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<title>Experimental Oncology, 2012, № 3</title>
<link href="http://dspace.nbuv.gov.ua:80/handle/123456789/133132" rel="alternate"/>
<subtitle/>
<id>http://dspace.nbuv.gov.ua:80/handle/123456789/133132</id>
<updated>2026-04-06T22:03:34Z</updated>
<dc:date>2026-04-06T22:03:34Z</dc:date>
<entry>
<title>Neutrophil-tumor cell phagocytosis (cannibalism) in human turoms: an update and literature review</title>
<link href="http://dspace.nbuv.gov.ua:80/handle/123456789/139087" rel="alternate"/>
<author>
<name>Caruso, R.A.</name>
</author>
<author>
<name>Fedele, F.</name>
</author>
<author>
<name>Finocchiaro, G.</name>
</author>
<author>
<name>Arena, G.</name>
</author>
<author>
<name>Venuti, A.</name>
</author>
<id>http://dspace.nbuv.gov.ua:80/handle/123456789/139087</id>
<updated>2018-06-20T00:11:25Z</updated>
<published>2012-01-01T00:00:00Z</published>
<summary type="text">Neutrophil-tumor cell phagocytosis (cannibalism) in human turoms: an update and literature review
Caruso, R.A.; Fedele, F.; Finocchiaro, G.; Arena, G.; Venuti, A.
The recognition and removal of apoptotic cells by tissue macrophages and nonprofessional phagocytes, in a process called efferocytosis, is critical for development, tissue homeostasis and resolution of inflammation. Apoptotic bodies arising in tumor tissue are ingested by viable neoplastic cells and by resident macrophages. We described tumor cell phagocytosis of apoptotic neutrophils in human gastric carcinomas. This phenomenon is analogous to neutrophil efferocytosis performed by macrophages and by nonprofessional phagocytes during inflammatory reaction but is distinct by other types of cell-in-cell phenomena including emperipolesis and entosis both cytologically and biologically. In this review, we discussed them in their ultrastructural morphology, physiolo­gical roles, and clinicopathologic implications. This article is part of a Special Issue entitled “Apoptosis: Four Decades Later”.
</summary>
<dc:date>2012-01-01T00:00:00Z</dc:date>
</entry>
<entry>
<title>Splice variants in apoptotic pathway</title>
<link href="http://dspace.nbuv.gov.ua:80/handle/123456789/139085" rel="alternate"/>
<author>
<name>Miura, K.</name>
</author>
<author>
<name>Fujibuchi, W.</name>
</author>
<author>
<name>Unno, M.</name>
</author>
<id>http://dspace.nbuv.gov.ua:80/handle/123456789/139085</id>
<updated>2018-06-20T00:11:22Z</updated>
<published>2012-01-01T00:00:00Z</published>
<summary type="text">Splice variants in apoptotic pathway
Miura, K.; Fujibuchi, W.; Unno, M.
Elimination of superfluous or mutated somatic cells is provided by various mechanisms including apoptosis, and deregulation of apoptotic signaling pathways contributes to oncogenesis. 40 years have passed since the term “apoptosis” was introduced by Kerr et al. in 1972; among the programmed cell death, a variety of therapeutic strategies especially targeting apoptotic pathways have been investigated. Alternative precursor messenger RNA splicing, by which the process the exons of pre-mRNA are spliced in different arrangements to produce structurally and functionally distinct mRNA and proteins, is another field in progress, and it has been recognized as one of the most important mechanisms that maintains genomic and functional diversity. A variety of apoptotic genes are regulated through alternative pre-mRNA splicing as well, some of which have important functions as pro-apoptotic and anti-apoptotic factors. In this article we summarized splice variants of some of the apoptotic genes including BCL2L1, BIRC5, CFLAR, and MADD, as well as the regulatory mechanisms of alternative splicing of these genes. If the information of the apoptosis and aberrant splicing in each of malignancies is integrated, it will become possible to target proper variants for apoptosis, and the trans-elements themselves can become specific targets of cancer therapy as well. This article is part of a Special Issue entitled “Apoptosis: Four Decades Later”.
</summary>
<dc:date>2012-01-01T00:00:00Z</dc:date>
</entry>
<entry>
<title>Targeting the anti-apoptotic BCL-2 family members for the treatment of cancer</title>
<link href="http://dspace.nbuv.gov.ua:80/handle/123456789/139083" rel="alternate"/>
<author>
<name>Weyhenmeyer, B.</name>
</author>
<author>
<name>Murphy, A.C.</name>
</author>
<author>
<name>Prehn, J.H.M.</name>
</author>
<author>
<name>Murphy, B.M.</name>
</author>
<id>http://dspace.nbuv.gov.ua:80/handle/123456789/139083</id>
<updated>2018-06-20T00:04:49Z</updated>
<published>2012-01-01T00:00:00Z</published>
<summary type="text">Targeting the anti-apoptotic BCL-2 family members for the treatment of cancer
Weyhenmeyer, B.; Murphy, A.C.; Prehn, J.H.M.; Murphy, B.M.
Most cells express a variety of both anti-apoptotic and pro-apoptotic Bcl-2 proteins and the interaction within this family dictates whether a cell survives or dies. The dysregulation of the anti-anti-apoptotic Bcl-2 family members is one of the defining features of cancer cells in comparison to normal cells, and significantly contributes to the resistance of cancer cells to current treatment modalities. This anti-apoptotic subfamily of proteins is now a major target in the development of new methods to improve treatment outcomes for cancer patients. Several drugs directed at inhibiting Bcl-2 and related anti-apoptotic proteins have been developed with some showing considerable promise in the clinic. This Review presents the current knowledge of the role of the anti-apoptotic Bcl-2 family in cancer cells, as well as current and future perspectives on targeting this subfamily of proteins for therapeutic intervention in human malignancies. This article is part of a Special Issue entitled “Apoptosis: Four Decades Later”.
</summary>
<dc:date>2012-01-01T00:00:00Z</dc:date>
</entry>
<entry>
<title>The change of cellular membranes on apoptosis: fluorescence detection</title>
<link href="http://dspace.nbuv.gov.ua:80/handle/123456789/139071" rel="alternate"/>
<author>
<name>Demchenko, A.P.</name>
</author>
<id>http://dspace.nbuv.gov.ua:80/handle/123456789/139071</id>
<updated>2018-06-20T00:11:56Z</updated>
<published>2012-01-01T00:00:00Z</published>
<summary type="text">The change of cellular membranes on apoptosis: fluorescence detection
Demchenko, A.P.
The strong plasma membrane asymmetry existing in living cells is lost on apoptosis, and it is commonly detected with the probes interacting strongly and specifically with phosphatidylserine (PS). This phospholipid becomes exposed to the cell surface, and the labeled annexin V is used for its detection. The requirement for early and Ca2+-independent detection of apoptosis in the formats of spectroscopy of cell suspensions, flow cytometry, microarray technology and confocal or two-photon microscopy stimulated efforts for the development of new methods. Since the PS exposure must produce integrated changes of electrostatic potential and hydration in the outer leaflet of cell membrane, its detection can be provided by direct response of smart fluorescence probes. This review is focused on basic mechanisms underlying the loss of membrane asymmetry during apoptosis and the principles lying in the background of new methods that demonstrate essential advantages over the annexin V-binding assay. The convenient wavelength-ratiometric technique based on fluorescent probe F2N12S is described in detail. It incorporates spontaneously into outer leaflet of cell membrane and the color change of its fluorescent emission associated with apoptosis can be easily detected. This article is part of a Special Issue entitled “Apoptosis: Four Decades Later”.
</summary>
<dc:date>2012-01-01T00:00:00Z</dc:date>
</entry>
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