Avid Bioservices Inc (CDMO)

[entdoc]

Cloaked:the following is a bit of my own due diligence on the subject this morning for about 30 minutes. Hope it helps
Adv Cancer Res. 2011;111:39-96.
The essential role of evasion from cell death in cancer.
Kelly GL, Strasser A.
SourceThe Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia.
Abstract
The link between evasion of apoptosis and the development of cellular hyperplasia and ultimately cancer is implicitly clear if one considers how many cells are produced each day and, hence, how many cells must die to make room for the new ones (reviewed in Raff, 1996). Furthermore, cells are frequently experiencing noxious stimuli that can cause lesions in their DNA and faults in DNA replication can occur during cellular proliferation. Such DNA damage needs to be repaired efficiently or cells with irreparable damage must be killed to prevent subsequent division of aberrant cells that may fuel tumorigenesis (reviewed in Weinberg, 2007). The detection of genetic lesions in human cancers that activate prosurvival genes or disable proapoptotic genes have provided the first evidence that defects in programmed cell death can cause cancer (Tagawa et al., 2005; Tsujimoto et al., 1984; Vaux, Cory, and Adams, 1988) and this concept was proven by studies with genetically modified mice (Egle et al., 2004b; Strasser et al., 1990a). It is therefore now widely accepted that evasion of apoptosis is a requirement for both neoplastic transformation and sustained growth of cancer cells (reviewed in Cory and Adams, 2002; Hanahan and Weinberg, 2000; Weinberg, 2007). Importantly, apoptosis is also a major contributor to anticancer therapy-induced killing of tumor cells (reviewed in Cory and Adams, 2002; Cragg et al., 2009). Consequently, a detailed understanding of apoptotic cell death will help to better comprehend the complexities of tumorigenesis and should assist with the development of improved targeted therapies for cancer based on the direct activation of the apoptotic machinery (reviewed in Lessene, Czabotar, and Colman, 2008).

Copyright © 2011 Elsevier Inc. All rights reserved.

Biochim Biophys Acta. 2011 November; 1808(11-15): 2638–2645.
doi: 10.1016/j.bbamem.2011.07.026 PMCID: PMC3175029

Copyright © 2011 Elsevier B.V.
In search of a novel target — Phosphatidylserine exposed by non-apoptotic tumor cells and metastases of malignancies with poor treatment efficacy
Sabrina Riedl,a1 Beate Rinner,b1 Martin Asslaber,c Helmut Schaider,be Sonja Walzer,d2 Alexandra Novak,b Karl Lohner,a and Dagmar Zweyticka
aInstitute of Biophysics and Nanosystems Research, Austrian Academy of Sciences, Schmiedlstraße 6, A-8042 Graz, Austria
Received April 1, 2011; Revised July 19, 2011; Accepted July 19, 2011.
This document may be redistributed and reused, subject to certain conditions.
This document was posted here by permission of the publisher. At the time of the deposit, it included all changes made during peer review, copy editing, and publishing. The U. S. National Library of Medicine is responsible for all links within the document and for incorporating any publisher-supplied amendments or retractions issued subsequently. study was performed in the aim to identify potential targets for the development of novel therapy to treat cancer with poor outcome or treatment efficacy. We show that the negatively charged phospholipid phosphatidylserine (PS) is exposed in the outer leaflet of their plasma membrane not only in tumor cell lines, but also in metastases and primary cultures thereof, which contrasts with a lack of PS exposure by differentiated non-tumorigenic counterparts. Studied tumor cell lines were derived from non-tumorigenic and malignant melanomas, prostate- and renal cancer, glioblastoma and a rhabdomyosarcoma. Importantly, also metastases of melanoma expose PS and there is a correlation between malignancy of melanoma cell lines from different stages of tumor progression and PS exposure. The PS exposure we found was neither of apoptotic nor of experimental artificial origin. Finally potentially malignant and non-malignant cells could be differentiated by sorting of a primary cell culture derived from a glioblastoma based on PS exposure, which has so far not been possible within one culture due to lack of a specific marker. Our data provide clear evidence that PS could serve as uniform marker of tumor cells and metastases as well as a target for novel therapeutic approaches based on e.g. PS-specific host defense derived peptides.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3175029/

Annu Rev Physiol. 2003;65:701-34. Epub 2002 May 1.
Aminophospholipid asymmetry: A matter of life and death.
Balasubramanian K, Schroit AJ.

Cancer Res. 1991 Jun 1;51(11):3062-6.
Elevated expression of phosphatidylserine in the outer membrane leaflet of human tumor cells and recognition by activated human blood monocytes.
Utsugi T, Schroit AJ, Connor J, Bucana CD, Fidler IJ.

Anatomic Pathology / Annexin-V in Ovarian Carcinoma
CME/SAM
Evaluation of Cell Surface Expression of
Phosphatidylserine in Ovarian Carcinoma Effusions
Using the Annexin-V/7-AAD Assay
Clinical Relevance and Comparison With Other Apoptosis
Parameters
Hiep Phuc Dong, MSc,1 Arild Holth, BSc,1 Lilach Kleinberg, PhD,1 Marit Gunhild Ruud, BSc,1
Mari Bunkholt Elstrand, MD,2 Claes G. Tropé, MD, PhD,2,3 Ben Davidson, MD, PhD,1,3
and Björn Risberg, MD, PhD1,4
http://ajcp.ascpjournals.org/content/132/5/756.full.pdf