tbuckley/cabot-search huggingface dataset:
Long-Term Outcome of 309 Young Patients Affected by Diffuse Large B-Cell Lymphoma (DLBCL) with a Poor-Prognosis at Diagnosis: a Pooled Analysis From Four Consecutive Trials of GIMURELL and Italian Lymphoma Intergroup (IIL).
Authors: Annalisa Chiappella, Maria Giuseppina Cabras, Anna Marina Liberati, Chiara Bottelli, Giovannino Ciccone, Emanuele Angelucci, Luca Baldini, Barbara Botto, Nicola Cascavilla, Sergio Cortelazzo, Pasqualina De Masi, Lorenzo Falchi, Giuseppe Fioritoni, Chiara Frairia, Roberto Freilone, Alessandro Levis, Lorella Orsucci, Guido Parvis, Enrico Maria Pogliani, Delia Rota-Scalabrini, Flavia Salvi, Giorgina Specchia, Anna Tonso, Alessandra Tucci, Umberto Vitolo
Journal: Blood (2009)
Sorafenib-Resistant Hepatocellular Carcinoma Stratified by Phosphorylated ERK Activates PD-1 Immune Checkpoint
Authors: Jiang Chen, Tong Ji, Jie Zhao, Gaofeng Li, Xiao Liang, Anyong Xie, Hui Lin, Yong Cang, Xiujun Cai
Journal: Clinical Gastroenterology and Hepatology (2016)
Individualized Pazopanib Dosing—Response
Authors: Remy B. Verheijen, Alwin D.R. Huitema, Neeltje Steeghs
Journal: Clinical Cancer Research (2016)

We thank Mir and colleagues for their interest in our article Individualized Pazopanib Dosing: A Prospective Feasibility Study in Cancer Patients ([1][1]). Their letter addresses relevant points concerning the choice to escalate the once-daily dose (in contrast to switching to twice-daily dosing)
Comparison of hepatic MDCT, MRI, and DSA to explant pathology for the detection and treatment planning of hepatocellular carcinoma
Authors: Lauren M. Ladd, Temel Tirkes, Mark Tann, David M. Agarwal, Matthew S. Johnson, Bilal Tahir, Kumaresan Sandrasegaran
Journal: Clinical and Molecular Hepatology (2016)

The diagnosis and treatment plan for hepatocellular carcinoma (HCC) can be made from radiologic imaging. However, lesion detection may vary depending on the imaging modality. This study aims to evaluate the sensitivities of hepatic multidetector computed tomography (MDCT), magnetic resonance imaging (MRI), and digital subtraction angiography (DSA) in the detection of HCC and the consequent management impact on potential liver transplant patients.One hundred and sixteen HCC lesions were analyzed in 41 patients who received an orthotopic liver transplant (OLT). All of the patients underwent pretransplantation hepatic DSA, MDCT, and/or MRI. The imaging results were independently reviewed retrospectively in a blinded fashion by two interventional and two abdominal radiologists. The liver explant pathology was used as the gold standard for assessing each imaging modality.The sensitivity for overall HCC detection was higher for cross-sectional imaging using MRI (51.5%, 95% confidence interval [CI]=36.2-58.4%) and MDCT (49.8%, 95% CI=43.7-55.9%) than for DSA (41.7%, 95% CI=36.2-47.3%) (P=0.05). The difference in false-positive rate was not statistically significant between MRI (22%), MDCT (29%), and DSA (29%) (P=0.67). The sensitivity was significantly higher for detecting right lobe lesions than left lobe lesions for all modalities (MRI: 56.1% vs. 43.1%, MDCT: 55.0% vs. 42.0%, and DSA: 46.9% vs. 33.9%; all P<0.01). The sensitivities of the three imaging modalities were also higher for lesions ≥2 cm vs. <2 cm (MRI: 73.4% vs. 32.7%, MDCT: 66.9% vs. 33.8%, and DSA: 62.2% vs. 24.1%; all P<0.01). The interobserver correlation was rated as very good to excellent.The sensitivity for detecting HCC is higher for MRI and MDCT than for DSA, and so cross-sectional imaging modalities should be used to evaluate OLT candidacy.
Viral Respiratory Infections After Allogeneic Hemaotpoietic Stem Cell Transplantation: Outcome and Prognosis
Authors: Alice Wolfromm, Raphael Porcher, Jérome Legoff, Régis Peffault de Latour, Alienor Xhaard, Patricia Ribaud, Catherine Scieux, Anne Bergeron, Gerard Socie, Marie Robin
Journal: Blood (2011)
Recipient Langerhans Cells Are Neither Required Nor Sufficient for GVHD Induction in MHC-Matched Allogeneic BMT, but a Langerin+ Cell Is a Pivotal Regulator of Langerhans Cell Turnover Post Transplantation
Authors: Hongmei Li, Daniel Kaplan, Anthony Jake Demetris, Jennifer McNiff, Mark Shlomchik, Warren D. Shlomchik
Journal: Blood (2008)
Abstract 4211: The proteomic characterization of HNSCC patient-derived xenografts
Authors: Hua Li, Sarah E. Wheeler, Yongseok Park, Zhenlin Ju, Ann Marie Egloff, Michele Fichera, Sufi Thomas, Gordon B. Mills, Jennifer R. Grandis
Journal: Cancer Research (2015)

Abstract Head and neck squamous cell carcinoma (HNSCC) is the fifth most common cancer in the US and a leading cancer worldwide. There has been little change in the prognosis for these patients despite extensive research and FDA approval of the targeted therapy cetuximab. Cetuximab has been effective in immortalized HNSCC cell lines but demonstrates only a modest benefit for a subset of patients. This gap between pre-clinical discovery and testing and final clinical efficacy can be narrowed improving the translational relevance of preclinical model systems. Patient derived xenografts (PDXs) have emerged as a promising approach in several cancers. We sought to define and compare the protein expression patterns between primary HNSCC and PDXs derived from 13 patient tumors and test predictive biomarkers to cetuximab therapy. We compared 13 PDXs propagated at the University of Pittsburgh and analyzed for the expression levels of 190 proteins by reverse-phase protein array (RPPA) to 212 HNSCC specimens and 4566 cancer specimens from TCGA also analyzed by RPPA. We found that 12/13 PDXs were more like HNSCC than any of 14 other cancer types analyzed. Unsupervised clustering of the primary HNSCC and the PDXs demonstrated that PDXs clustered together, indicating some differences in protein expression between HNSCC and PDXs. Further analysis demonstrated that a subset of the proteins were different between the mouse derived PDXs and the primary HNSCC while a second subset were similar between mouse derived PDXs and primary HNSCC. Proteins that were different between these two groups may be poor candidates for translational models, but proteins that were similar may prove useful. We tested the different responses to cetuximab using the PDXs. We found that a PDX with high EGFR/pEGFR expression was more sensitive to cetuximab treatment than a PDX with low EGFR/pEGFR expression. These results suggest that improved model systems used for translational may predict clinical responses. RPPA measurement of protein expression in PDXs and primary cancers demonstrates that PDXs do represent HNSCC overall. Comparison of the PDXs specifically with primary HNSCC reveals that PDXs are not an appropriate model system for all targeted therapies/studies but provide an effective model for many studies of interest in the field. Citation Format: Hua Li, Sarah E. Wheeler, Yongseok Park, Zhenlin Ju, Ann Marie Egloff, Michele Fichera, Sufi Thomas, Gordon B. Mills, Jennifer R. Grandis. The proteomic characterization of HNSCC patient-derived xenografts. [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 4211. doi:10.1158/1538-7445.AM2015-4211
Rituximab Combined with M/VACOP-B and Radiotherapy in Primary Mediastinal Large B-Cell Lymphoma (PMLBCL): A Prospective Italian Phase II IIL Study.
Authors: Maurizio Martelli, Vittorio Stefoni, Giuseppina Cabras, Sergio Cortellazzo, Ercole Brusamolino, Alessandro Levis, Barbara Botto, Antonio De Vivo, Fiammetta Natalino, Finolezzi Erica, Robert Foa, Pier Luigi Zinzani
Journal: Blood (2006)
Imatinib Resistance Mutation Analysis Pattern In Chronic Myeloid Leukemia (CML) Patients on Imatinib In Indian Population.
Authors: Mukul Goyal, K.C. Lakshmaiah, K.Govind Babu, Amit Rauthan, Linu Abraham Jacob, Singh Tejinder, L.K. Rajeev, G.Mehar Kumar, Vineetha Unnikrishnan
Journal: Blood (2010)
Abstract 3647: Targeting cancer-induced anemia with hepcidin lowering ALK2 inhibitors
Authors: Peter W. Peterson
Journal: Cancer Research (2015)

Abstract Anemia of cancer (AOC) is a cytokine driven condition that frequently occurs in patients due to chronic inflammation associated with cancer development. It differs from chemotherapy-induced anemia because the anemia is a result of the disease itself and not a side effect of a treatment regimen, although the both causes can work in concert. AOC is caused by high levels of the liver peptide hormone, hepcidin, which sequesters iron in epithelial cells and macrophages, thereby limiting bioavailable iron required for erythropoiesis. Reducing elevated hepcidin levels in cancer patients can reverse the hypoferremia and anemia seen in AOC. Hepcidin levels are controlled by inflammatory cytokines through pathways dependent on bone morphogenetic proteins (BMP). BMPs up-regulate hepcidin by activating the SMAD signaling pathway through the activin-like kinase receptor 2 (ALK2). Therefore, ALK2 has emerged as an attractive therapeutic target to modulate hepcidin levels in cancer patients and treat their AOC. We have developed novel small molecule ALK2 inhibitors which have shown promising results in tissue culture models as well as a preclinical cancer model of AOC. The two most promising compounds downregulate hepcidin expression in BMP-induced cell culture studies at concentrations of 100 nM or lower. Importantly, this activity was observed at concentrations that exhibited little cytotoxicity suggesting the compounds have a clean selectivity profile. The two compounds have been tested in a TC-1 syngeneic mouse model of AOC where anemia is induced after tumor formation, in a manner similar to human cancer caused anemia. Treatment with the lead candidates reversed the induction of hepcidin expression and also decreased the symptoms of anemia as measured by serum iron and red blood cell levels. From these data, we have nominated a candidate to advance into IND-enabling studies that has favorable drug-like properties. We anticipate a clinical development strategy that focuses on AOC. Citation Format: Peter W. Peterson. Targeting cancer-induced anemia with hepcidin lowering ALK2 inhibitors. [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 3647. doi:10.1158/1538-7445.AM2015-3647
An antidote for <i>Staphylococcus aureus</i> pneumonia?
Authors: Frank R. DeLeo, Michael Otto
Journal: The Journal of Experimental Medicine (2008)

In the third sentence under the subheading "A role for other toxins?," the word "consistent" appeared as "wconsistent."In addition, in the third sentence of the second paragraph under the subheading "Virulence factors and immune evasion," the word "proteins" should have been "molecules."The corrected sentence appears below: S. aureus makes several molecules, including protein A, serotype 5 or 8 capsular polysaccharide (CP5 or CP8), and clumping factor A (ClfA), which inhibit phagocytosis (12-14).
Abstract 4613: MDM4 SNP 34091 (rs4245739) effect on risk of breast, colon, lung, prostate, endometrial and ovarian cancer
Authors: Liv B. Gansmo, Merete Bjørnslett, Anne Dørum, Helga Salvesen, Pål Romundstad, Kristian Hveem, Lars Vatten, Per Eystein Lønning, Stian Knappskog
Journal: Cancer Research (2015)

Abstract Background MDM4 enhances MDM2's E3 ligase activity causing ubiquitin-proteasome-dependent degradation of p53. Thus, elevated levels of both MDM4 and MDM2 may result in p53 inactivation and elevated cancer risk. A single nucleotide polymorphism in the MDM4 3′ UTR (SNP34091A&amp;gt;C; rs4245739) has been found to exert biological function as the SNP34091C allele creates a putative target site for hsa-miR-191 leading to specific hsa-miR-191 down-regulation of MDM4. Further, the SNP34091AA genotype is associated with increased risk for both recurrence and tumor related death in estrogen negative ovarian cancer patients. In the present study we assessed the potential effect of MDM4 SNP34091A&amp;gt;C on cancer risk in six major cancer forms. Materials and methods We analyzed 1717 breast-, 1331 lung-, 1531 colon-, 2501 prostate cancer cases and 3747 healthy controls form the same population based study (CONOR) as well as 1404 endometrial- and 1699 ovarian cancer cases from hospital based studies. All samples were genotyped for MDM4 SNP34091A&amp;gt;C using custom Light-SNiP assay on a LightCycler 480 II instrument. Potential associations between MDM4 SNP34091 and cancer risk were estimated by calculating Odds Ratio (OR) with 95% confidence intervals (CI). All statistical analyses were performed using the IBM SPSS 19 software. Results We observed no significant association between MDM4 SNP34091A&amp;gt;C status and cancer risk in any of the analyzed cancer forms. Interestingly, stratifying the ovarian cancer samples according to grade and histology, we observed a reduced risk of high grade serous ovarian cancer in patients harboring the MDM4 SNP34091AA genotype (OR = 0.80; 95% CI = 0.65 - 0.98). Stratifying according to MDM2 SNP309 status we found the MDM4 SNP34091A allele to be associated with increased risk for breast cancer (OR = 2.10; 95% CI = 1.08 - 4.10) in patients carrying the SNP309 GG genotype. Conclusions The data presented here indicate that the effect of MDM4 SNP34091 on cancer risk may be tissue specific and that there may be cooperative effects with MDM2 SNP309. Citation Format: Liv B. Gansmo, Merete Bjørnslett, Anne Dørum, Helga Salvesen, Pål Romundstad, Kristian Hveem, Lars Vatten, Per Eystein Lønning, Stian Knappskog. MDM4 SNP 34091 (rs4245739) effect on risk of breast, colon, lung, prostate, endometrial and ovarian 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 4613. doi:10.1158/1538-7445.AM2015-4613
Abstract 5047: Role of estrogen receptors alpha and beta in the balance between proliferation and surveillance
Authors: D. Joseph Jerry, Karen A. Dunphy, Amy L. Roberts, Margarita Brown
Journal: Cancer Research (2015)

Abstract Estrogens have paradoxical effects in both promoting and preventing breast cancer. The proliferative actions of estrogens promote the expansion of both normal mammary epithelium and breast cancer. But estrogen also activates p53-mediated surveillance and apoptotic pathways to eliminate cells with potential oncogenic mutations. This is exemplified by tumor regression in response to high dose estrogen-treatment in postmenopausal breast cancer. Estrogens mediate their effects through the activation of two estrogen receptor subtypes: Estrogen Receptor alpha (ERα)and Estrogen Receptor beta (ERβ). Our objective is to examine the contribution of these receptors in mediating surveillance as opposed to proliferation by comparing selective estrogen receptor agonists with 17β-estradiol (E2) for induction of proliferation and surveillance in three model systems: (1) in vivo mouse model, (2) in vitro MCF7-tet-off-ERβ model, and (3) an ex-vivo human mammary explant model. Selective activation of ERβ with the agonist diarylpropionitrile (DPN) in vivo enhances p53-mediated apoptosis in the mouse mammary epithelium without stimulating proliferation. In addition, radiation-induced apoptosis is significantly reduced in mice lacking ERβ (βERKO). E2 or the ERα selective agonist pyrazole triol (PPT) induced the expression of estrogen response genes including progesterone receptor and amphiregulin in all three models. DPN-mediated activation of ERβ failed to induce the expression of these genes. The ERβ agonist DPN selectively induced the expression of genes that repress proliferation including TGFβ and inhibitors of canonical WNT signaling, WNT5a and AXIN2. DPN was also more potent in stimulating EGR1, a modulator of p53 activity, and CEBPd, a pro-apoptotic gene. Conclusions: The ability of DPN and ERβ to potentiate surveillance pathways while limiting proliferation suggests that ERβ agonists may provide a new approach for chemoprevention of breast cancer. Citation Format: D. Joseph Jerry, Karen A. Dunphy, Amy L. Roberts, Margarita Brown. Role of estrogen receptors alpha and beta in the balance between proliferation and surveillance. [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 5047. doi:10.1158/1538-7445.AM2015-5047
456. Pharmacodynamics and GMP Development of a Lentivirus-Induced DC Vaccine for Accelerated Adaptive Immune Reconstitution Against Cytomegalovirus after Stem Cell Transplantation
Authors: Bala Sai Sundarasetty, Sonja Naundorf, Klaus Kuehlcke, Candida Deves Roth, Valery Volk, Eliana Ruggiero, Manfred Schmidt, Ulrike Koehl, Arnold Ganser, Renata Stripecke
Journal: Molecular Therapy (2015)

Effective immunization of patients shortly after allogeneic hematopoietic stem cell transplantation (allo-HSCT) is an unmet clinical need due to delayed de novo development of T and B cells. We demonstrated a recombinant, donor-derived cell vaccine against cytomegalovirus that can be easily manufactured, cryopreserved and, upon thaw and administration, turn themselves into highly-viable dendritic cells (DCs). The cell source consisted of monocytes from peripheral blood or cord blood (CB), transduced with an integrase-defective lentiviral vector (IDLV, co-expressing GM-CSF, IFN-α and the cytomegalovirus antigen pp65). The pharmacodynamics of the frozen/thawed vaccine ("SmyleDCpp65") was evaluated by immunization of NOD.Rag1–/–.IL2rγ–/– mice transplanted with human CD34+ CB stem cells. SmyleDCpp65 stimulated in vivo thymic and extrathymic expansion of human cytotoxic T cells (CTL) reactive against pp65, and high levels of human immunoglobulins and immune-stimulatory cytokines in plasma. Standardized production of the IDLV and SmyleDCpp65 was established using Good Manufacturing Practices (GMP). Analytical parameters for quality control demonstrated high recovery, uniformity, purity and viability of SmyleDCpp65 after thawing. Stimulation of autologous T cells by GMP-grade SmyleDCpp65 was validated. SmyleDCpp65 showed only residual and polyclonal IDLV integration, unbiased to protooncogenic hot-spots. These results underscore further developments of this individualized cell vaccine to accelerate immune reconstitution against cytomegalovirus after allo-HSCT.
Delirium
Authors: Michael E. Zenilman
Journal: JAMA (2017)

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OC-019 Should all patients with anaemia undergo ferritin testing to exclude iron deficiency anaemia?
Authors: S Menon, C Kothari, N Trudgill
Journal: Gut (2010)

<h3>Introduction</h3> A low ferritin in the setting of microcytic anaemia is both sensitive and specific for iron deficiency anaemia (IDA) but its role in normocytic anaemia is unclear. Many laboratories do not offer ferritin testing in normocytic anaemia. We have investigated the prevalence of microcytic and normocytic anaemia in patients presenting with upper and lower gastrointestinal (GI) cancer and assessed the cost-benefit of ferritin in models of microcytic and normocytic anaemia. <h3>Methods</h3> Two decision-analysis models were created to evaluate a hypothetical cohort of postmenopausal women and men with microcytic anaemia. Two strategies were investigated for each type of anaemia: microcytic – ferritin and GI endoscopy (gastroscopy, D2 biopsy and colonoscopy) if IDA or no ferritin and GI endoscopy for all; normocytic—ferritin and GI endoscopy if IDA or no ferritin and no GI endoscopy. A ferritin level &lt;20 μg/ml was used to determine iron deficiency. Baseline prevalence variables were obtained after a literature search. Records of patients with upper and lower gastrointestinal cancers at our hospital in the last year were audited to determine the prevalence and type of anaemia. Costs of endoscopic procedures were derived from HRG tariffs. Costs for advanced cancer were obtained from published literature. Monte-Carlo and sensitivity analysis were carried out. <h3>Results</h3> Of 75 upper GI cancers, 51 (68%) were anaemic on presentation (82% normocytic, 18% microcytic). Of 75 lower GI cancers, 59 (79%) were anaemic (75% normocytic, 25% microcytic). The average cost of evaluating a patient with microcytic anaemia when ferritin was used was £1106, compared to £1526 when not, yielding a cost-saving of £420 per patient. With normocytic anaemia, the average cost of investigation was £223 per patient when ferritin was used to determine further investigations compared to £243 per patient when not, yielding a cost-difference of £20 per patient. This difference was due to a number of cancers presenting late in the arm where ferritin was not used to determine IDA. Monte Carlo simulation and sensitivity analysis on cost of ferritin showed a consistent cost-difference in favour of using ferritin in microcytic anaemia for a cost per test from £5 to £15. In normocytic anaemia, the percentage presenting at an inoperable stage of GI malignancy was critical in determining whether ferritin was cost-effective. So long as at least 40% of GI cancers were inoperable, ferritin was cost-effective in normocytic anaemia. <h3>Conclusion</h3> Ferritin is associated with cost-savings in the investigation of suspected IDA and should be used as a baseline investigation in planning endoscopic investigations. It has clear value in microcytic anaemia and is marginally cost-effective in normocytic anaemia, where it is dependent on the rate of GI cancers in patients with IDA with normocytic anaemia and how many are inoperable.