Author: Yifan Zhai
Publisher:
ISBN:
Category : Breast
Languages : en
Pages : 296

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Author:
Publisher:
ISBN:
Category :
Languages : en
Pages :

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The folder may include clippings, announcements, small exhibition catalogs, and other ephemeral items.

Author: Benjamin G. Neel
Publisher: Springer
ISBN: 1493936492
Category : Medical
Languages : en
Pages : 362

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This book aims to bridge the gap in understanding how protein-tyrosine phosphatases (PTPs), which carry out the reverse reaction of tyrosine phosphorylation, feature in cancer cell biology. The expertly authored chapters will first review the general features of the PTP superfamily, including their overall structure and enzymological properties; use selected examples of individual PTP superfamily members, to illustrate emerging data on the role of PTPs in cancer; and will review the current status of PTP-based drug development efforts. Protein Tyrosine Phosphatases in Cancer,from renowned researchers Benjamin Neel and Nicholas Tonks, is invaluable reading for researchers in oncology, stem cell signaling,and biochemistry.

Author:
Publisher:
ISBN:
Category : Medicine
Languages : en
Pages : 1860

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Author:
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ISBN:
Category :
Languages : en
Pages : 0

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Overexpression of DNA polymerase beta in the breast epithelial cell line, MCF-lOA, resulted in loss of proliferative potential, most probably due to the upregulation of pro- apoptotic proteins, such as Hax. The ras-transformed MCF-1OAT cell line is more tolerant of pol-beta overexpression, possibly due to the increased levels of Bcl-2 protein in these cells. However, the MCP-lOAT cells continue to display a progressive loss of proliferative potential resulting from pol-beta overexpression. We observed an alteration in MCF-lCAT cell phenotype from an adherent to a floating cell morphology after pol-beta overexpression. This is a novel observation and may be related to underlying genomic changes resulting from increased pol-beta protein levels. MCFlOAT cells overexpressing poln displayed a tumor incidence and latency similar to parental cells. Thus, in contrast to what we observe in cell culture, a subpopulation of pol-beta overexpressing cells retains proliferative potential in vivo. We hypothesize that biologic selection occurs for a mutant, MCE-l0AT/WTpol-beta cell variant within the mouse environment. The requisite genetic variation may be related to the adherent to floating morphology change. The observations that the MCF-lOAT/pol-beta tumors are sac-like rather than solid, and that animals bearing MCF-lOAT/pol-beta tumors progressed to form lung metastases, further supports our hypothesis.

Author: Sanaz Manteghi
Publisher:
ISBN:
Category :
Languages : en
Pages :

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"Histidine Domain containing Protein Tyrosine Phosphatase (HD-PTP/PTPN23) is part of the ESCRT (Endosomal Sorting Complex Required for Transport) complex with previously established function in cell surface receptor sorting, signaling and multi-vesicular body biogenesis. HD-PTP is encoded by the PTPN23 gene, which maps to chromosomal region 3p21.3, reported to be frequently deleted in various human cancers. However, the bona fide tumor suppressive role of HD-PTP has not been demonstrated yet. In this study we have investigated Ptpn23's tumor suppressor function in vivo and we further assessed its role in cellular transformation and NF-[kappa]B pathway modulation in vitro.Components of the ESCRT complex have long been proposed to act as tumor suppressors. Here we show for the first time that PTPN23/HD-PTP, an ESCRT associated protein, exhibits tumor suppressor function in vivo. Ptpn23 hemizygous knockout mice are susceptible to the development of spontaneous B-cell lymphoma and lung adenocarcinoma. Moreover, B-cell lymphoma onset and dissemination were significantly potentiated by hemizygous loss of Ptpn23 in the transgenic Eμ-myc mouse model. Tumors derived from the Ptpn23+/- mice maintained HD-PTP expression and exhibited impaired apoptosis together with reduced levels of the ARF tumor suppressor. In addition, PTPN23 hemizygous loss resulted in partial cell transformation and increased migration/invasion. Furthermore, analysis of human cancer gene expression data revealed that heterozygous loss of PTPN23 is common in many human cancers, which is correlated with poor survival. This suggests that PTPN23/HD-PTP is a prominent tumor suppressor gene in human malignancies. Moreover, we identified a new function for HD-PTP in TNF[alpha]-induced canonical NF-[kappa]B activation downstream of TNFR1 receptor. We have shown that HD-PTP depleted cells have increased cell surface TNFR1 and increased TNFR1 signaling complex formation which occurs due to defect in TNFR1 degradation in the context of HD-PTP deficiency. Furthermore, we have identified HD-PTP as a negative regulator of NF-[kappa]B pathway via TNFR1 receptor. We have shown that HD-PTP depleted cells display faster kinetics of NF-[kappa]B activation, increased target gene expression and inflammatory cytokine secretion upon TNF[alpha] stimulation. This suggests that HD-PTP inhibits NF-[kappa]B activation by controlling cell surface TNFR1 levels and recruitment of adaptor molecules to TNFR1 in order to attenuate the signaling cascade.In conclusion, these data suggest that PTPN23 is a haplo-insufficient tumor suppressor gene involved in tumor initiation, progression and NF-[kappa]B signaling, demonstrating for the first time the importance of an ESCRT component, HD-PTP, in tumorigenesis and immunity. Further investigation is required to determine the exact molecular mechanism of HD-PTP in tumorigenesis, inflammation and cancer." --

Author:
Publisher:
ISBN:
Category : Medicine
Languages : en
Pages : 742

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Author:
Publisher:
ISBN:
Category : Cancer
Languages : en
Pages : 690

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Author: Manfred Wirth
Publisher: Walter de Gruyter
ISBN: 3110807270
Category : Medical
Languages : en
Pages : 220

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Author:
Publisher:
ISBN:
Category : Dissertations, Academic
Languages : en
Pages : 658

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