tbuckley/cabot-search huggingface dataset:
Abstract P6-08-09: Leptin and Estrogen Receptor Expression in Patients Suffered with Breast Cancer and Fibroadenoma
Authors: EV Peredereeva, AA Lushnikova, LN Lyubchenko, AA Parokonnaya, EB. Polevaya
Journal: Cancer Research (2010)

Abstract Introduction: Leptin is a multifunctional hormone produced by adipocytes. It plays important role in angiogenesis. Induction of cell proliferation, survival and anchorage-independent growth. These leptin activities are mediated through leptin receptor (ObR) that binds leptin molecule and stimulates Jak/STAT 3, ERK ½, cyclin D1 expression and other signal pathways. A recent data show that targeting leptin signaling may reduce mammary carcinogenesis and breast cancer (BC) progression. However, the link between obesity and leptin expression in serum/breast tumor as well as its role in modulation of estrogen receptors (EsR) and HER2/neu expression is not clear. Material and methods: We studied leptin, ObR, EsR, HER2/neu expression in patients with sporadic, familial and pregnancy-associated BC by RT PCR using BC fresh tissue and primers for genes encoding leptin, ObR, EsR-α, β. Leptin level in the patient sera was estimated also by ELISA (Leptin Sandwich DRG, DRG Diagnostics, Germany) followed by comassie staining. The data on immunohistochemical staining of HER2/neu, EsR and PrR were also obtained. In control group were patients with benign fibroadenoma (BFa) and healthy women of comparable age. Results: RT PCR results and immunohistochemistry method are mainly concordant : only 5% (5/29) of data were different. In triplonegative tumors (n=40) leptin overexpression was significantly higher than in other tumor types. Blood sera leptin level was correlates positively with ObR expression. Leptin expression in tumor tissue also correlates with HER2/neu over expression in all BC groups except triplonegative ones: Esr (-), PrR(-), HER2/neu(-). Serum leptin levels in BFa patients was higher (100-300 ng/ml) than in healthy women and the mean leptin level in BC patient of comparable age and body weight. Moreover, leptin serum level was positively correlates with ObR expression in tumors on I-III BC stages and with high body weight index (obesity). Conclusions: The data obtained indicate that leptin/ObR maight involved in BC progression. It indicates that ObR suppression isthe possible way for target BC therapy, especially of triplonegative tumors which do not express HER2/neu, so hormone therapy is not effective for these neoplasia. Citation Information: Cancer Res 2010;70(24 Suppl):Abstract nr P6-08-09.
Abstract 2776: Establishment of patient non-small cell lung cancer derived models for test of anticancer drugs.
Authors: Changnian Liu, Connie Sun, Wenwei Li, Wen Zhou, Yong Liu, Rui Zhou, Fang He, Chang Bai
Journal: Cancer Research (2013)

Abstract BACKGROUND Human tumor xenograft models established by transplantation of human tumor cell lines into immunodifficient mice have been routinely used for preclinical test of anticancer agents. But tumor cell lines have a relatively low transplantability and resulted in a limited number of tumor models available for selection of right models for testing novel agents based on their antitumor mechanism. Recently, we have developed a large number of patient primary non-small cell lung cancer (NSCLC) xenograft models by transplanting patients’ fresh tumor tissues into nude mice, which have been employed for preclinical test of anticancer agents. METHODS The fresh NSCLC tissues were collected from local hospitals. The tumor fragments of 1-2 mm were subcutaneously implanted in the flanks of the nude mice by trocar needle. Sixteen tumor fragments were grafted into four mice from one patient tumor tissue (passage 0). All therapeutic efficacy experiments used female mice bearing passage 5 xenografts. The test drugs included cisplatin, carboplatin, paclitaxel, docetaxel, gemcitabine, erlotinib, gefitinib, and pemetrexed. RESULTS A total of 213 patient primary NSCLC samples were implanted into nude mice, and 107 primary tumor models have been established with a tumor taking rate of 50% for the first passage. The tumor taking rates were higher (80-100) in the later passages. The therapeutic efficacy of the test drugs in these models is consistent with their clinical findings. The histopathology and gene sequence of the established primary tumor xenografts were analyzed; their architecture, histopathological morphology, and genomic mutation status from five generations of xenografts retained the patients’ original tumor characteristics. CONCLUSIONS The patient primary NSCLC models can be established in a large number for right models selection in preclinical setting, and have been employed for test of standard of care drugs and novel anticancer agents. The primary tumor models retain a similarity in histology and genomic mutation status to their patients’ original tumors. They may predict more relevant clinical response rate and higher correlation with clinical findings than use of traditional xenograft models established from long-term cultured cancer cell lines. Especially, they have advantages for test of target-oriented therapeutics in new drugs discovery and development programs. Citation Format: Changnian Liu, Connie Sun, Wenwei Li, Wen Zhou, Yong Liu, Rui Zhou, Fang He, Chang Bai. Establishment of patient non-small cell lung cancer derived models for test of anticancer drugs. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2776. doi:10.1158/1538-7445.AM2013-2776
VALORACIÓN ENDOSCÓPICA DE LA AFECTACIÓN GASTROINTESTINAL DE LA ENFERMEDAD INJERTO CONTRA HUÉSPED: COMPARATIVA DEL RENDIMIENTO DIAGNÓSTICO SEGÚN EL ÁREA ANATÓMICA BIOPSIADA
Authors: FJ García-Alonso, V Busto Bea, R Martín-Mateos, S Lozano-Cerrada, I Lucea, AI González-Tallón, M Calbacho, JÁ González Martín, D Boixeda de Miquel
Journal: Endoscopy (2011)

Introducción: La enfermedad injerto contra huesped (EICH) implica una importante mortalidad tras el trasplante de progenitores hematopoyéticos (TPH). La afectación gastrointestinal (GI) es frecuente, pero clínicamente indiferenciable de la secundaria a fármacos o infecciones. El diagnóstico es histológico, pero carecemos de consenso acerca del mejor enfoque endoscópico. Nuestro objetivo es evaluar la sensibilidad de distintas áreas de biopsia en el diagnóstico de EICH.
Endoscopic findings of indolent systemic mastocytosis involving the colon
Authors: Shuji Kochi, Shotaro Nakamura, Yumi Oshiro, Koichi Kurahara, Keisuke Kawasaki, Hiroki Yaita, Tadahiko Fuchigami
Journal: Endoscopy (2014)

A 64-year-old Japanese woman visited our hospital in July 2013 with a complaint of intermittent abdominal pain for 1 month. She had a history of maculopapular rashes on the neck over a period of 14 years. Colonoscopy using indigo carmine dye spraying revealed a few yellowish-white polypoid lesions ([Fig. 1 a, b]) and yellowish-white nodular or granular mucosal lesions in the ascending colon ([Fig. 1 c]) and the cecum ([Fig. 1 d]).
Increased Susceptibility to Infection in a Patient with Type II Essential Hypercatabolism of C3
Authors: Chester A. Alper, Kurt J. Bloch, Fred S. Rosen
Journal: New England Journal of Medicine (1973)

In a patient with partial lipodystrophy and increased susceptibility to infection, no abnormalities were found in humoral antibody, cellular immunity or leukocyte function. In contrast, the patient's serum complement-mediated functions were grossly deficient. The concentrations of the components of the serum complement and properdin systems were normal, except for that of C3, which was markedly reduced and consisted of native C3 and an inactive conversion product, C3c. The patient's serum contained an enzyme, C3ase, capable of cleaving C3 in vitro and in vivo. Addition of purified C3 to the patient's serum improved complement-mediated phagocytosis and killing of bacteria. In this Type II disorder, low serum C3 levels are ascribable to both hyposynthesis and hypercatabolism of this component of complement.
THU0069 Increased rate of diastolic heart failure in rheumatoid arthritis correlates with systemic inflammation and persistent disease activity, independent from treatment strategy
Authors: M. Gottwald, T. Schau, M. Neuss, D. Ridjab, I. Fischer, C. Butter, M. Zaenker
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Increased prevalence of chronic heart failure is observed in patients with rheumatoid arthritis (RA) and heart failure with normal ejection fraction (HFNEF) is the predominant type. Although traditional cardiovascular risk factors are overrepresented in RA patients, they alone do not sufficiently explain higher morbidity. Chronic inflammation is a suspected contributor to myocardial dysfunction. Further data is necessary to elucidate the influence of persistent RA disease activity and RA treatment on HFNEF. <h3>Objectives</h3> To correlate clinical signs, laboratory findings and echocardiographic markers of heart failure in a well-characterized cohort of RA-patients with cardiovascular risk factors and comorbidity <h3>Methods</h3> Prospective cross-sectional study including all RA-patients consecutively treated in our community based outpatient-clinic in a 3 months period. Inclusion criteria were written consent and diagnosis of RA, fulfilling ACR/EULAR-criteria. All patients were interviewed using a standardized questionnaire. Clinical signs were evaluated based upon Framingham criteria. Laboratory tests included NT-proBNP. Echocardiography contained tissue doppler and global longitudinal strain (GLS) imaging. <h3>Results</h3> 162 patients with RA, n=110 (68%) female, mean (SD) age 61.3 (±13.1) years, mean disease duration 12.5 (±11.4) years, mean DAS<sub>28</sub> 2.8 (±1.0), mean FFbH 68 (±27)%, mean HAQ 1.3 (±0.9) were included. Rate of remission or low-disease-activity (DAS<sub>28</sub> and lower remission rates in the biologic groups according to more severe disease state and longer disease duration. However, no significantly differences were found for HFNEF rates and cardiovascular comorbidity. <h3>Conclusions</h3> Traditional risk factors as well as RA-related factors are responsible for HFNEF in RA. RA-duration, persistent disease activity with DAS<sub>28</sub>&gt;2.6, increased ESR as markers of chronic inflammation were shown to be significant and independent contributors. The reduced GLS in HFNEF patients supports a putative role of endomyocardial fibrosis as a link between inflammation and impaired myocardial function. <h3>Disclosure of Interest</h3> None Declared
Pill scare linked to rise in abortions
Authors: L. Dillner
Journal: BMJ (1996)

It is argued that the British media exposure of the potential harmful side effects from oral contraceptive use contributed to raising fears and panic among users. The government in 1995 announced that there was double the risk of deep vein thrombosis from use of contraceptive pills containing gestodene or desogestrel. The government was advised by the Committee on Safety of Medicines. The British Pregnancy Advisory Service (BPAS) announced that the rise in abortions after the announcement could have been due to the pill scare. BPAS reported that during December 1995-February 1996 the number of abortions performed increased by 823 over the number reported in the same period a year before. The increase reversed a declining trend in abortions performed by a service that carries out 20% of all abortions in Great Britain. A BPAS spokesperson suggested that women panicked and stopped taking their pills, even though the government warned against an abrupt stop in usage. Women appeared to have not understood that risk was highest among overweight women and women with a prior history of thromboses. Findings from a BPAS survey that was conducted among almost 300 women with unplanned pregnancies showed that over 40% of women stopped taking their contraceptive pills immediately after the government's warning. 61% did not finish taking their remaining pills in the month's cycle. Under 20% of women switched to another contraceptive method. Another BPAS survey among 90 women that sought contraceptive advice at BPAS clinics found that nearly 50% of women expected the pill to be an unsafe method. It was suggested that media messages should have emphasized that the risk of unplanned pregnancies was much greater than the risks of deep vein thromboses.
Abstract A31: The Myb transcription factor links the ERα and EGFR pathways in breast cancer cells
Authors: Jing Bi, Nick Gilbert
Journal: Cancer Research (2011)

Abstract Drug resistance in breast cancer remains a big challenge, with many patients relapsing on endocrine therapies. To investigate growth-dependent signaling pathways in cancer we have generated a novel long-term estrogen-deprived cell line in serum-free conditions called DH as a model for antiestrogen treatment. DH cells are sensitive to ICI 182780, showing they are estrogen receptor (ERα)-dependent, they upregulate estrogen (E2)-dependent genes, indicating they are E2 responsive and are highly tamoxifen sensitive. This led us to hypothesize that in the total absence of E2 these cells might evolve to become highly E2 responsive and be capable of activating other growth-promoting pathways. We find that unliganded ERα is a negative regulator of EGFR expression but E2 stimulation triggers a slow upregulation of EGFR and a rapid reduction in ERα levels. After initial stimulation, EGFR expression is maintained despite E2 withdrawal, indicating a stable epigenetic modification at the EGFR promoter. E2 activates the growth-promoting MAPK pathway in an EGFR-dependent manner and we show a 5-day E2 pulse substantially increases the resistance of DH, MCF7, and ZR75-1 cells to tamoxifen and is accompanied by EGFR upregulation and phosphorylation. The cells remain sensitive to AG1478, an EGFR inhibitor, demonstrating a surprising functional switch between ERα and EGFR survival pathways, triggered by E2. To further investigate the relationship between ERα and EGFR, we used expression microarrays to identify MYB, a transcription factor, which is upregulated in response to E2. Upon E2 treatment, ERα binds to MYB intron 1, promoting MYB expression and consequently MYB is transiently located upstream of the EGFR promoter. MYB depletion by siRNA abrogates E2-dependent EGFR expression showing a direct link between these two pathways. These findings maybe significant for understanding acquired drug resistance on endocrine therapies. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the Second AACR International Conference on Frontiers in Basic Cancer Research; 2011 Sep 14-18; San Francisco, CA. Philadelphia (PA): AACR; Cancer Res 2011;71(18 Suppl):Abstract nr A31.
Changing paradigms in lower extremity reconstruction in war-related injuries
Authors: Margaret Connolly, Zuhaib R. Ibrahim, Owen N. Johnson
Journal: Military Medical Research (2016)

Ballistic high-energy trauma has substantially increased the severity of non-fatal extremity injuries incurred in modern warfare. Expedient medical care, refinement in surgical techniques, and soft tissue coverage have brought about a paradigm shift in the management of lower extremity wounds during the last decade with an increased emphasis on limb salvage. A literature-based study was conducted to analyze reconstructive modalities based on the location, depth, and severity of wounds, as well as mechanism of injury, concomitant vascular injuries and open fractures, choice of flap, timing of definitive reconstruction, and complications. Extremity injuries account for over 60 % of injuries in the recent conflicts in Iraq and Afghanistan, with the majority secondary to explosive devices. The severity of these injuries is profound compared with civilian registries, and conventional injury scoring systems have failed to accurately predict outcomes in combat trauma. The mainstay of treatment is serial debridement, negative pressure therapy, fracture stabilization, and treatment of concomitant injuries by the forward medical teams with subsequent definitive reconstruction after transport to an advanced military treatment facility. Autologous reconstruction with free tissue transfer and pedicled flaps remains the primary modality for soft tissue coverage in limb salvage. Adjunct innovative modalities, such as external tissue expansion, dermal substitutes, and regenerative matrices, have also been successfully utilized for limb salvage. Lower extremity injuries account for the vast majority of injuries in modern warzones. Explosive devices represent the most common mechanism of injury, with blast impact leading to extensive soft tissue injuries necessitating complex reconstructive strategies. Serial debridement, negative pressure therapy, and autologous reconstruction with free tissue transfer and pedicled flaps remain the mainstay of treatment in recent conflicts.
Abstract LB-444: Transforming growth factor beta polymorphisms and breast cancer survival among Chinese women
Authors: Alicia C. Beeghly-Fadiel, Wei Zheng, Wei Lu, Hui Cai, Jirong Long, Yu-Tang Gao, Ryan J. Delahanty, Qiuyin Cai, Xiao-Ou Shu
Journal: Cancer Research (2011)

Abstract Aberrant transforming growth factor-beta (TGFB) signaling contributes to tumor progression. To clarify the role of TGFB pathway variants and breast cancer survival, we conducted a two stage study among 4,535 breast cancer patients recruited in two studies conducted in Shanghai, China. In Stage I, 111 variants in TGFB, TGFBR1, and TGFBR2 were evaluated for associations with disease-free (DFS) and overall survival (OS) among 2,923 participants with a median of 5.5 years of follow-up time after their cancer diagnosis. Nominally significant associations with either DFS or OS were found for 31 variants, which after considering linkage disequilibrium, were found to represent 13 independent loci. Stage II genotyping was conducted among 1,612 additional participants with a median follow-up time of 5.1 years; data was available for 11 loci. Genetic variants in 6 loci were not associated with breast cancer outcomes in Stage II. Variants in 4 loci showed associations in Stage II that were generally consistent, but did not reach statistical significance. One variant was significantly associated with overall breast cancer survival in both study stages, and overall and disease free survival in analyses of the two study stage samples combined. Specifically, women with two copies of the rare variant of TGFBR1 rs3773651 (GG) had increased hazards of recurrence or breast cancer specific mortality (HR: 2.05, 95% CI: 1.28–3.27) and overall mortality (HR: 2.44, 95% CI: 1.50–3.95) compared to women with one or more common alleles (AG, AA) in age adjusted analyses. Additional adjustment for disease stage, ER, PR, or treatment including surgery, chemotherapy, radiotherapy, and tamoxifen did not attenuate these effects. Further, the statistical significance of these associations was retained after consideration was made for multiple comparisons (DFS p-value 0.0027; OS p-value 0.0003). rs3773651 is located in intron six of TGFBR2, a TGFB ligand specific receptor critical for transduction of TGFB signaling. Our data support a role for individual variation in TGFBR2 in breast cancer survival outcomes; additional investigation is warranted. 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 LB-444. doi:10.1158/1538-7445.AM2011-LB-444
Abstract 3577: Sensitivity and resistance of non-small cell lung cancer to the telomerase inhibitor imetelstat
Authors: Robin E. Frink, Michael Peyton, James P. Sullivan, Woodring E. Wright, Joan Schiller, Jerry W. Shay, John D. Minna
Journal: Cancer Research (2010)

Abstract Telomerase is expressed in the majority of lung cancers and functions to extend telomeres allowing for unlimited replication potential. Telomerase may also be essential in maintaining a cancer stem cell population making it an attractive therapeutic target. A new telomerase inhibitor, imetelstat (GRN163L), is currently in clinical trials for non-small cell lung cancer (NSCLC). Imetelstat, a lipidated 13-mer oligonucleotide N3′ P5′-thio-phosphoramidate, binds the functional RNA template of telomerase preventing telomerase from extending telomeres and thus potentially leading to telomere loss associated cancer cell death. In the present studies we treated multiple NSCLC cell lines (representing the full spectrum of oncogenotypes and chemotherapy drug response phenotypes) with imetelstat (1 μM, a concentration achieved in patients) continuously over several months and all tumor lines showed loss of telomerase activity and shortening of telomeres. NSCLC lines with initially short telomeres (NCI-H2073-initial telomere length (ITL) 2.7 Kb, Calu-3 (ITL 1.5 Kb), and NCI-H2087 (ITL 3 Kb)) either suffered massive apoptotic associated cell death (H2073) within one week, or developed very short telomeres and ceased proliferating at 2.5 weeks (Calu-3) or 20 weeks (H2087) of treatment, demonstrating primary sensitivity. However, a small subpopulation in H2073 continues to grow in culture in the presence of drug and is being tested for telomere length and sensitivity to higher concentrations of imetelstat. NSCLC lines with long telomeres (NCI-H1819 (ITL 15Kb) and NCI-H157 (ITL 14.5Kb)) treated with 1 µM imetelstat twice weekly for 32 weeks showed reduction of telomeres to 1.8 and 2 Kb respectively with no effect on mass culture proliferation but, in some cases, showed inhibition of colony formation. Removal of imetelstat resulted in return of telomerase activity and telomere re-growth. With continued 1 μM treatment, however, H1819 telomere length stabilized at 1.8Kb while H157 cells showed re-growth of telomeres to parental length and now requires &amp;gt;5 μM imetelstat to robustly inhibit telomerase. In summary, we have found a panel of NSCLC lines demonstrate several imetelstat response phenotypes: extreme initial sensitivity, maintenance of shortened telomeres with inhibition of colony formation, and acquired resistance to imetelstat therapy. We conclude that NSCLCs exhibit a diverse spectrum of responses to telomerase targeted therapy emphasizing the need to have tumor biomarker signatures for personalizing imetelstat therapy in NSCLC. 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 3577.
Surgical Oncology Research is Relatively Meager
Authors: T. Reynolds
Journal: JNCI Journal of the National Cancer Institute (1991)

Journal Article Surgical Oncology Research is Relatively Meager Get access Tom Reynolds Tom Reynolds Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 83, Issue 6, 20 March 1991, Pages 390–392, https://doi.org/10.1093/jnci/83.6.390 Published: 20 March 1991
Intense Ga-67 Accumulation in Pure Primary Mediastinal Seminomas
Authors: Makoto Hosono, Kikuo Machida, Norinari Honda, Takeo Takahashi, Akio Kashimada, Osamu Murata, Hisato Osada, Nobuyuki Ohtawa, Shinji Itoyama
Journal: Clinical Nuclear Medicine (2003)

The authors examined three patients with pure primary mediastinal seminomas, all of whom had marked Ga-67 uptake on scintigraphy. The unusual presentation of sclerotic bone metastases with remarkable extraosseous soft tissue involvement was observed in one patient. Another had a seminoma associated with a multiloculated thymic cyst, which is a rare lesion.
Potentiatied antitumor effectiveness of combined chemo-immunotherapy with Interleukin-12 and 5-fluorouracil of L1210 leukemia in vivo
Authors: J Goła̧b, R Zagożdżon, R Kamiński, K Kozar, K Gryska, D Iżycki, A Mackiewicz, T Stokłosa, A Giermasz, W Lasek, M Jakóbisiak
Journal: Leukemia (2001)