Database : MEDLINE
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[PMID]: 29520195
[Au] Autor:Zhang W; Zhou Y; Xu XQ; Kong LY; Xu H; Yu TF; Shi HB; Feng Q
[Ad] Address:Department of Radiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210000, China.
[Ti] Title:A Whole-Tumor Histogram Analysis of Apparent Diffusion Coefficient Maps for Differentiating Thymic Carcinoma from Lymphoma.
[So] Source:Korean J Radiol;19(2):358-365, 2018 Mar-Apr.
[Is] ISSN:2005-8330
[Cp] Country of publication:Korea (South)
[La] Language:eng
[Ab] Abstract:Objective: To assess the performance of a whole-tumor histogram analysis of apparent diffusion coefficient (ADC) maps in differentiating thymic carcinoma from lymphoma, and compare it with that of a commonly used hot-spot region-of-interest (ROI)-based ADC measurement. Materials and Methods: Diffusion weighted imaging data of 15 patients with thymic carcinoma and 13 patients with lymphoma were retrospectively collected and processed with a mono-exponential model. ADC measurements were performed by using a histogram-based and hot-spot-ROI-based approach. In the histogram-based approach, the following parameters were generated: mean ADC (ADC ), median ADC (ADC ), 10th and 90th percentile of ADC (ADC and ADC ), kurtosis, and skewness. The difference in ADCs between thymic carcinoma and lymphoma was compared using a test. Receiver operating characteristic analyses were conducted to determine and compare the differentiating performance of ADCs. Results: Lymphoma demonstrated significantly lower ADC , ADC , ADC , ADC , and hot-spot-ROI-based mean ADC than those found in thymic carcinoma (all values < 0.05). There were no differences found in the kurtosis ( = 0.412) and skewness ( = 0.273). The ADC demonstrated optimal differentiating performance (cut-off value, 0.403 × 10 mm /s; area under the receiver operating characteristic curve [AUC], 0.977; sensitivity, 92.3%; specificity, 93.3%), followed by the ADC , ADC , ADC , and hot-spot-ROI-based mean ADC. The AUC of ADC was significantly higher than that of the hot spot ROI based ADC (0.977 vs. 0.797, = 0.036). Conclusion: Compared with the commonly used hot spot ROI based ADC measurement, a histogram analysis of ADC maps can improve the differentiating performance between thymic carcinoma and lymphoma.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.3348/kjr.2018.19.2.358

  2 / 267602 MEDLINE  
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[PMID]: 29517616
[Au] Autor:Robertson MJ; Stamatkin CW; Pelloso D; Weisenbach J; Prasad NK; Safa AR
[Ad] Address:Lymphoma Program and Bone Marrow and Stem Cell Transplantation Program, Department of Medicine, Division of Hematology/Oncology.
[Ti] Title:A Dose-escalation Study of Recombinant Human Interleukin-18 in Combination With Ofatumumab After Autologous Peripheral Blood Stem Cell Transplantation for Lymphoma.
[So] Source:J Immunother;, 2018 Mar 06.
[Is] ISSN:1537-4513
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Interleukin-18 (IL-18) is an immunostimulatory cytokine that augments antibody-dependent cellular cytotoxicity mediated by human natural killer cells against antibody-coated lymphoma cells in vitro and that has antitumor activity in animal models. Ofatumumab is a CD20 monoclonal antibody with activity against human B-cell lymphomas. A phase I study of recombinant human (rh) IL-18 given with ofatumumab was undertaken in patients with CD20 lymphoma who had undergone high-dose chemotherapy and autologous peripheral blood stem cell transplantation. Cohorts of 3 patients were given intravenous infusions of ofatumumab 1000 mg weekly for 4 weeks with escalating doses of rhIL-18 as a intravenous infusion weekly for 8 consecutive weeks. Nine male patients with CD20 lymphomas were given ofatumumab in combination with rhIL-18 at doses of 3, 10, and 30 µg/kg. No unexpected or dose-limiting toxicities were observed. The mean reduction from predose levels in the number of peripheral blood natural killer cells after the first rhIL-18 infusion was 91%, 96%, and 97% for the 3, 10, and 30 µg/kg cohorts, respectively. Serum concentrations of interferon-γ and chemokines transiently increased following IL-18 dosing. rhIL-18 can be given in biologically active doses by weekly infusions in combination with ofatumumab after peripheral blood stem cell transplantation to patients with lymphoma. A maximum tolerated dose of rhIL-18 plus ofatumumab was not determined. Further studies of rhIL-18 and CD20 monoclonal antibodies in B-cell malignancies are warranted.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher
[do] DOI:10.1097/CJI.0000000000000220

  3 / 267602 MEDLINE  
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[PMID]: 29515122
[Au] Autor:Müller A; Gillissen B; Richter A; Richter A; Chumduri C; Daniel PT; Scholz CW
[Ad] Address:Department of Hematology, Oncology and Tumor Immunology, Charité - University Medicine Berlin, Campus Berlin-Buch, Lindenberger Weg 80, Berlin, 13125, Germany.
[Ti] Title:Pan-class I  PI3-kinase inhibitor BKM120 induces MEK1/2-dependent mitotic catastrophe in non-Hodgkin lymphoma leading to apoptosis or polyploidy determined by Bax/Bak and p53.
[So] Source:Cell Death Dis;9(3):384, 2018 Mar 07.
[Is] ISSN:2041-4889
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Constitutive signaling of PI3K/Akt/mTOR plays a prominent role in malignant transformation and progression of B-cell non-Hodgkin lymphomas (B-NHL) underscoring the need for PI3K targeted therapies. The pan-class I PI3-kinase inhibitor BKM120 has shown preclinical activity in distinct malignancies and is currently tested in clinical trials. Intratumor heterogeneity is an intrinsic property of cancers that contributes to drug resistance and tumor recurrence. Here, we demonstrate that inhibition of PI3-kinases by BKM120 attenuates growth and survival of B-NHL cell lines by inducing mitotic arrest with subsequent induction of intrinsic apoptosis. BKM120-mediated downregulation of Cyclin A and activation of the CDK1/Cyclin B1 complex facilitates mitotic entry. In addition, concomitant BKM120-mediated upregulation of Cyclin B1 expression attenuates completion of mitosis, which results in mitotic catastrophe and apoptotic cell death. In Bax and Bak deficient B-NHL, which are resistant to BKM120-induced apoptosis, BKM120-induced mitotic catastrophe results in polyploidy. Upon re-expression of wt p53 in these p53 mutated cells, BKM120-induced polyploidy is strongly reduced demonstrating that the genetic status of the cells determines the outcome of a BKM120-mediated pathway inhibition. Mitotic catastrophe and unfavorable induction of polyploidy can be prevented in this setting by additional inhibition of MEK1/2 signaling. Combining MEK1/2 inhibitors with BKM120 enhances the anti-tumor effects of BKM120, prevents prognostic unfavorable polyploidy and might be a potential strategy for the treatment of B-NHL.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1038/s41419-018-0413-4

  4 / 267602 MEDLINE  
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[PMID]: 29510739
[Au] Autor:Steele KE; Tan TH; Korn R; Dacosta K; Brown C; Kuziora M; Zimmermann J; Laffin B; Widmaier M; Rognoni L; Cardenes R; Schneider K; Boutrin A; Martin P; Zha J; Wiestler T
[Ad] Address:MedImmune, One MedImmune Way, Gaithersburg, MD, 20878, USA. SteeleK@MedImmune.com.
[Ti] Title:Measuring multiple parameters of CD8+ tumor-infiltrating lymphocytes in human cancers by image analysis.
[So] Source:J Immunother Cancer;6(1):20, 2018 Mar 06.
[Is] ISSN:2051-1426
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Immuno-oncology and cancer immunotherapies are areas of intense research. The numbers and locations of CD8+ tumor-infiltrating lymphocytes (TILs) are important measures of the immune response to cancer with prognostic, pharmacodynamic, and predictive potential. We describe the development, validation, and application of advanced image analysis methods to characterize multiple immunohistochemistry-derived CD8 parameters in clinical and nonclinical tumor tissues. METHODS: Commercial resection tumors from nine cancer types, and paired screening/on-drug biopsies of non-small-cell lung carcinoma (NSCLC) patients enrolled in a phase 1/2 clinical trial investigating the PD-L1 antibody therapy durvalumab (NCT01693562), were immunostained for CD8. Additional NCT01693562 samples were immunostained with a CD8/PD-L1 dual immunohistochemistry assay. Whole-slide scanning was performed, tumor regions were annotated by a pathologist, and images were analyzed with customized algorithms using Definiens Developer XD software. Validation of image analysis data used cell-by-cell comparison to pathologist scoring across a range of CD8+ TIL densities of all nine cancers, relying primarily on 95% confidence in having at least moderate agreement regarding Lin concordance correlation coefficient (CCC = 0.88-0.99, CCC_lower = 0.65-0.96). RESULTS: We found substantial variability in CD8+ TILs between individual patients and across the nine types of human cancer. Diffuse large B-cell lymphoma had several-fold more CD8+ TILs than some other cancers. TIL densities were significantly higher in the invasive margin versus tumor center for carcinomas of head and neck, kidney and pancreas, and NSCLC; the reverse was true only for prostate cancer. In paired patient biopsies, there were significantly increased CD8+ TILs 6 weeks after onset of durvalumab therapy (mean of 365 cells/mm over baseline; P = 0.009), consistent with immune activation. Image analysis accurately enumerated CD8+ TILs in PD-L1+ regions of lung tumors using the dual assay and also measured elongate CD8+ lymphocytes which constituted a fraction of overall TILs. CONCLUSIONS: Validated image analysis accurately enumerates CD8+ TILs, permitting comparisons of CD8 parameters among tumor regions, individual patients, and cancer types. It also enables the more complex digital solutions needed to better understand cancer immunity, like analysis of multiplex immunohistochemistry and spatial evaluation of the various components comprising the tumor microenvironment. TRIAL REGISTRATION: ClinicalTrials.gov identifier: NCT01693562 . Study code: CD-ON-MEDI4736-1108. Interventional study (ongoing but not currently recruiting). Actual study start date: August 29, 2012. Primary completion date: June 23, 2017 (final data collection date for primary outcome measure).
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1186/s40425-018-0326-x

  5 / 267602 MEDLINE  
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[PMID]: 29501729
[Au] Autor:Miloudi H; Leroy K; Jardin F; Sola B
[Ad] Address:Normandie Univ, INSERM UMR1245, UNICAEN, Caen, France. Electronic address: hadjer.miloudi@unicaen.fr.
[Ti] Title:STAT6 is a cargo of exportin 1: Biological relevance in primary mediastinal B-cell lymphoma.
[So] Source:Cell Signal;46:76-82, 2018 Mar 01.
[Is] ISSN:1873-3913
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Primary mediastinal B-cell lymphoma (PMBL) is a distinct B-cell lymphoma subtype with unique clinicopathological and molecular features. PMBL cells are characterised by several genetic abnormalities that conduct to the constitutive activation of the Janus kinase 2/signal transducer and activator of transcription 6 (JAK2/STAT6) signalling pathway. Among recurrent genetic changes in PMBL, we previously reported that the XPO1 gene encoding exportin 1 that controls the nuclear export of cargo proteins and RNAs, is mutated (p.E571K) in about 25% of PMBL cases. We therefore hypothesized that STAT6 could be a cargo of XPO1 and that STAT6 cytoplasm/nucleus shuttle could be altered in a subset of PMBL cells. Using immunocytochemistry techniques as well as the proximity ligation assay, we showed that STAT6 bound XPO1 in PBML cell lines and in HEK-293 cells genetically engineered to produce STAT6. Moreover, XPO1-mediated export of STAT6 occurs in cells expressing either a wild-type or the E571K mutated XPO1 protein.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  6 / 267602 MEDLINE  
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[PMID]: 29246942
[Au] Autor:Cooney JD; Lin AP; Jiang D; Wang L; Suhasini AN; Myers J; Qiu Z; Wölfler A; Sill H; Aguiar RCT
[Ad] Address:Division of Hematology and Medical Oncology, Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas.
[Ti] Title:Synergistic Targeting of the Regulatory and Catalytic Subunits of PI3Kδ in Mature B-cell Malignancies.
[So] Source:Clin Cancer Res;24(5):1103-1113, 2018 Mar 01.
[Is] ISSN:1078-0432
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Aberrant activation of the B-cell receptor (BCR) is implicated in the pathogenesis of mature B-cell tumors, a concept validated in part by the clinical success of inhibitors of the BCR-related kinases BTK (Bruton's tyrosine kinase) and PI3Kδ. These inhibitors have limitations, including the paucity of complete responses, acquired resistance, and toxicity. Here, we examined the mechanism by which the cyclic-AMP/PDE4 signaling axis suppresses PI3K, toward identifying a novel mechanism-based combinatorial strategy to attack BCR-dependency in mature B-cell malignancies. We used and diffuse large B-cell lymphoma (DLBCL) cell lines and primary chronic lymphocytic leukemia (CLL) samples to preclinically evaluate the effects of the combination of the FDA-approved phosphodiesterase 4 (PDE4) inhibitor roflumilast and idelalisib on cell survival and tumor growth. Genetic models of gain- and loss-of-function were used to map multiple signaling intermediaries downstream of the BCR. Roflumilast elevates the intracellular levels of cyclic-AMP and synergizes with idelalisib in suppressing tumor growth and PI3K activity. Mechanistically, we show that roflumilast suppresses PI3K by inhibiting BCR-mediated activation of the P85 regulatory subunit, distinguishing itself from idelalisib, an ATP-competitive inhibitor of the catalytic P110 subunit. Using genetic models, we linked the PDE4-regulated modulation of P85 activation to the oncogenic kinase SYK. These data demonstrate that roflumilast and idelalisib suppress PI3K by distinct mechanisms, explaining the basis for their synergism, and suggest that the repurposing of PDE4 inhibitors to treat BCR-dependent malignancies is warranted. .
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1158/1078-0432.CCR-17-2218

  7 / 267602 MEDLINE  
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[PMID]: 29230015
[Au] Autor:Bu Y; Yoshida A; Chitnis N; Altman BJ; Tameire F; Oran A; Gennaro V; Armeson KE; McMahon SB; Wertheim GB; Dang CV; Ruggero D; Koumenis C; Fuchs SY; Diehl JA
[Ad] Address:Department of Biochemistry and Molecular Biology and Hollings Cancer Center, Medical University of South Carolina, Charleston, SC, USA.
[Ti] Title:A PERK-miR-211 axis suppresses circadian regulators and protein synthesis to promote cancer cell survival.
[So] Source:Nat Cell Biol;20(1):104-115, 2018 Jan.
[Is] ISSN:1476-4679
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The unfolded protein response (UPR) is a stress-activated signalling pathway that regulates cell proliferation, metabolism and survival. The circadian clock coordinates metabolism and signal transduction with light/dark cycles. We explore how UPR signalling interfaces with the circadian clock. UPR activation induces a 10 h phase shift in circadian oscillations through induction of miR-211, a PERK-inducible microRNA that transiently suppresses both Bmal1 and Clock, core circadian regulators. Molecular investigation reveals that miR-211 directly regulates Bmal1 and Clock via distinct mechanisms. Suppression of Bmal1 and Clock has the anticipated impact on expression of select circadian genes, but we also find that repression of Bmal1 is essential for UPR-dependent inhibition of protein synthesis and cell adaptation to stresses that disrupt endoplasmic reticulum homeostasis. Our data demonstrate that c-Myc-dependent activation of the UPR inhibits Bmal1 in Burkitt's lymphoma, thereby suppressing both circadian oscillation and ongoing protein synthesis to facilitate tumour progression.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1038/s41556-017-0006-y

  8 / 267602 MEDLINE  
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[PMID]: 29205808
[Au] Autor:Zhao N; Zeng Z; Zu Y
[Ad] Address:Department of Pathology and Genomic Medicine, Houston Methodist Hospital, Cancer Pathology Laboratory, Houston Methodist Research Institute, 6565 Fannin St., Houston, TX, 77030, USA.
[Ti] Title:Self-Assembled Aptamer-Nanomedicine for Targeted Chemotherapy and Gene Therapy.
[So] Source:Small;14(4), 2018 Jan.
[Is] ISSN:1613-6829
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:Chemotherapy is the mainstream treatment of anaplastic large cell lymphoma (ALCL). However, chemotherapy can cause severe adverse effects in patients because it is not ALCL-specific. In this study, a multifunctional aptamer-nanomedicine (Apt-NMed) achieving targeted chemotherapy and gene therapy of ALCL is developed. Apt-NMed is formulated by self-assembly of synthetic oligonucleotides containing CD30-specific aptamer and anaplastic lymphoma kinase (ALK)-specific siRNA followed by self-loading of the chemotherapeutic drug doxorubicin (DOX). Apt-NMed exhibits a well-defined nanostructure (diameter 59 mm) and stability in human serum. Under aptamer guidance, Apt-NMed specifically binds and internalizes targeted ALCL cells. Intracellular delivery of Apt-NMed triggers rapid DOX release for targeted ALCL chemotherapy and intracellular delivery of the ALK-specific siRNA induced ALK oncogene silencing, resulting in combined therapeutic effects. Animal model studies reveal that upon systemic administration, Apt-NMed specifically targets and selectively accumulates in ALCL tumor site, but does not react with off-target tumors in the same xenograft mouse. Importantly, Apt-NMed not only induces significantly higher inhibition in ALCL tumor growth, but also causes fewer or no side effects in treated mice compared to free DOX. Moreover, Apt-NMed treatment markedly improves the survival rate of treated mice, opening a new avenue for precision treatment of ALCL.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1002/smll.201702103

  9 / 267602 MEDLINE  
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[PMID]: 29524233
[Au] Autor:Bartholomä MD
[Ad] Address:Department of Nuclear Medicine, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
[Ti] Title:Radioimmunotherapy of solid tumors: Approaches on the verge of clinical application.
[So] Source:J Labelled Comp Radiopharm;, 2018 Mar 09.
[Is] ISSN:1099-1344
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:While radioimmunotherapy (RIT) for the treatment of hematological malignancies such as indolent B-cell lymphoma has proven quite successful, clinical results of RIT in solid tumors have only been moderate in the past. The reasons were manifold and can be mostly attributed to the different biological properties of solid tumors vs. hematological cancers. Furthermore, the slow clearance of the radiolabelled antibody prevents the use of radiation doses necessary to achieve clinical responses. The long biological half-life of radioimmunoconjugates results in high background levels and is the main reason for radiation related toxicities. In recent years, researchers and clinicians have developed solutions for the successful application of RIT for the treatment of solid tumors. These include compartmental route of administration, neoadjuvant therapies and pretargeting approaches. In this review, recent developments in RIT for the treatment of solid tumors that address these restrictions as well as future perspectives will be highlighted from a clinical perspective.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1002/jlcr.3619

  10 / 267602 MEDLINE  
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[PMID]: 29524215
[Au] Autor:Ye X; Zhang G; Righolt C; Johnston JB; Banerji V; Gibson SB; Mahmud SM
[Ad] Address:Department of Community Health Sciences, University of Manitoba, Winnipeg, Manitoba, Canada.
[Ti] Title:Associations between Statin Use and Risk of Non-Hodgkin Lymphomas by Subtype.
[So] Source:Int J Cancer;, 2018 Mar 10.
[Is] ISSN:1097-0215
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Non-Hodgkin lymphomas (NHL) are a group of cancers with highly heterogeneous biology and clinical features. Statins are increasingly prescribed to prevent cardiovascular diseases. Early evidence shows a preventive effect of statins for some cancers, but their effect on NHL risk is unclear. We conducted a population-based nested case-control study involving 5,541 NHL cases and 27,315 controls matched for gender, age, place of residence, and length of period of available prescription drug data. We assessed the use of statins prior to diagnosis (excluding the 12 months prior to the index date). We used conditional logistic regression models to estimate odds ratio (OR) and 95% confidence interval (CI) for use of any statin, adjusting for medical conditions, number of family physician visits for 5 years prior to index date, healthcare utilization, income, and use of other medications. Over one-quarter of cases and controls were prescribed statins. Ever-use of any statin was associated with lower risk of Total NHL (OR=0.82, 95% CI 0.76-0.89) and of certain subtypes including diffuse large B-cell lymphomas (DLBCL, OR=0.77, 95% CI 0.65-0.92), plasma cell neoplasms (PCN, OR=0.76, 95% CI 0.63-0.91) and other B-cell NHL (0.75, 0.59-0.95). Analysis by statin type suggested that the association was limited to high potency statin and lipophilic statin users. No clear duration- or dose-response relationships were observed. Our findings provide evidence that statin use can reduce the risk of DLBCL and plasma cell lymphomas, but not other NHL types. Further studies are warranted to verify these associations and to examine the biological mechanisms. This article is protected by copyright. All rights reserved.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1002/ijc.31373


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