tbuckley/cabot-search huggingface dataset:
The use of<i>O</i>-(2-<sup>18</sup>F-fluoroethyl)-L-tyrosine PET in the diagnosis of gliomas located in the brainstem and spinal cord
Authors: Caroline Tscherpel, Veronika Dunkl, Garry Ceccon, Gabriele Stoffels, Natalie Judov, Marion Rapp, Philipp T. Meyer, Elena Rota Kops, Johannes Ermert, Gereon R. Fink, Nadim J. Shah, Karl-Josef Langen, Norbert Galldiks
Journal: Neuro-Oncology (2016)

Despite an increasing number of O-(2-18F-fluoroethyl)-L-tyrosine (18F-FET) PET studies in supratentorial gliomas, studies regarding the usefulness of 18F-FET PET in brainstem and spinal cord gliomas to date remain scarce.Thirty-six 18F-FET PET scans were performed in 29 patients with brainstem (n = 29 scans) or spinal cord glioma (n = 7 scans). In 32 of 36 PET scans, a dynamic acquisition was performed. Fifteen scans in 15 patients were performed to assess newly diagnosed lesions, and 21 scans were obtained during follow-up: for diagnosing tumor progression (n = 15 scans in 14 patients) as well as for treatment monitoring (n = 6 scans in 3 patients). Four patients underwent additional serial scans (range, 1-2), and 3 of these 4 patients were examined for more than one indication. Maximum and mean tumor/brain ratios (TBRmax/mean) of 18F-FET uptake (20-40 min post injection) as well as kinetic 18F-FET uptake parameters were determined. Final diagnoses were confirmed histologically (54%) or by clinical follow-up (46%).In all newly diagnosed high-grade (n = 3 patients) and in 5 of 11 patients with low-grade gliomas, 18F-FET uptake was increased (TBRmax ≥2.5 and/or TBRmean ≥1.9). In 2 patients with newly diagnosed gliomas without MR contrast enhancement, 18F-FET PET nevertheless showed increased metabolism. At suspected progression, the combination of TBRs with kinetic 18F-FET parameters correctly identified presence or absence of progressive disease in 9 of 11 patients (82%).This preliminary study suggests that 18F-FET PET adds valuable diagnostic information in brainstem and spinal cord glioma, particularly when the diagnostic information derived from MRI is equivocal.
Presentation of Epstein Barr Virus (EBV) Epitopes by Activated Human γδ T Cells Induces Peptide-Specific Cytolytic CD8+ T Cell Expansion.
Authors: Silke Landmeier, Bianca Altvater, Sibylle Pscherer, Lena Varnholt, Catherine M. Bollard, Heribert Juergens, Claudia Rossig
Journal: Blood (2006)
Clinical and laboratory features of minor ABO incompatible reduced intensity blood hematopoietic cell transplantation using cyclosporin vs CsA/mycophenolate mofetil for graft-vs-host disease prophylaxis
Authors: A. Reese, W. T. Stevens, T. Donohue, S. Chakrabarti, R. Wesley, K. Castro, D. Fowler, M. R. Bishop, D. Stroncek, S. Leitman, R. W. Childs, C. D. Bolan
Journal: Blood (2003)
Abstract 5030: Polarizing tumor associated macrophages (TAMs) towards an anti-tumor phenotype with a novel compound reveals a new subset of TAMs within breast tumors which facilitate tumor regression
Authors: Alaba O. Sotayo, Jennnifer L. Guerriero, Holly E. Ponichtera, Anthony G. Letai
Journal: Cancer Research (2015)

Abstract Manipulation of the innate immune system is a relatively understudied strategy for anti-cancer immunotherapy. The current focus on immunotherapy is centered on the adaptive immune system. However, there is growing evidence that manipulation of the innate immune system, including macrophages, is also a promising method to combat cancer. Tumor associated macrophages (TAMs) are one of the major infiltrating leukocyte populations associated with solid tumors. There are two major types of macrophages: classically activated macrophages, which can kill bacteria, pathogens, and similarly tumor cells; and alternatively activated macrophages which facilitate wound repair and are generally found in the tumor microenvironment. TAMs are generally alternatively activated cells with immunosuppressive properties that have been shown to enhance tumorogenesis by facilitating metastasis, angiogenesis, and inhibiting a protecting adaptive immune response. The presence of macrophages in the tumor microenvironment correlates with poor prognosis. Here we describe a novel, first in class compound that activates macrophages to an anti-tumor phenotype. While this compound has no direct cytotoxic activity, we show in the PyMT mouse model of breast cancer that breast tumors regress in response to therapy in a manner dependent on myeloid cells. Through the use of flow cytometry, we have been able to identify different subpopulations of TAMs using the markers CD45, MHCII, and CD11b. Correlating with tumor regression, we see an increase in PARP and cleaved caspase 3, indicating apoptotic cell death. Here we show that a novel compound effectively polarize macrophages to an anti-tumor phenotype to induce tumor regression. This strategy may have great therapeutic promise. Citation Format: Alaba O. Sotayo, Jennnifer L. Guerriero, Holly E. Ponichtera, Anthony G. Letai. Polarizing tumor associated macrophages (TAMs) towards an anti-tumor phenotype with a novel compound reveals a new subset of TAMs within breast tumors which facilitate tumor regression. [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 5030. doi:10.1158/1538-7445.AM2015-5030
Abstract 5526: Deciphering the basis of CendR-mediated penetration into tumors
Authors: Hongbo Pang, Gary B. Braun, Tomas Friman, Erkki Ruoslahti
Journal: Cancer Research (2015)

Abstract Cell-penetrating peptides (CPPs) have proven their usefulness in overcoming barriers (such as the cell membrane) of drug delivery into tumor cells. We recently discovered a novel class of cell-penetrating peptides that also have tumor-penetrating properties. These so-called, CendR peptides,bind to neuropilin-1 (NRP1) and initiate an active endocytic process into tumor cells. Subsequent studies showed that CendR-initiated endocytosis is a receptor-dependent macropinocytosis process, and that its activity is stimulated by mTOR inhibition and nutrient deprivation. In vivo, CendR peptides penetrate across tumor vessels deeply into the extravascular tumor tissue, and show ability to improve the tumor accumulation and antitumor efficacy of coupled, and even co-administrated, drugs. Further understanding of the CendR-mediated cell and tissue penetration is of value to cell biology and cancer therapy. Here, we report ultrastructural studies to unveil the subcellular transport route for CendR peptide. After synchronized cell entry, transmission electron microscopy (TEM) imaging shows that CendR cargo is transported from early endosomes to late endosomes and lysosomes. We have also identified some of the genes important for this transport. Moreover, magnetic isolation of intracellular vesicles containing CendR cargo and proteomics analysis identified signature molecules associated with these vesicles. Studies with TAT peptide comprised of D-amino acids (D-TAT), included in these studies as a non-CendR CPP, indicate that D-TAT also penetrates into tumor cells through a variation of macropinocytosis independent of NRP1. The uniqueness of CendR pathway lies in the linkage of CendR endocytosis to mTOR and cellular nutrient status. We provide evidence that a transcription factor, Sp1, serves as a link between mTOR and CendR endocytosis by regulating the NRP1 level on the cell surface. Additionally, we have shown the intercellular transport of CendR cargo that affords tissue penetration and is also stimulated by nutrient deprivation. Here we identify genes critical to the export and re-entry of CendR cargo during intercellular transport. These results shed light into the mechanism of action of CPPs, and endocytosis in general. They also have implications in cancer metabolism and drug delivery. Citation Format: Hongbo Pang, Gary B. Braun, Tomas Friman, Erkki Ruoslahti. Deciphering the basis of CendR-mediated penetration into tumors. [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 5526. doi:10.1158/1538-7445.AM2015-5526
Metastatic potential and prognosis of mucinous adenocarcinoma of the endometrium.
Authors: F. Musa, B. Adams, M. Huang, E. C. Pirog, K. Holcomb
Journal: Journal of Clinical Oncology (2011)

e15575 Background: Mucinous adenocarcinoma of the endometrium (MAC) is a rare histological variant of endometrial cancer accounting for 1-9% of endometrioid tumors. It is thought to originate from mucinous metaplasia of the endometrium and prior studies have implicated the anti-estrogenic effects of tamoxifen and progesterone in its carcinogenesis. This study compares the risk factors and clinical course of MAC relative to endometrioid adenocarcinoma. Methods: This is a case-control study including patients treated for endometrial cancer from 1996-2006. 41 cases of MAC were identified and matched with two controls of endometrioid histology by age and histological grade. Cases and controls were compared with regard to known risk factors for endometrial cancer and the extent of disease at diagnosis. Chi-square tests were used to compare proportions and student T-tests for the comparison of means. Multivariate regression was used to identify the independent predictors of lymph node metastases. Overall survival was calculated using the Kaplan-Meier method and compared with the Log-rank test. P<0.05 was considered significant for all tests. Results: No difference was found between cases and controls with regard to ethnicity, BMI, history of diabetes, hypertension, prior hormone replacement, or tamoxifen use. Prior oral contraceptive use was less common among women with MAC compared to controls (6.5% vs 32.3%, P= 0.01). No difference in myometrial invasion (MI) > 50% or the presence of LVSI was found between cases and controls, however, 17% of patients with MAC had lymph node metastases compared to 3% of controls (P= 0.01). Multivariate analysis controlling for both tumor grade and depth of MI identified mucinous histology as an independent predictor of lymph node metastasis (P =0.02). Adjuvant radiation or chemotherapy was used in 60% of cases compared to 42% of controls (P =0.05). No difference in recurrence or survival was identified between the two groups. Conclusions: MAC is associated with an increased risk of lymph node metastases that is independent of tumor grade and depth of MI. Comprehensive surgical staging including retroperitoneal node dissection should be strongly considered in all patients with mucinous differentiation.
Abstract 4182: Gemcitabine triggers angiogenesis-promoting molecular signals in pancreatic cancer cells: Therapeutic implications
Authors: Mohammad Aslam Khan, Sanjeev K. Srivastava, Arun Bhardwaj, Seema Singh, James E. Carter, Ajay P. Singh
Journal: Cancer Research (2015)

Abstract Pancreatic tumor microenvironment (TME) is characterized by poor tumor vasculature and extensive desmoplasia that together contribute to poor response to chemotherapy. It was recently shown that targeting of TME to inhibit desmoplastic reaction in a mouse model of pancreatic cancer resulted in increased microvessel density and intratumoral drug concentration, leading to improved therapeutic response. This approach; however, failed to generate a favorable response in a clinical trial. In that regard, we have previously demonstrated that gemcitabine-treatment of pancreatic cancer cells induces CXCR4 expression in a counter-defense mechanism and promotes pancreatic tumor cell invasiveness. The goal of present study was to examine the effect of chemotherapy on endothelial cell growth and migration. Pancreatic cancer cells were treated with gemcitabine or vehicle for 8 h and subsequently incubated in fresh low serum-containing media for next 48 h. Conditioned media was collected from vehicle- (V-CM) and gemcitabine-treated (Gem-CM) pancreatic cancer cells and used for the treatment of human umbilical vein endothelial cells (HUVEC). The data demonstrated stimulatory effects of Gem-CM on endothelial cell proliferation, migration, invasion and capillary-like structure (CLS) formation. Expression analysis of vehicle- and gemcitabine-treated pancreatic cancer cells and their conditioned-media revealed an upregulation of CXCL8/IL8, which is a known regulator of angiogenesis. Currently, we are investigating whether IL8 mediates the effect of Gem-CM on endothelial cells. Together, our findings suggest that gemcitabine triggers angiogenesis-promoting molecular signals in pancreatic cancer cells, which, in light of our previous observations, may hold important clinical and translational significance. Citation Format: Mohammad Aslam Khan, Sanjeev K. Srivastava, Arun Bhardwaj, Seema Singh, James E. Carter, Ajay P. Singh. Gemcitabine triggers angiogenesis-promoting molecular signals in pancreatic cancer cells: Therapeutic implications. [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 4182. doi:10.1158/1538-7445.AM2015-4182
Methylation Status of the Collagen Prolyl-3 Hydroxylases (C-P3H) and C-P4H Genes in Multiple Myeloma: P3H2 Is Selectively Methylated
Authors: Eleftheria Hatzimichael, Aggeliki Dasoula, Konstantinos Lagos, Georgianna Kartalou, George Dranitsaris, Evangelos Briasoulis, Tim Crook
Journal: Blood (2011)
Extended Study for Topotecan, Idarubicin, and Intermediate-Dose Cytarabine Combination Chemotherapy in Patients with Refractory or Relapsed Acute Myelogenous Leukemia and High-Risk Myelodysplastic Syndrome.
Authors: Yuri Kim, June-Won Cheong, Jin Seok Kim, In Hae Park, Sun Young Park, Seung Tae Lee, Yoo-Hong Min
Journal: Blood (2005)
Somatic STAT5b gain-of-function mutations in early onset nonclonal eosinophilia, urticaria, dermatitis, and diarrhea
Authors: Chi A. Ma, Liqiang Xi, Brian Cauff, Adam DeZure, Alexandra F. Freeman, Sophie Hambleton, Gary Kleiner, T. Ronan Leahy, Maureen O’Sullivan, Michelle Makiya, Grainne O’Regan, Stefania Pittaluga, Julie Niemela, Jennifer Stoddard, Sergio D. Rosenzweig, Mark Raffeld, Amy D. Klion, Joshua D. Milner
Journal: Blood (2016)
Autologous transplant vs oral chemotherapy and lenalidomide in newly diagnosed young myeloma patients: a pooled analysis
Authors: F Gay, S Oliva, M T Petrucci, V Montefusco, C Conticello, P Musto, L Catalano, A Evangelista, S Spada, P Campbell, R Ria, M Salvini, M Offidani, A M Carella, P Omedé, A M Liberati, R Troia, A M Cafro, A Malfitano, A P Falcone, T Caravita, F Patriarca, A Nagler, A Spencer, R Hajek, A Palumbo, M Boccadoro
Journal: Leukemia (2016)
Abstract 4422: TTT-28, a newly synthesized thiazole-valine peptide, antagonizes multidrug resistance by inhibiting the efflux activity of the ABCB1 transporter
Authors: Yi-Jun Wang, Nagaraju Anreddy, Bhargav A. Patel, Eduardo E. Chufan, Satyakam Singh, Guan-Nan Zhang, Yun-Kai Zhang, Anna Maria Barbuti, Suresh V. Ambudkar, Tanaji T. Talele, Zhe-Sheng Chen
Journal: Cancer Research (2015)

Abstract Cancer cells often exhibit either intrinsic or acquired resistance to chemotherapy through a phenomenon known as multidrug resistance (MDR). Different mechanisms contribute to the development of MDR, preeminent among them being the accelerated drug efflux mediated by overexpression of ATP-binding cassette (ABC) transporters. Currently, it has been found that some small molecule tyrosine kinase inhibitors (TKIs), such as motesanib, linsitinib, masitinib and nilotinib, were able to modulate the activity of ABC transporters. Thus, the aim of this study was to determine whether TTT-28, a newly synthesized thiazole-valine peptide, could reverse ABCB1-mediated MDR. The results showed that TTT-28 significantly sensitized both ABCB1-transfected and drug-selected cell lines overexpressing this transporter to its substrate anticancer drugs. Using calcein-AM efflux assay, we identified TTT-28 (IC50 = 1.0 μM) carrying 3,4,5-trimethoxybenzoyl and 2-aminobenzophenone groups, respectively, at the amino and carboxyl termini of the monothiazole zwitterion. TTT-28 significantly increased the accumulation of [3H]-paclitaxel in ABCB1 overexpressing cells by blocking the efflux function of ABCB1 transporter. Furthermore, TTT-28 inhibited the photolabeling of ABCB1 with [125I]-iodoarylazidoprazosin with IC50 = 0.75 μM and stimulated the basal ATP hydrolysis of ABCB1 in a concentration-dependent manner (EC50 ATPase = 0.027 μM). Consistent with these findings, biochemical and docking studies showed site-1 to be the preferable binding site for TTT-28 within the drug-binding pocket of human ABCB1. Therefore, we report that TTT-28 antagonizes MDR by inhibiting the efflux activity of the ABCB1 transporter. These findings reveal high clinical values for the co-administration of TTT-28 and ABCB1 substrate chemotherapeutic drugs in cancer patients that overexpress ABCB1 and stimulate further research on circumventing the ABCB1-mediated MDR in cancers. Citation Format: Yi-Jun Wang, Nagaraju Anreddy, Bhargav A. Patel, Eduardo E. Chufan, Satyakam Singh, Guan-Nan Zhang, Yun-Kai Zhang, Anna Maria Barbuti, Suresh V. Ambudkar, Tanaji T. Talele, Zhe-Sheng Chen. TTT-28, a newly synthesized thiazole-valine peptide, antagonizes multidrug resistance by inhibiting the efflux activity of the ABCB1 transporter. [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 4422. doi:10.1158/1538-7445.AM2015-4422
Second primary cancers: Early detection strategies needed.
Authors: M. Blanco Villalba, A. PINI, S. Bogado, F. Dimase, E. Molinas, D. Schulz, C. Gonzalez Palacios, J. P. Re, G. J. Streich, M. P. Bramajo
Journal: Journal of Clinical Oncology (2011)

e12009 Background: One of the most serious events experienced by cancer survivors is the diagnosis of a new cancer. The number of patients with second cancers is growing rapidly, comprising about 16% of incident cancers reported to the National Cancer Institute. Second cancers can reflect the late sequelae of treatment, as well as the effect of shared etiologic factors, environmental exposures, host characteristics, and combinations of influences, including gene-environment and gene-gene interactions. This study describes stages and anatomic sites of second primary cancers observed in the selected population and time between first diagnosis and second cancer. Methods: This is an observational retrospective study that included 31 adult patients with second primary cancers registered in an oncology centre in Buenos Aires city. Results: The mean age was 66 years and 54% were female. Five patients presented synchronous primary cancers. The mean time between first and second cancer was 72, 24 months. Familiar cancer history was present in 37, 5% of patients who presented second cancer before the mean time. Only 11% referred familiar history in the group of patients with longer time between first and second cancer. Advanced stages (III-IV) accounted for 16% of the first cancers, being breast (25, 8%) and prostate (22%) the most frequent anatomic sites. Second cancers presented as advanced stages in 26% of cases being colon (25, 8%) breast (9, 6%), bladder (9, 6%) and lung (9, 6%) the most frequent anatomic sites. Conclusions: There has been a substantial progress in the description of second cancers specially concerning treatment related cancers and syndromic cancers together with early detection strategies and chemoprevention approaches. However the optimal screening modality and strategies to reduce mortality from second cancer remain to be defined as it is reflected in our study where the incidence of late stage second cancers is greater.
The influence of sociodemographic factors on breast cancer tumor biology.
Authors: K. A. Dookeran, K. Ferrer, M. Sekosan, N. Holloway, W. J. McCaskill-Stevens, S. J. Gehlert
Journal: Journal of Clinical Oncology (2011)

1553 Background: African American (AA) race is often associated with lower socioeconomic status (SES) and features of aggressive tumor biology in breast cancer, including: ER/PR-negative (-) subtypes, p53-positive (+) disease, and high grade. We attempt to disaggregate the influence of race and SES on tumor biology. Methods: Logistic regression models [odds ratios (ORs), 95% confidence intervals (CIs)] were used to select and evaluate sociodemographic factors at diagnosis related to tumor biology in a cohort of 534 women (331 AA, 203 non-AA) with breast cancer. Results: Table shows baseline covariates. After adjustment for age and race, multivariate independent predictors were: (a) all ER/PR- subtypes: higher parity, with a borderline relationship with worsening poverty/education status; (b) p53+ disease: only younger age at menarche; and (c) grade 3 disease, not having a FH, with a borderline relationship with higher parity. Conclusions: Results suggest that early menarche may predispose diagnosis with p53+ disease [OR, 1.2; 95% CI, 1.06-1.37; p=0.005], while higher parity and worse poverty/education status may predispose diagnosis with high-grade, ER/PR- subtype disease, and race may exert its effects through such factors. Tumor biology covariates. ER/PR- Triple negative Basal type p53+ Grade 3 Sociodemographic factors OR 95% CI OR 95% CI OR 95% CI OR 95% CI OR 95% CI Race (AA/non-AA) 1.11 0.77-1.59 1.29 0.87-1.90 1.65 1.01-2.69 0.92 0.60-1.42 1.04 0.73-1.48 Age (per year) 0.98 0.96-0.99 0.98 0.96-0.99 0.97 0.95-0.99 0.99 0.97-1.01 0.99 0.98-1.01 Comorbidity (+/-) 0.79 0.54-1.15 0.71 0.48-1.07 0.68 0.42-1.11 0.97 0.62-1.52 0.96 0.65-1.40 Family history (+/-) 0.82 0.55-1.24 0.79 0.51-1.23 0.67 0.38-1.16 0.87 0.53-1.42 0.49 0.33-0.74 Age at menarche (per year) 0.97 0.88-1.08 0.98 0.88-1.10 0.97 0.85-1.10 0.83 0.73-0.94 0.97 0.88-1.08 Parity (per birth) 1.08 0.99-1.17 1.13 1.04-1.23 1.11 1.00-1.23 1.00 0.90-1.10 1.07 0.99-1.16 BMI (≥ 30/ < 30) 0.86 0.59-1.28 0.94 0.62-1.42 0.94 0.58-1.53 1.01 0.64-1.60 0.81 0.55-1.19 Poverty status (> 1999 U.S. mean/ ≤) 1.65 1.06-2.57 2.01 1.21-3.34 1.83 1.00-3.36 1.02 0.61-1.71 1.16 0.76-1.77 Education status (< 1999 U.S. mean/ ≥) 1.59 0.99-2.53 1.86 1.10-3.17 1.98 1.02-3.84 1.79 0.97-3.29 0.91 0.58-1.42
Activated Protein C Resistance (APC-R) Analyzed as a Continuous Variable Is Significantly Decreased In Patients with Multiple Myeloma (MM) Compared to Normal Individuals
Authors: Tamara Berno, Kenneth Boucher, Fenghuang Zhan, Louis M. Fink, Guido J. Tricot, Benjamin Mughal, Maurizio Zangari
Journal: Blood (2010)
Elevated Serum Lactate Dehydrogenase (LDH) Should Be Included Among the Variables Which Define High Risk Multiple myeloma
Authors: Meletios A. Dimopoulos, Efstathios Kastritis, Maria Roussou, Maria Gkotzamanidou, Magdalini Migkou, Maria Gavriatopoulou, Dimitra Gika, Charis Matsouka, Despoina Mparmparoussi, Agapi Parcharidou, Evangelos Terpos
Journal: Blood (2010)
Primary Cutaneous Marginal Zone B-Cell Lymphoma Treated with Intralesional Rituximab: Experience of a Single Center
Authors: Eva Domingo-Domenech, Queralt Salas, Fina Climent, Carmen Aguilera, Helena Pomares, Eva González-Barca, Santiago Mercadal, Anna Lucas, Alberto Fernandez de Sevilla, Anna Sureda, Octavio Servitje
Journal: Blood (2015)
Ad-ISF35- Transduced Autologous Cells Promote In Vitro and In Vivo Chemosensitization to FCR and Durable Complete Responses In Patients with Del(17p)/P53 Defective Chronic Lymphocytic Leukemia.
Authors: Januario E Castro, Johanna Melo-Cardenas, Juan Sebastian Barajas-Gamboa, Mauricio Urquiza, Mark J. Cantwell, Thomas J. Kipps
Journal: Blood (2010)