tbuckley/cabot-search huggingface dataset:
Prognostic Factors for Locoregional Recurrence in Operable Breast Cancer Patients Treated with Preoperative Systemic Chemotherapy.
Authors: S. Jung, S. Min, S. Lee, C. Park, Y. Kwon, E. Kim, K. Ko, K. Lee, I. Park, J. Jeong, K. Shin, S. Lee, S. Kim, H. Kang, J. Ro
Journal: Cancer Research (2009)

Abstract Background: We aimed to evaluate the clinicopathologic factors affecting locoregional recurrence (LRR) in potentially operable breast cancer patients receiving preoperative systemic chemotherapy (PST).Methods: We reviewed the records of 316 breast cancer patients treated with PST (doxorubicin/cyclophosphamide, 101; docetaxel /capecitabine, 103; paclitaxel/gemcitabine, 43; doxorubicin/docetaxel, 69) followed by surgery and adjuvant radiotherapy between 2002 and 2006. The majority of patients had clinical positive axillary lymph nodes. To define the prognostic factors for LRR, age, clinical stage, hormone receptor (HR) and HER2 status, clinical and pathologic response, type of operation, pathological characteristics including tumor size, tumor grade, nodal status, number of positive axillary nodes, size of metastatic lymph node and status of resection margin and tumor multiplicity before and after PST were analyzed.Results: Overall 52 patients (16.5%) in the primary tumor and 87 patients (27.5%) in the axillary nodes achieved a pathologic complete response (pCR), and 206 patients (65.2%) underwent breast conserving surgery (BCS). With a median follow-up of 52.4 month (range: 4.7 - 89.4), total 18 (5.7%) patients developed LRR; 2 of 110 (1.8%) patients with mastectomy vs. 16 of 206 (7.7%) patients with BCS (p=0.04). Other significant factors in the univariate analysis were clinical T stage, HR status, clinical response and tumor multiplicity. A pCR in the primary tumor or node was not a prognostic factor for LRR in this study. In multivariate analysis, clinical T stage (T3/4, HR 7.8; 95% CI, 2.33-26.24; P=0.001), hormone receptor status (negative, HR 6.2; 95% CI, 1.91-20.22; P=0.002) and type of surgery (BCS, HR 9.5; 95% CI, 1.97-46.37; P=0.005) were independent prognostic factors. Among patients with BCS, advanced clinical T stage (HR 12.4; 95% CI, 3.45-44.56; P&amp;lt;0.001), negative hormone receptor (HR 4.74; 95% CI, 1.33-16.96; P=0.02), non-responding disease (HR 6.54; 95% CI, 1.07-40.12; P=0.04) and multiple tumors (HR 4.36; 95% CI, 1.06-17.90; P=0.04) developed more frequent LRR.Conclusions: Significantly more patients with advanced clinical T stage, negative HR status and BCS developed LRR in operable breast cancer treated with PST. Moreover, in patients with BCS after PST, clinically non-responding disease and multiple tumors showed unfavorable prognosis besides the larger tumors and negative hormone receptor.Partly supported by NCC Grant No 0610240 Citation Information: Cancer Res 2009;69(24 Suppl):Abstract nr 1095.
SP0176 Measuring outcomes in a busy practice
Authors: M.L. Hetland
Journal: Annals of the Rheumatic Diseases (2013)

Observational outcomes captured in routine care are a significant source of research data that complements results obtained from randomized clinical trials. It is a challenge to organize the clinical work in a busy department in ways that enables such data collection. Web-based registration of clinical data has evolved as a feasible tool for the busy clinician. By entering patient-reported and clinical outcomes in real-time, the rheumatologist gets a very good overview of the disease course in the individual patient. Data can then also be used for research purposes. In Denmark, the nationwide DANBIO database has been in use since year 2000. It is based on open source technology, which has advantages in requiring less economic resources. It has been demonstrated that electronic registration of PROs is equivalent to paper-based registrations [1]. Data from DANBIO on indications for biological treatment [2,3], treatment effect of biological therapies in RA [4,5], PsA [6]and AS [7], switching [8] have been published. Also data on HR-QoL [9], gender differences [10], radiographic progression [11] and health economy [12-13] have been published. <h3>References</h3> Schefte DB et al. Rheumatology 2010;49(1):99-104. Hjardem et al. Ann Rheum Dis 2005;64(8):1220-3. Hetland ML et al. Ann Rheum Dis 2008;67(7):1023-6. Hetland ML et al. Arthritis Rheum 2010;62(1):22-32. Leffers HC et al. Ann Rheum Dis 2011;70(7):1216-22. Glintborg B et al. Arthritis Rheum 2011;63(2):382-90. Glintborg B et al. Ann Rheum Dis 2010;69(11):2002-8. Hjardem E et al. Ann Rheum Dis 2007;66(9):1184-9. Linde L et al. J Rheumatol 2010;37(2):285-90. Jawaheer D et al. J Rheumatol 2012;39(1):46-53. Ørnbjerg LM et al. Ann Rheum Dis, in press 2012. Søgaard R et al. ClinicoEconomics and Outcomes Research 2010; 2: 105-12. Sørensen J et al. Value in Health, in press 2012. <h3>Disclosure of Interest</h3> None Declared
In vitro IL-12 treatment of peripheral blood mononuclear cells from patients with leukemia or myelodysplastic syndromes: increase in cytotoxicity and reduction in WT1 gene expression
Authors: L Pan, K Ohnishi, WJ Zhang, H Yoshida, L Maksumova, F Muratkhodjaev, K Shigeno, S Nakamura, JM Luo, HL Hao, S Fujisawa, K Naito, K Shinjo, A Takeshita, R Ohno
Journal: Leukemia (2000)
Abstract 4670: Polymorphisms in DNA repair genes, chemotherapy and survival in bladder cancer
Authors: Fulvio Ricceri, Carlotta Sacerdote, Silvia Polidoro, Simonetta Guarrera, Alessandra Allione, Rossana Critelli, Rossana Critelli, Alessia Russo, Paolo Gontero, Paolo Destefanis, Giuseppe Matullo, Paolo Vineis
Journal: Cancer Research (2011)

Abstract Bladder cancer (BC) survival is highly influenced by environmental and predisposing genetic factors. In the last decades growing evidence of the major role played by DNA repair systems in the survival after a BC has been provided. The objectives of the study are to assess the relationship between DNA Repair Genes polymorphisms and survival by treatment in bladder cancer patients. We conducted a hospital-based case-control investigation at S. Giovanni Battista hospital in Turin, where about half of the incident BC in the Turin metropolitan area are treated. Cases are histologically confirmed incident BC patients, male, aged 40 to 75 years and resident in the Turin metropolitan area. Each patient filled in a questionnaire on history of tobacco smoking, occupational history, 24-hours medication use recall and food habits, and provided a blood sample. We followed up BC patients for death and recurrences using municipal registry office, death's certificate, hospital discharge, medical records and pathologists’ reports. In the cohort of BC patients, we genotyped 36 Single Nucleotide Polymorphisms (SNPs) in 10 DNA Repair Genes. We analyzed survival on BC patients using a Cox proportional-hazards regression model for codominant and per-allele scenario, adjusted for age, stage and grading and stratified by therapy (chemotherapy vs no or other therapies). Chemotherapy group include patients tretated with systemic and local chemotherapy with different therapeutic plans (Carboplatinum doublets, Gencitabin, Epirubicin, etc). We identified 456 BC patients which were followed-up for mortality (median follow-up 62 months). In multivariate analysis both stage and grade predicted the outcome in a statistically significant way, after adjustment for age. Our preliminary analyses showed that the variant alleles in two SNPs in XRCC1 gene (rs 2854509 and rs 3213255) confer a significant lower risk of death and one SNP in ERCC2 gene (rs 171140) confers a significant higher risk of death compared to the wild type (analyses adjusted by age, stage and grading) only in the group of treated with chemotherapy. Our findings suggest a link between DNA repair genes variation and survival in BC patients that become evident only in patients treated with chemotherapy. We hypothesize that levels of DNA adducts or other DNA damages inducted by chemotherapy, are partially due to the individual DNA repair activity, resulting in a different response to chemotherapy and, consequentially, in different survival rates. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 4670. doi:10.1158/1538-7445.AM2011-4670
Epidemic Staphylococcal Pyoderma Associated with Ritters Disease and the Appearance of Phage Type 3B/71
Authors: Russell R. Rygheck, Paul M. Taylor, Horace M. Gezon
Journal: New England Journal of Medicine (1963)

RITTER'S disease, exfoliative dermatitis of the newborn, was first described by Ritter von Ritter-shain in 1878. Many investigators, since the work of Winternitz,1 in 1898, suggested Staphylococcus aureus and albus as the etiologic agents, have considered Ritter's disease to be an unusual manifestation of staphylococcal skin disease. The well documented epidemic of staphylococcal pyoderma reported by Lee et al.,2 in which 5 cases of Ritter's disease occurred in the middle of each wave of a biphasic outbreak, as well as similar outbreaks described by Howells and H. Everley Jones3 and Benson, Rankin and Rippey,4 suggests that Ritter's disease and simple . . .
Abstract 4087: Microbiomic subprofiles and MDR1 promoter methylation in head and neck squamous cell carcinoma
Authors: Gurkan Bebek, Kristi L. Bennett, Pauline Funchain, Rebecca Campbell, Rahul Seth, Joseph Scharpf, Brian Burkey, Charis Eng
Journal: Cancer Research (2012)

Abstract Background: Clinical observations and epidemiologic studies suggest that the incidence of head and neck squamous cell carcinoma (HNSCC) correlates with dental hygiene, implying a role for bacteria-induced inflammation in its pathogenesis. Differences in microbiota in HNSCC compared to matched normal oral mucosa, and whether these differences are accompanied by epigenetic modifications in selected HNSCC-associated genes and clinico-pathologic features has not yet been investigated. Standard microbiologic culturing techniques miss many fastidious organisms. Methods: Human genomic DNA and associated microbial DNA were isolated from 42 prospectively accrued consecutive HNSCC tumors and paired normal oral mucosae. Microbiomic profiling was carried out by serially characterizing bacteria-specific 16S rRNA and taxa classified by the presence of specific polymorphisms in the 16S rDNA genes. Promoter methylation and microbial populations of each sample was determined. Microbiomic profiles were compared between HNSCC and matched normal mucosa, to specific promoter methylation in four genes (MDR1, IL8, RARB, TGFBR2) previously linked to HNSCC or inflammation, and to clinico-pathologic features. Results: Specific microbiomic profiles significantly associate with HNSCC over normal mucosae. While methylation of both MDR1 (p&amp;lt;10-9) and IL8 (p&amp;lt;0.02) genes significantly associate with HNSCC, only MDR1 methylation associates with specific microbiomic profiles in HNSCC over normal mucosae. Furthermore, MDR1 methylation correlates with regional nodal metastases in the context of two specific bacterial taxa, Enterobacteriaceae and Tenericutes. Additionally, microbial populations can separate tumors by tobacco status (p&amp;lt;0.005), but not by alcohol status (p=0.37). Conclusions: Specific microbial populations may contribute to HNSCC pathogenesis, possibly by triggering inflammation and consequent aberrant DNA methylation. These associations could lead to better understanding of the pathogenesis and treatment of HNSCC, suggesting novel roles for demethylating agents and probiotic adjuncts particularly for patients with advanced or refractory disease. 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 4087. doi:1538-7445.AM2012-4087
Abstract 2178: Survivin appears to act as a transcription factor or co-factor to transcriptionally downregulate p21 gene expression via a p53 status-dependent manner
Authors: Lei Tang, Xiang Ling, Wensheng Liu, Gokul M. Das, Fengzhi Li
Journal: Cancer Research (2011)

Abstract Survivin, a unique member of the inhibitor of apoptosis (IAP) family proteins, is highly expressed in cancers but undetectable in most normal adult tissue. Survivin shows both inhibition of apoptosis and promotion of cell division. It plays a central role in cancer cell signaling network. Recent studies indicate that survivin may also play an important role in G1/S transition during cell cycle regulation. However, the underlying mechanism is unclear. Furthermore, although upregulation of p21WAF1/CIP1 (p21) expression by p53 plays an important role in p53-mediated cell G1 arrests in response to various distressing stimuli, it is unknown whether survivin plays a role in the regulation of p21 expression. Here, we report that forced expression of survivin in p53-wild type MCF-7 breast cancer cells inhibits the expression of the cell cycle inhibitor p21 protein, mRNA and promoter activity, while the survivin C84A mutant and survivin antisense failed to do so. Cotransfection experiments in the p53 mutant H1650 lung cancer cell line showed that exogenous survivin expression neutralizes p53-induced p21 expression and promoter activity. Both p53 and survivin interacts on two p53 binding sites in the p21 promoter (−2313 to -2212; -1452 to -1310), and survivin protein physically interacts with p53 protein in cancer cells. Additionally, we identified a PKC phosphorylation site at T127 that plays a critical role in inhibition of p21 promoter activity by survivin. Together, we propose that survivin acts as a transcription factor or cofactor to interact with p53 on the p21 promoter leading to transcriptional inhibition of p21 expression at least in part by neutralizing p53-mediated transcriptional activation of the p21 gene. *LT was a pre-doctoral Chinese fellowship student (Second West China Hospital, Sichuan University, Sichuan 610041, China) at the time this work was performed in the Li laboratory Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2178. doi:10.1158/1538-7445.AM2011-2178
Pancreatoduodenectomy with Portal Vein Resection is Feasible and Beneficial for Elderly Patients with Pancreatic Cancer
Authors: Mitsuro Kanda, Tsutomu Fujii, Hideki Takami, Hisaharu Ohya, Masaya Suenaga, Suguru Yamada, Daisuke Kobayashi, Chie Tanaka, Goro Nakayama, Hiroyuki Sugimoto, Masahiko Koike, Shuji Nomoto, Michitaka Fujiwara, Yasuhiro Kodera
Journal: Annals of Oncology (2013)
PTU-068 Response to antiviral therapy in genotype 3 hepatitis C—cirrhosis and diabetes but not ethnicity reduce response rates
Authors: D Shoeb, I Rowe, A Brown, R Marley, D Freshwater, S Moreea, D Mutimer, G Foster
Journal: Gut (2010)

<h3>Introduction</h3> The impact of ethnic background on response to antiviral therapy in patients with genotype 3 chronic hepatitis C infection remains unclear. <h3>Methods</h3> We performed a large retrospective analysis of 535 patients (268 Caucasian, 267 South Asian) treated with pegylated interferon and ribavirin at four UK centres. <h3>Results</h3> At baseline age, sex and proportions with cirrhosis were compared between the South Asians and Caucasians and cirrhosis was the only factor more common in people from South Asia 83/267(31%) vs Caucasian 56/268 (20.8%) and this was statistically significant (p=&lt;0.05). The overall sustained virological response rate (SVR) was 77.6%. In univariate analysis, age, diabetes, cirrhosis and need for dose reduction were associated with treatment failure. Ethnicity (Caucasian vs South Asian) did not affect SVR (proportions achieving SVR were 210/268=78.3%% in Caucasians and 209/267=78.2% in South Asians). In a multivariable analysis cirrhosis and presence of diabetes were the only factors significantly associated with a reduction in the proportion who achieved an SVR. Treatment failure was due to relapse in the majority of patients (70/535 patients relapsed (13.08%) while 46/535 (8.59%) had a breakthrough or no response. Relapse was inevitable in patients who did not achieve an early virological response (all 32 patients without an EVR relapsed) and was more common in those who did not have a rapid virological response (relapse occurred in18/96–18.7% who did not have an RVR compared to 8/153, 5.2% who did have a RVR, p=&lt;0.001). <h3>Conclusion</h3> The SVR in patients with genotype 3 chronic HCV infection is similar in patients from South Asia and Caucasians. The presence of cirrhosis significantly reduces the response to therapy and relapse is the most common mode of treatment failure.
AB1099 Outcome of Undifferentiated Arthritis- A Study of 154 Patients:
Authors: S. Rodríguez-Muguruza, M. Martinez-Morillo, A. Olive, A. Riveros-Frutos, J. Sanint, A. Prior, S. Holgado, L. Mateo, G. Cañellas, X. Tena
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Undifferentiated arthritis (UA) is defined as an inflammatory arthritis in which no definitive diagnosis can be made. The prognosis of patients with UA may vary from spontaneous remission, to severe defined inflammatory joint disease. Patients UA poses a challenging problem to the rheumatologist. It is important to identify patients who will develop a persistent and/or erosive disease because early treatment might offer an effective means to slow disease progression. <h3>Objectives</h3> To describe the outcome of patients with UA after 30 months of follow up. <h3>Methods</h3> Design retrospective (2006 - 2011) in an academic tertiary hospital with a reference area of 850,000 inhabitants. We reviewed the medical records of patients with “undifferentiated arthritis” from the database of rheumatology Department. We reviewed the pattern of involvement at the onset of the disease and final diagnosis in December 2013. <h3>Results</h3> A hundred and fifty four patients were included. The involvement, at the beginning of the disease was: 36 (23.3%) monoarticular, 71 (46.1%) oligoarticular and 47 (30.5%) polyarticular. During follow-up, it was observed that 30 (19.5%) patients went into remission spontaneously, 57 (64.9%) evolved to a defined inflammatory joint disease and 67 (43.5%) continued under the diagnosis of undifferentiated arthritis. Among those patients were a definite inflammatory joint disease was established: 38 (66.6%) continued follow up controls, 16 (28%) discontinued the follow-up and 3 (5.3%) were discharged. A progression to extended polyarthitis was observed in 3 patients with an oligoarticular pattern. Four patients with monoarthitis developed oligoarthritis. The knee was the most commonly involved joint (58.3%). <h3>Conclusions</h3> The most common pattern of joint involvement in UA is oligoarticular. Furthermore half of patients with UA went into remission. Patients with a monoarticular pattern had a greater chance of spontaneous remission compared with patients with oligo and polyarticular involvement. The frequency of follow up was also significantly higher in patients with definite inflammatory joint disease compared with patients with persistent UA (66.6% versus 47.7%). <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.2933
Abstract 5689: Phtalates toxicity on normal lymphocytes
Authors: Carlos A. Rosado, Christian Velez, Beatriz Zayas
Journal: Cancer Research (2010)

Abstract The main purpose of this study is to determine the toxicity and cell death mechanism of the phthalate Di-ethylhexyl (DEHP) and its principal metabolite, Mono-ethylhexyl (MEHP) on the TK-6 human lymphocytic cell line. Phthalates are a family of compounds used widely in the manufacturing industry and in the production of plastics. Exposure to these compounds can be through plastic items and personal care products. Phthalates are considered estrogen disrupters and effects on the reproductive and respiratory systems have also been reported by the scientific community. Studies, of the effect of phthalates on the immune system however are limited. The analysis of the effects of phthalates on normal lymphocytes could allow the development biomarkers of exposure to phthalates. TK-6 lymphocytes cells were cultured on 25cm2 flasks on modified RPMI culture media with 10% FBS, and incubated at 37oC and 5% CO2. TK-6 cells were exposed to DEHP or MEHP at doses ranging from 5μM, to 350μM for 48 and 72 hours. Cytotoxicity, ROS generation and mitochondrial membrane permeabilization were measured by Trypan Blue exclusion, DCFH-DA ROS assay and Mito PT assay respectively. Cytotoxicity results indicated higher resistance of TK-6 to the parent compound DEHP in comparison to the metabolite MEHP with IC50s of 100uM and 75uM respectively. Preliminary ROS generation analyses suggest induction of ROS generation by both parent and metabolite. mitochondrial membrane permeability analysis also indicated some degree of mitochondrial interaction. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 5689.
Abstract 438: The importance of estrogen-ERβ axis in racial disparity of prostate cancer
Authors: Zakaria Y. Abd Elmageed, Krzysztof Moroz, Sudesh K. Srivastav, Byron E. Crawford, Krishnarao Moparty, Raju Thomas, Asim B. Abdel-Mageed
Journal: Cancer Research (2012)

Abstract Purpose: The role of estrogens and estrogen receptors (ERs) in the disproportionate incidence and mortality of prostate cancer (PCa) has not been established. Although ERβ has been implicated in PCa progression, its ethnic-based expression and underlying mechanisms are not fully understood. The aim of this study is to establish correlation between estrogen-ERβ axis and clinical outcome in African American (AA) in comparison to Caucasian American (CA) men. Patients and Methods: 17β-Estradiol (E2) was determined in the blood procured from normal (n=30) and PCa patients (n=50) by ELISA. The expression of ERβ was assessed using an NCI-designed ethnicity-based tissue microarray (TMA) slide encompassing 150 each of AA and CA PCa tissue cores, 17 BPH, 13 normal biopsies, and 3 PCa cell lines (LNCaP, DU-145 and PC-3). Validation of ERβ in situ was validated by qRT-PCR in matched microdissected tumors and normal glands from both populations. Results: In comparison to normal subjects, circulating E2 levels were significantly (p=0.0160) elevated in AA-men than in CA-men with PCa. Additionally, a significant difference in E2 blood levels (p=0.0015) was observed between AA and AA PCa patients. Histoscore analysis demonstrate intense nuclear immunoreactivity (p=0.0018) against ERβ in tumors of AA than CA men. This notion was further validated by qRT-PCR on LCM-procured tumor cells (p=0.0315). In the adjusted multivariate analysis there was no correlation between ERβ expression and any clinical parameters in PCa tissues. In AA, there was a positive correlation between Gleason score (GS) and age but a negative correlation was found between GS, age and PSA-recurrence free. However, no correlation was found in CA. Conclusion: Together, high circulating levels of blood estrogens and mRNA levels coupled with a differential expression of ERβ in PCa tissues suggest a potential role for estrogen-ERβ axis in the development of castrate-resistant prostate cancer in AA men. Key words: E2, ER beta, mRNA, TMA, histoscore, African Americans, health disparities. 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 438. doi:1538-7445.AM2012-438