Apoptosis: New Approaches To Cancer Therapy

emise of cells by programmed cell death referred toapoptosis-triggering drugs. A large number of
as apoptosis, a Greek word that meansadenoviral agents are being constructed, including
“dropping off“ or “fallingreplication-incompetent and replication-selective
off“ as in leaves from a tree, has beenoncolytic adenoviruses. One of them is ONYX-015, a
recently a topic of intense interest in biomedicalreplication-competent virus genetically engineered to
sciences. Apoptosis is a well-defined sequence ofselectively replicate in and lyse p53-deficient cancer
morphological changes of cells that shrink andcells. Other agent, INGN 201, was shown to deliver a
condense and then fragment, releasing smallp53 expression.
membrane-bound apoptotic bodies, which arePreclinical studies in human cell lines and animals with
phagocytosed by other cells. Importantly, thehead and neck cancers have shown that the p53
intracellular constituents are not released into thegene is transcribed and translated into p53 protein.
extracellular milieu where they might have deleteriousRespectively, 5% and 58% of patients receiving
effects on neighboring cells. On the contrary, cellsthree intratumoral injections of INGN 201 in
that die in response to tissue damage or otherconjunction with radiation therapy for over 6 weeks
reasons exhibit very different morphological changeswere shown to have achieved complete and partial
generally called necrosis. The cells that undergo thisresponses. Other example may be a gene encoding
process swell and burst, releasing their intracellularthe proapoptotic Vpr protein that was successfully
contents, which can damage surrounding cells andtransferred into cancer cells by the HIV-1 virion.
often cause inflammation. Apoptosis refers to aThese agents are introduced by intravascular infusion
particular morphology in which a chromatin condensesor intratumoral or epitumoral injections. An example
or coalesces to a heterochromatin in one or moreof a target therapy against cancer is an intravenous
masses in the nucleus. It usually settles alongadministration of liposomal form of tretinoin (ATRA).
still-intact nuclear membrane referred to asTreatment of acute promyelocytic leukemia (APL)
margination of the chromatin. One of the essentialwith ATRA alone or in combination with
functions of apoptosis is the elimination of cells inchemotherapy results in an almost complete remission
which DNA damages, faulty proliferation or improperrate as high as 85% to 95%.
adhesion to extracellular matrix that cannot beOther proapoptotic anticancer therapeutics is
repaired. In cancer cells, the mechanism of apoptosisGenasense developed by the Genta Company.
induction is broken. Therefore, more and more ideasGenasense is a phosphothioate oligonucleotide
and hypotheses for selective inducing apoptosis inconsisting of 18 modified DNA bases. First, the
cancer cells are tested in a growing number ofsingle-stranded DNA molecule must be incorporated
laboratories all over the world. The subject ofinto a cancer cell and then target the mRNA by
programmed cell death has been recently discussed inhaving a complementary sequence to it.
almost 80 000 publications. As it is known, cellThis drug inhibits the production of a protein known
apoptosis may be induced by various stress factorsas Bcl-2 that is widely expressed in many types of
(e.g. hypoxia, expression of oncogenes, mutations,cancer. This up-regulation of Bcl-2 blocks the release
DNA damages). On the other hand, apoptosis may beof cytochrome C from the mitochondria thereby
induced via internal or external signals, for instancepreventing apoptosis. Furthermore, Bcl-2 appears to
proteins. Some of such endogenous and exogenousbe a major contributor to both inherent and acquired
proapoptotic proteins have been found and described.resistance to current anticancer treatments. By
Their genes may be used in modern anticancerinhibiting production of Bcl-2, Genasense enables the
therapies.cancer cells to be killed by apoptosis when treated
For example, introducing into cancer cells proapoptoticwith current state of the art therapy. Interesting
genes as Bax, Bcl-X5 or E2F-1 significantly increasesapoptosis-inducing drug is Velcade jointly developed
induction of apoptosis. Some clinical trials concernby NCI and Millenium Pharmaceuticals. Activity of
therapeutic application of a 121-amino acids apoptinVelcade is mainly associated with reversible inhibition
originated from chicken anemia virus (CAV). Recentof the proteasome and building up many proteins
data suggest that apoptosis induced by this proteinincluding BAX. In the normal cells, the BAX protein
involves caspases, a family of cysteinylinduces apoptosis by blocking the activity of Bcl-2.
aspartate-specific proteinases. In vitro results showWhen BAX level increases, BAX inhibition of Bcl-2 also
that apoptin is very active against cancer cellsincreases and the cells undergo apoptosis. Non-clinical
without inducing toxicity to normal cells. Thisstudies have demonstrated that cancer cells are
tumor-specific effect may be explained by themore sensitive to the effects of the proteasome
nuclear localization of the protein in tumor cellsinhibition than normal cells.
required for its action. Moreover, apoptin is equallySelected references
active, such as p53-mutant, Bcl-2-overexpressing orAdachi, S.L.L., Carson, D.A., Nakahata, T., 2004.
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induction of apoptosis by introducing genes encodingFerreira, C.G., Epping, M., Kruyt. F.A.E., Giaccone, G.,
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One possible mechanism is associated withCancer Research 8, 2024-2034.
destruction of mitochondrial membranes and, inGhobrial, I.M., Witzig, T.E., Adjei, A.A., 2005. Targeting
consequence, disturbing electrons transport, oxidativeApoptosis Pathways in Cancer Therapy. CA: A
phosphorylation and ATP synthesis. Finally, the cellCancer Journal for Clinicians 55, 178-194.
dies but the death is slightly different than that duringHengartner, M.O., 2000. The biochemistry of
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Proapoptotic proteins cannot be directly introducedCarcinogenesis 21, 485-495.
to cancer cells because there are no specificTamm, I., Dorken, B., Hartmann G., 2001. Antisense
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Other method is introducing them as genes byTamm, I., Schriever, F., Dorken, B., 2001. Apoptosis:
vectors and this approach has been alreadyimplications of basic research for clinical oncology.
successfully applied. Clinical trials are presentlyLancet Oncology 2, 33-42.
underway to test efficiency of new