tbuckley/cabot-search huggingface dataset:
Lack of Benefit for Liraglutide in Heart Failure
Authors: Salvatore Carbone, Ross Arena, Antonio Abbate
Journal: JAMA (2016)

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Salvage tyrosine kinase inhibitor therapy for differentiated and medullary thyroid cancer.
Authors: R. P. Chowdry, C. Bhimani, S. S. Ramalingam, F. R. Khuri, T. K. Owonikoko
Journal: Journal of Clinical Oncology (2011)

e16036 Background: Thyroid cancer is the most common endocrine cancer worldwide. Frontline therapy with multikinase inhibitors in medullary and radioiodine-refractory thyroid cancer is very promising. Majority of patients eventually progress and therefore require salvage therapy. The benefit associated with the use of biologic agents as salvage therapy has, however, not been well studied. We reported on the clinical outcome of salvage therapy of thyroid cancer using biologic agent. Methods: Seven patients who progressed on a combination therapy with sunitinib and bortezomib were subsequently treated with another biologic agent as salvage therapy. We compared the clinical benefit attained on protocol with benefit in the salvage setting. Biochemical response was assessed by blood-based tumor marker assessment and anatomic response was assessed by cross-sectional imaging. Results: Seven thyroid cancer patients were included in this analysis. All patients were initially treated with bortezomib weekly plus sunitinib daily for 4 out of 6 weeks in a 6 week-cycle schedule. Median age at enrolment was 67 years, M/F - 5/2, ECOG performance status of 1 or 2: (100%). Tumor histology: medullary 2 (28%), papillary 3 (43%), Hurthle 2 (28%). Median duration of time on the initial therapy with the combination of Bortezomib and Sunitinib was 11 months (range: 3-18 months). Four of seven patients achieved metabolic response; best anatomic response was stable disease in 5/7 (71%) and partial response in 2/7 patient (29%). Salvage therapy off protocol included sorafenib (5 patients), sandostatin (1 patient), and best supportive care only (1 patient). Median duration of salvage therapy was 3 months (range 0-13 months). Best anatomic response was stable disease in 4 of 7 (57%) patients without any partial response. One patient died within 5 months of stopping active therapy. The remaining six patients are alive (1-22 months) after failing the initial therapy. Conclusions: Additional therapy using receptor kinase inhibitors in the salvage setting is associated with modest clinical benefit. Increased rate of toxicity however, limits prolonged treatment course.
Characterization of TPO Kinetics within 60 Days of Allogeneic Hematopoietic Stem Cell Transplantation and Its Correlation with Megakaryocyte Ploidy Distribution
Authors: Xiao-hui Zhang, Hai-xia Fu, Dai-Hong Liu, Lan-Ping Xu, Kai-Yan Liu, Xiao-Jun Huang
Journal: Blood (2012)
670. Probing the Stability of rAAV Capsids and Genomic Constructs Using Differential Scanning Calorimetry in Concert With Mobile Phase Modifiers
Authors: James D. Maratt, Samantha F. Povlich, Christopher J. Morrison, Gwendolyn M. Wilmes, Samuel C. Wadsworth, K. Reed Clark
Journal: Molecular Therapy (2015)

The recent resurgence of using rAAV vectors as commercially viable therapeutic agents has highlighted the need to identify stable capsid/genomic construct combinations which can both endure a typical cGMP manufacturing process and possess a long product shelf life. In this work we investigate the inherent stability of various capsids and genomic constructs using differential scanning calorimetry (DSC). DSC measures the amount of energy required to increase the temperature of a sample and reference and can be used to determine the Tm of the molecule in question. Numerous commercially relevant rAAV serotypes containing several genomic constructs (self-complimentary and oversized genomes) were subjected to melting curve analysis using DSC to compare stability. Additionally, various mobile phase modifiers were added to solution in order to probe the stability of rAAV vector, using organics and kosmotropic/chaotropic salts. These results demonstrate DSC as an effective tool to examine inherent rAAV vector capsid stability and support a role for the serotype and vector genome structure to affect the observed stability.
Development of Mek inhibition (MEK-I)-Based Therapeutic Strategies in Acute Myeloid Leukemia (AML)
Authors: Michele Milella, Maria Rosaria Ricciardi, Paola Bergamo, Maria Cristina Scerpa, Jacopo Gervasoni, Maria Teresa Petrucci, Sabina Chiaretti, Simona Tavolaro, Ludovica Ciuffreda, Samantha Decandia, Francesco Libotte, Stephen Lee Abrams, Linda S Steelman, Marina Konopleva, Francesco Cognetti, Robert Foa, Michael Andreeff, James McCubrey, Agostino Tafuri
Journal: Blood (2008)
Abstract 3201: Complement component C3 and complement factor B regulate growth of cutaneous squamous cell carcinoma
Authors: Pilvi Riihila, Mehdi Farshchian, Markku Kallajoki, Atte Kivisaari, Seppo Meri, Reidar Grenman, Ritva Heljasvaara, Taina Pihlajaniemi, Juha Peltonen, Sirkku Peltonen, Veli-Matti Kahari
Journal: Cancer Research (2015)

Abstract Cutaneous squamous cell carcinoma (cSCC) is the most common metastatic skin cancer and its incidence is increasing globally. We have examined the role of complement component C3 and complement factor B (CFB) in the progression of cSCC. Significantly elevated mRNA levels for C3 and CFB were detected din cSCC cell lines (n = 8) compared to normal human epidermal keratinocytes (n = 11) by quantitative real-time reverse transcriptase-PCR. Increased production of C3 and CFB by cSCC cell lines was detected by western blotting. The mRNA levels for C3 and CFB were also markedly higher in cSCC tumors (n = 6) than in normal skin (n = 10). Tumor cell specific staining for C3 and CFB was detected in cSCC tumors in vivo by immunohistochemistry and the staining intensity was stronger in invasive cSCCs (n = 71) than in cSCC in situ (n = 69), premalignant epidermal lesions (actinic keratoses, n = 65) and normal skin (n = 5). Significant upregulation of C3 and CFB mRNA expression was also noted in chemically induced mouse skin cSCCs (n = 27) compared to benign papillomas (n = 17). The expression of C3 and CFB at mRNA and protein level was markedly higher in invasive tumorigenic Ha-ras-transformed HaCaT cell line than in benign tumorigenic ras-transformed HaCaT cells and parental non-tumorigenic HaCaT cells. The expression of both C3 and CFB was significantly upregulated by IFN-γ and TNF-α in cSCC cells. Knockdown of CFB and C3 by specific siRNAs inhibited migration of cSCC cells. Knockdown of CFB inhibited proliferation of cSCC cells and this was associated with potent inhibition of ERK1/2 activation. Knockdown of C3 and CFB also significantly inhibited growth of human cSCC xenograft tumors in vivo in SCID mice. These results provide evidence for the role of C3 and CFB in progression of cSCC and identify them as specific biomarkers and putative therapeutic targets for invasive cSCC. Citation Format: Pilvi Riihila, Mehdi Farshchian, Markku Kallajoki, Atte Kivisaari, Seppo Meri, Reidar Grenman, Ritva Heljasvaara, Taina Pihlajaniemi, Juha Peltonen, Sirkku Peltonen, Veli-Matti Kahari. Complement component C3 and complement factor B regulate growth of cutaneous squamous cell carcinoma. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 3201. doi:10.1158/1538-7445.AM2015-3201
Splenectomy in a Child of X-Linked Thrombocytopenia with Thalassemia and Bone Marrow Fibrosis : Hemoglobin and Platelet Count Were Improved
Authors: Yang Wan, Xiaofan Zhu, Xiaojuan Chen, Wenbin An, Peihong Zhang, Yingchi Zhang, Ye Guo
Journal: Blood (2014)
Adoptive Transfer of EBNA1-Specific T-Cells as a Treatment of Epstein-Barr-Virus Reactivation Following Allogeneic Stem Cell Transplantation
Authors: Vanya Icheva, Kathrin Opherk, Wolfgang A. Bethge, Simone Kayser, Johann Greil, Rupert Handgretinger, Peter Lang, Tobias F. Feuchtinger
Journal: Blood (2010)
A Facile and Versatile Method to Endow Biomaterial Devices with Zwitterionic Surface Coatings
Authors: Volkan Yesilyurt, Omid Veiseh, Joshua C. Doloff, Jie Li, Suman Bose, Xi Xie, Andrew R. Bader, Michael Chen, Matthew J. Webber, Arturo J. Vegas, Robert Langer, Daniel G. Anderson
Journal: Advanced Healthcare Materials (2016)

The surface modification of implantable biomaterials with zwitterionic phosphorylcholine polymer is demonstrated through mussel-mimetic catecholamine polymer thin films. Using this method, the surfaces of alginate hydrogel microspheres and polystyrene microbeads, a model material known to produce robust foreign body responses and fibrosis, are successfully modified to reduce the tissue reaction by reducing the fibrosis in immunocompetent C57BL/6J mice. As a service to our authors and readers, this journal provides supporting information supplied by the authors. Such materials are peer reviewed and may be re-organized for online delivery, but are not copy-edited or typeset. Technical support issues arising from supporting information (other than missing files) should be addressed to the authors. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.
Randomized phase II study of ficlatuzumab (formerly AV-299), an anti-hepatocyte growth factor (HGF) monoclonal antibody (MAb) in combination with gefitinib (G) in Asian patients (pts) with NSCLC.
Authors: T. Mok, E. Tan, K. Park, J. Jac, M. Han, F. C. Payumo, M. Credi, K. McKee, M. M. Cotreau, P. Bhargava, W. Slichenmyer
Journal: Journal of Clinical Oncology (2011)

TPS213 Background: Ficlatuzumab is a humanized anti-HGF IgG1 MAb that inhibits activation of the c-Met receptor by neutralizing its only known natural ligand, HGF. HGF/c-Met pathway activation has been implicated in EGFR TKI resistance in NSCLC. In an ongoing phase Ib trial, the combination of ficlatuzumab + G was found to be well tolerated up to the maximum tested dose of 20 mg/kg of ficlatuzumab and 250 mg of G, and demonstrated clinical activity in pts with NSCLC. Methods: It is a multi-center, open-label, 2-arm, randomized study comparing ficlatuzumab + G versus G alone in clinically selected Asian pts with previously untreated lung adenocarcinoma (never- or former-light smokers) who have a high likelihood of harboring activating EGFR mutations. Stratification is by ECOG performance status (0-1 vs. 2), smoking status (nonsmoker vs. light ex-smoker) and gender. Pts will be treated in continuous 28-day cycles, during which all pts will receive G daily (250 mg/day PO), and pts randomized to ficlatuzumab + G will also receive ficlatuzumab (20 mg/kg IV) on Days 1 and 15 of each cycle. Pts who progress after achieving initial disease control (CR, PR, or SD for 12 weeks or longer) in the G alone arm may cross over to the combination arm. The primary objective is to compare the Objective Response Rate (ORR) between the arms. Secondary objectives are to evaluate the safety and tolerability of ficlatuzumab + G, response duration, Progression-Free Survival (PFS), and Overall Survival (OS), to investigate the relationship between the anti-tumor activity of ficlatuzumab + G and molecular markers such as activating EGFR mutations, c‐Met and EGFR gene copy numbers (FISH positivity), HGF, c-Met and p-Met expression, HGF serum levels, and to assess whether acquired resistance to G can be overcome with the addition of ficlatuzumab in pts who progressed after initial demonstration of disease control (CR, PR, or SD for 12 weeks or longer) in the G alone arm. Estimated sample size is 170 pts.
Low Risk of Pneumonia From Pneumocystis jirovecii Infection in Patients With Inflammatory Bowel Disease Receiving Immune Suppression
Authors: Thomas G. Cotter, Nicola Gathaiya, Jelena Catania, Edward V. Loftus, William J. Tremaine, Larry M. Baddour, W. Scott Harmsen, Alan R. Zinsmeister, William J. Sandborn, Andrew H. Limper, Darrell S. Pardi
Journal: Clinical Gastroenterology and Hepatology (2016)
The PRAME and WT1 Transcripts Constitute a Good Molecular Marker Combination for Monitoring Minimal Residual Disease in Myelodysplastic Syndromes
Authors: Yazhen Qin, Honghu Zhu, Yan-rong Liu, Ya-zhe Wang, Hong-Xia Shi, Yue-yun Lai, Lan-Ping Xu, Daihong Liu, Xiaojun Huang
Journal: Blood (2012)
The role of bile acids in morphological changes оf gastric mucosa in rats
Authors: A.I. Rudenko, L.M. Mosiychuk, N.Y. Oshmyanska
Journal: GASTROENTEROLOGY (2014)

The present study was conducted on 60 white male laboratory rats in order to investigate the role of bile acids in morphofunctional changes of gastric mucosa in rats with due regard to exposure of bile and its concentration. It was found that in the early stages of duodenogastric reflux in experiment bile in low concentrations carries protective adaptive-trophic function and promotes cell renewal of the surface epithelium. At the same time long-term exposure to the bile acids regardless of its concentration can lead to the significant dystrophic changes in gastric mucosa, pilorization and atrophy of the gastric glands. In the case of the oral administration of bile followed by «immobilization and cold stress» for one hour (I group) experiment’s results can confirm that the combined effects of several aggressive factors lead to the more severe pathological changes in the gastric mucosa: first erosive and later ulcerative lesions.
Abstract 219: Fluorescence-guided surgery with an anti-CA 19-9-conjugated fluorophore in combination with neoadjuvant chemotherapy inhibits metastatic recurrence in a pancreatic cancer patient derived orthotopic xenograft (PDOX) nude mouse model
Authors: Yukihiko Hiroshima, Ali Maawy, Yong Zhang, Takashi Murakami, Masashi Momiyama, Ryutaro Mori, Ryusei Matsuyama, Matthew H. Katz, Jason B. Fleming, Takashi Chishima, Kuniya Tanaka, Yasushi ichikawa, Itaru Endo, Robert M. Hoffman, Michael Bouvet
Journal: Cancer Research (2015)

Abstract The efficacy of fluorescence-guided surgery (FGS) in combination with neoadjuvant chemotherapy (NAC) with gemcitabine (GEM) on a pancreatic cancer patient derived orthotopic xenograft (PDOX) model was determined. A PDOX model was established from a CA19-9-positive, CEA-negative tumor from a patient who had undergone a pancreaticoduodenectomy for pancreatic adenocarcinoma. Mice were randomized to 4 groups: bright light surgery (BLS) only; BLS + NAC; FGS only; and FGS + NAC. An anti-CA19-9 or anti-CEA antibody conjugated to DyLight 650 was administered intravenously via the tail vein of mice with the pancreatic cancer PDOX 24 hours before surgery. The PDOX was brightly labeled with fluorophore-conjugated anti-CA19-9, but not with a fluorophore-conjugated anti-CEA antibody. FGS was performed using the fluorophore-conjugated anti-CA19-9 antibody. FGS + NAC significantly reduced the metastatic recurrence frequency to one of 8 mice, compared to FGS only after which metastasis recurred in 6 out of 8 mice, and BLS + NAC with metastatic recurrence in 7 out of 8 mice (p = 0.041). Thus NAC in combination with FGS can reduce or even eliminate metastatic recurrence of pancreatic cancer sensitive to NAC. The present study further emphasizes the power of the PDOX model which enables metastasis to occur and thereby identify the efficacy of FGS in combination with NAC on metastatic recurrence. Citation Format: Yukihiko Hiroshima, Ali Maawy, Yong Zhang, Takashi Murakami, Masashi Momiyama, Ryutaro Mori, Ryusei Matsuyama, Matthew H. Katz, Jason B. Fleming, Takashi Chishima, Kuniya Tanaka, Yasushi ichikawa, Itaru Endo, Robert M. Hoffman, Michael Bouvet. Fluorescence-guided surgery with an anti-CA 19-9-conjugated fluorophore in combination with neoadjuvant chemotherapy inhibits metastatic recurrence in a pancreatic cancer patient derived orthotopic xenograft (PDOX) nude mouse model. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 219. doi:10.1158/1538-7445.AM2015-219
An in vitro model for oral cancer progression: Transformation of the oral keratinocyte cell line (MSK Leuk1) by benzopyrene-7,8-dihydrodiol-9,10-epoxide
Authors: Qing Zhong, Jia-Long Fang, Peter Sacks, Philip Lazarus
Journal: Cancer Research (2004)

788  Leukoplakia is a highly prevalent premalignant disease state of the oral cavity with a relatively high tumorigenic potential. MSK Leuk1 is an oral keratinocyte cell line spontaneously-derived from an oral leukoplakia lesion that exhibits an immortalized but non-tumorigenic phenotype. In an attempt to obtain an in vitro model for oral cancer progression from leukoplakia to oral cancer, MSK Leuk1 cells were treated with benzo[a]pyrene (BaP)- 7,8-diol-9,10-epoxide (BPDE), the ultimate carcinogenic metabolite of BaP, a potent and abundant tobacco smoke carcinogen. MSK Leuk1 cells were exposed to titrated doses of BPDE (0.2 through 1.6 μM) for up to 8 hours of treatment. BPDE-treated cells were then continuously sub-cultured and tested for neoplastic transformation as determined by anchorage-independent growth in semisolid agar (0.3% Noble soft agar with DMEM/F-12 medium) in colony formation assays. In addition, morphologic alterations, growth rates and foci formation were monitored in regular culture medium. BPDE-treated but not vehicle-treated MSK Leuk1 cells formed colonies after growth in soft agar, with the colony forming efficiency of BPDE-treated cells increasing in a dose-dependent manner. Similarly, foci formation was observed for BPDE-treated but not vehicle-treated MSK Leuk1 cells, with the foci-forming efficiency of BPDE-treated cells increasing in a dose-dependent manner. BPDE (1.6 uM)-treated cells had a growth rate that was significantly (p
Abstract 3021: FoxP1 increases nucleotide excision repair capacity through activating xeroderma pigmentosum group C in human breast cancer
Authors: Haesung Kim, Lee-Su Kim, Jae-yong Lee, Jeong-Hyeon Kim, Jeong-Min Lee, Chea-Ha Kim
Journal: Cancer Research (2015)

Abstract Breast cancer is the most common cancer in the women. Recent study revealed that nucleotide excision repair (NER) deficiency might play an important role in the cause of sporadic breast cancer, showing significant reduction of five NER gene products including xeroderma pigmentosum group C (XPC) in human breast cancer tissue. Thus, XPC inactivation might be related to occurrence and progression of breast cancer. FoxP1 is a member of the forkhead O family of transcription factors which have a broad range of functions. FoxP1 is considered as a putative tumor suppressor in breast cancer because of its ability to cause apoptosis. The relationship between FoxP1 and XPC has been yet to be known in breast cancer. In our data, Western blot analysis of 8 human primary tumors showed that the high expression of FoxP1 was correlated with the high level of XPC. In three established mammary epithelial cell lines (MCF-7, MDA-MB-231, 4T1), FoxP1 expression in MCF-7 was higher than in MDA-MB-231 and 4T1. Similar to the result of primary tumors, the expression of XPC was also high in MCF-7 and low in MDA-MB-231 and 4T1. Next, we found that the level of XPC decreased with the knockdown of FoxP1 compared to control in MCF-7. On the other hand, the ectopic expression of FoxP1 in MDA-MB-231 and 4T1 elevated XPC expression for protein level. In real time RT-PCR, the level of XPC mRNA was the same as in Western blot analysis. We tested whether NER activity is dependent on FoxP1. In vitro NER activity increased by overexpression of FoxP1 in MB-231. Sh-FoxP1 transfected MCF-7 cell shows reduced in vitro NER activity. In addition, immunostaining assay showed that XPC expression was much accumulated in the nucleus of MDA-MB-231 with overexpression of FoxP1 than in control.Taken together, these data suggested FoxP1 could up-regulate NER activity by activating XPC in breast cancer. However, the way how FoxP1 can regulate XPC remained to be cleared. To clarify the mechanism, we are performing biological interaction between FoxP1 and XPC in both breast cancer cell lines and human primary breast tumors. Citation Format: Haesung Kim, Lee-Su Kim, Jae-yong Lee, Jeong-Hyeon Kim, Jeong-Min Lee, Chea-Ha Kim. FoxP1 increases nucleotide excision repair capacity through activating xeroderma pigmentosum group C in human breast cancer. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 3021. doi:10.1158/1538-7445.AM2015-3021