Δευτέρα 14 Ιανουαρίου 2019

The cellular effects of novel triazine nitrogen mustards in glioblastoma LBC3, LN-18 and LN-229 cell lines

Summary

1,3,5-triazine is an important heterocyclic skeleton for mono, two or three 2-chloroethylamine groups. The study presented here provides novel information on cellular effects of 1,3,5-triazine with mono, two or three 2-chloroethylamine groups in glioblastoma LBC3, LN-18 and LN-229 cell lines. In our study, the most cytotoxic effect was observed in 1,3,5-triazine with three 2-chloroethylamine groups (12f compound). It has been demonstrated that 12f induce time- and dose-dependent cytotoxicity in all investigated glioma cell lines. Apart from that in glioblastoma cells, treated with 12f compound, we noticed strong induction of apoptosis. In conclusion, this research provides novel information concerning cellular effects of apoptosis in LBC3, LN-18 and LN-229 cell lines. Moreover, we suggest that 12f compound may be a candidate for further evaluation as an effective chemotherapeutic agent for human glioblastoma cells.



http://bit.ly/2DbbATC
Αναρτήθηκε από στις Δεν υπάρχουν σχόλια:

The cellular effects of novel triazine nitrogen mustards in glioblastoma LBC3, LN-18 and LN-229 cell lines

Summary

1,3,5-triazine is an important heterocyclic skeleton for mono, two or three 2-chloroethylamine groups. The study presented here provides novel information on cellular effects of 1,3,5-triazine with mono, two or three 2-chloroethylamine groups in glioblastoma LBC3, LN-18 and LN-229 cell lines. In our study, the most cytotoxic effect was observed in 1,3,5-triazine with three 2-chloroethylamine groups (12f compound). It has been demonstrated that 12f induce time- and dose-dependent cytotoxicity in all investigated glioma cell lines. Apart from that in glioblastoma cells, treated with 12f compound, we noticed strong induction of apoptosis. In conclusion, this research provides novel information concerning cellular effects of apoptosis in LBC3, LN-18 and LN-229 cell lines. Moreover, we suggest that 12f compound may be a candidate for further evaluation as an effective chemotherapeutic agent for human glioblastoma cells.



http://bit.ly/2DbbATC
Αναρτήθηκε από στις Δεν υπάρχουν σχόλια:

Risk Factors for Relapse of Hyperglycemia after Laparoscopic Roux-en-Y Gastric Bypass in T2DM Obese Patients: a 5-Year Follow-Up of 24 Cases

Abstract

Objectives

To explore the risk factors for relapse of hyperglycemia in obese patients with type II diabetes mellitus (T2DM) who received laparoscopic Roux-en-Y gastric bypass (LRYGB) surgery.

Methods

A retrospective analysis was performed on all obese patients with T2DM who underwent a LRYGB during the period 2011–2013. Demographics, preoperative body mass index (BMI), preoperative glycated hemoglobin A1c (HbA1c), adherence to lifestyle intervention, preoperative medication of insulin, and the time interval between surgery and diagnosis of T2DM were investigated and compared.

Results

A total of 24 patients were included in our study. The median age was 45.5 years, the median BMI was 29.9 kg/m2, and the median HbA1c was 7.9%. Out of 24 patients, 54.2% (13/24) experienced a relapse of hyperglycemia. The 1-year, 3-year, and 5-year relapse rates were 4.2%, 12.5%, and 50.0%, respectively. The preoperative HbA1c level, C-peptide (2 h) level, and C-peptide (3 h) level were identified as independent variables for the relapse of hyperglycemia (8.11 ± 0.48 vs 7.72 ± 0.37 kg/m2, p = 0.036; 4.35 ± 1.46 vs 7.13 ± 4.10 ng/ml, p = 0.032; 3.76 ± 0.61 vs 5.99 ± 3.39 ng/ml, p = 0.029). Lifestyle intervention could reduce the hyperglycemia relapse rate (66.7 vs 41.7%) after LRYGB surgery.

Conclusions

The preoperative HbA1c level and C-peptide level at surgery have an important significance in predicting the relapse of hyperglycemia after LRYGB surgery; lifestyle intervention is crucial for these patients.



http://bit.ly/2AN27Rb
Αναρτήθηκε από στις Δεν υπάρχουν σχόλια:

Cancer Cell

  1. Previews

    1. Mini reviewAbstract only

      Hijacking EMT: Better Fat Than Dead

      Stefan Hinz, Mark A. LaBarge
      Pages 1-2
      Purchase PDF

      Potential for cancers to form metastases requires cell dissemination utilizing epithelial-to-mesenchymal transition (EMT) program. In this issue of Cancer Cell, Ishay-Ronen et al. show that plasticity intrinsic to the EMT program can be exploited to divert cancer cells into becoming post-mitotic adipocytes, thus preventing formation of metastases.

    2. Mini reviewAbstract only

      Tumor Extracellular Vesicles Impede Interferon Alert Responses

      Candia M. Kenific, Gang Wang, David Lyden
      Pages 3-5
      Purchase PDF

      Tumor-derived extracellular vesicles promote metastasis by inducing functional changes in cells at pre-metastatic sites conducive for tumor cell colonization. In this issue of Cancer Cell, Ortiz and colleagues show that type I interferon regulates extracellular vesicle uptake and that modulating this pathway holds promise for treating metastasis.

    3. Mini reviewAbstract only

      The Deadly Bite of STAT3

      Hagen Schwenzer, Ariberto Fassati
      Pages 5-7
      Purchase PDF

      The Tasmanian devils' facial tumor disease (DFTD) is a transmissible cancer that spreads by biting and threatens extinction of this marsupial. In this issue of Cancer Cell, Kosack et al. describe how overexpression of ERBB and uncontrolled activation of STAT3 drive DFTD growth and immune evasion.

    4. Mini reviewAbstract only

      Tails of a Super Histone

      Patrick Sin-Chan, Iqra Mumal, Annie Huang
      Pages 7-9
      Purchase PDF

      Diffuse intrinsic brain stem gliomas (DIPGs) with characteristic K27M mutation of H3.3 are lethal and poorly understood childhood cancers. In this issue of Cancer Cell, Larson et al. exploit a unique murine DIPG model with inducible, endogenous K27M expression to reveal insights into mechanisms of K27M-mediated transformation in DIPG.

  2. Perspective

    1. Review articleAbstract only

      The Roles of Initiating Truncal Mutations in Human Cancers: The Order of Mutations and Tumor Cell Type Matters

      Arnold J. Levine, Nancy A. Jenkins, Neal G. Copeland
      Pages 10-15
      Purchase PDF

      We propose that initiating truncal mutations plays a special role in tumor formation by both enhancing the survival of the initiating cancer cell and by selecting for secondary mutations that contribute to tumor progression, and that these mutations often act in a tissue-preferred fashion. Here, we explain why inherited mutations often have different tissue specificities compared with spontaneous mutations in the same gene. Initiating truncal mutations make excellent neo-antigens for immunotherapy, and understanding why one mutation selects for a second mutation in a particular tissue type could one day aid in the design of gene-targeted combination therapies.

  3. Articles

    1. Research articleAbstract only

      Gain Fat—Lose Metastasis: Converting Invasive Breast Cancer Cells into Adipocytes Inhibits Cancer Metastasis

      Dana Ishay-Ronen, Maren Diepenbruck, Ravi Kiran Reddy Kalathur, Nami Sugiyama, ... Gerhard Christofori
      Pages 17-32.e6
      Purchase PDF
      Graphical Abstract

      Graphical abstract for this article

    2. Research articleAbstract only

      An Interferon-Driven Oxysterol-Based Defense against Tumor-Derived Extracellular Vesicles

      Angelica Ortiz, Jun Gui, Farima Zahedi, Pengfei Yu, ... Serge Y. Fuchs
      Pages 33-45.e6
      Purchase PDF
      Graphical Abstract

      Graphical abstract for this article

    3. Research articleAbstract only

      p62/SQSTM1 Fuels Melanoma Progression by Opposing mRNA Decay of a Selective Set of Pro-metastatic Factors

      Panagiotis Karras, Erica Riveiro-Falkenbach, Estela Cañón, Cristina Tejedo, ... María S. Soengas
      Pages 46-63.e10
      Purchase PDF
      Graphical Abstract

      Graphical abstract for this article

    4. Research articleAbstract only

      Tinagl1 Suppresses Triple-Negative Breast Cancer Progression and Metastasis by Simultaneously Inhibiting Integrin/FAK and EGFR Signaling

      Minhong Shen, Yi-Zhou Jiang, Yong Wei, Brian Ell, ... Yibin Kang
      Pages 64-80.e7
      Purchase PDF
      Graphical Abstract

      Graphical abstract for this article

    5. Research articleAbstract only

      Hyper-Editing of Cell-Cycle Regulatory and Tumor Suppressor RNA Promotes Malignant Progenitor Propagation

      Qingfei Jiang, Jane Isquith, Maria Anna Zipeto, Raymond H. Diep, ... Catriona Jamieson
      Pages 81-94.e7
      Purchase PDF
      Graphical Abstract

      Graphical abstract for this article

    6. Research articleAbstract only

      Comprehensive Analysis of Chromatin States in Atypical Teratoid/Rhabdoid Tumor Identifies Diverging Roles for SWI/SNF and Polycomb in Gene Regulation

      Serap Erkek, Pascal D. Johann, Martina A. Finetti, Yiannis Drosos, ... Marcel Kool
      Pages 95-110.e8
      Purchase PDF
      Summary

      Biallelic inactivation of SMARCB1, encoding a member of the SWI/SNF chromatin remodeling complex, is the hallmark genetic aberration of atypical teratoid rhabdoid tumors (ATRT). Here, we report how loss of SMARCB1 affects the epigenome in these tumors. Using chromatin immunoprecipitation sequencing (ChIP-seq) on primary tumors for a series of active and repressive histone marks, we identified the chromatin states differentially represented in ATRTs compared with other brain tumors and non-neoplastic brain. Re-expression of SMARCB1 in ATRT cell lines enabled confirmation of our genome-wide findings for the chromatin states. Additional generation of ChIP-seq data for SWI/SNF and Polycomb group proteins and the transcriptional repressor protein REST determined differential dependencies of SWI/SNF and Polycomb complexes in regulation of diverse gene sets in ATRTs.

    7. Research articleAbstract only

      Proteogenomic Characterization of Human Early-Onset Gastric Cancer

      Dong-Gi Mun, Jinhyuk Bhin, Sangok Kim, Hyunwoo Kim, ... Daehee Hwang
      Pages 111-124.e10
      Purchase PDF
      Graphical Abstract

      Graphical abstract for this article

    8. Research articleOpen access

      The ERBB-STAT3 Axis Drives Tasmanian Devil Facial Tumor Disease

      Lindsay Kosack, Bettina Wingelhofer, Alexandra Popa, Anna Orlova, ... Andreas Bergthaler
      Pages 125-139.e9
      Download PDF
      Graphical Abstract

      Graphical abstract for this article

    9. Research articleAbstract only

      Histone H3.3 K27M Accelerates Spontaneous Brainstem Glioma and Drives Restricted Changes in Bivalent Gene Expression

      Jon D. Larson, Lawryn H. Kasper, Barbara S. Paugh, Hongjian Jin, ... Suzanne J. Baker
      Pages 140-155.e7
      Purchase PDF
      Graphical Abstract

      Graphical abstract for this article

  4. Correction

    1. ErratumFull text access

      CARM1 Is Essential for Myeloid Leukemogenesis but Dispensable for Normal Hematopoiesis

      Sarah M. Greenblatt, Na Man, Pierre-Jacques Hamard, Takashi Asai, ... Stephen D. Nimer
      Page 156
      Download PDF

Αναρτήθηκε από στις Δεν υπάρχουν σχόλια:
Εγγραφή σε: Αναρτήσεις (Atom)