemia
Authors: Hiwatari Mitsuteru , Takita Junko , Nishimura Riki , Okubo Jun , Oki Kentaro , Sanada Masashi , Sotomatsu Manabu , Kikuchi Akira , Igarashi Takashi , Hayashi Yasuhide , Ogawa Seishi 
Published: August 2012

Abstract
Recently, mutational and epigenetic profiling of a large acute myeloid leukemia (AML) patient cohort revealed that NADP+dependent isocitrate dehydrogenase (IDH)1/2-mutated AMLs display global DNA hypermethylation and a specific hypermethylation signature, suggesting a shared proleukemogenic effect. To explore the involvements of IDH1/2 in the pathogenesis in pediatric hematological malignancies. We analyzed mutations that involve the activation sites of IDH1/2 using polymerase chain reaction amplification/sequencing in a total of 244 samples of pediatric myeloid malignancies as well as infantile leukemia including 17 AML-derived cell lines, 115 primary cases of AML, 28 primary cases of MDS, 15 primary cases of juvenile myelomonocytic leukaemia (JMML), 6 chronic myeloid leukemia (CML)-derived cell line, 18 primary cases of CML and 45 infantile leukemia(6 AML and 39 acute lymphoblastic leukemia (ALL) patients). Moreover, to assess whetherIDH1/2 mutations overlap with known gene abnormalities, such as FLT3, c-KIT, and NPM1 mutations, mutational analyses of FLT3, c-KIT, and NPM1 were also performed. The common IDH2 R140Q mutation was detected in a single AML case, whereas no IDH1 mutation was detected in samples of myeloid malignancies. Although no IDH2 mutation was detected in infantile leukemias, novel P127S, H133I and I130V of IDH1 mutations were detected in 4 of 45 (8.9%) infantile ALL cases. No IDH1 and IDH2 mutations were detected in the JMML, MDS, or CML samples examined. Six AML samples including one cell line had c-KIT mutations (D816V, N822K, or D419fs), 12 AML cases had FLT3-ITD and 10 infantile leukemia cases had FLT3 mutations (D835E or I836). The NPM1 mutation was detected in 2 of 132 AML samples. The AML case harboring the IDH2 mutation, Case 39 was a 12-year-old boy diagnosed as AML-M2 according to the French-American-British cooperative group classification system having t(8;21)(q22;q22), showed no abnormalities of NPM1, c-KIT, and FLT3. Remarkably, among 4 infantile ALL cases with IDH1 mutations, 3 cases showed mixed lineage leukemia(MLL) rearrangements with t(4;11). The FLT3-D835 mutation was found in 1 of 4 patients with IDH1 mutations. These results suggest that although the involvements of IDH1/2 mutations in the pathogenesis of pediatric myeloid malignancies are extremely rare, closely positioned to near activation site, R132 IDH1, these IDH1 mutations are the candidate second genetic events in a subset of MLL-leukemia.
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 71. doi:1538-7445.AM2012-71