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MOLECULAR BASIS OF CANCER AND CLINICAL APPLICATIONS - 06/09/11

Doi : 10.1016/S0039-6109(05)70194-8 
Manuel G. Alvarez, MD, PhD a, Pelayo C. Besa, MD b
a Department of Medicine (MGA) 
b Radiology (PCB), Pontificia Universidad Católica de Chile, Santiago, Chile 

Résumé

When analyzing the trend in cancer mortality in developed countries during the last 3 decades, the authors agree with recent publications that report only a slight reduction or no reduction at all. They agree only in part with authorized opinions that insist on changing the present strategies in the “war against cancer”—moving them to the stages of prevention and early diagnosis, and recommend a review on the funding of cancer research with a reduction in the support for the search of new therapeutic options and basic biomolecular research.4, 5

Nonetheless, these publications, based exclusively on the analysis of the outcome in the global cancer mortality rate, cannot overlook the fact that the advances in the knowledge of cancer have been impressive, more so considering the complexity of this disease. Since the 1970s, the joint use of classic therapeutic strategies, such as chemotherapy, radiotherapy, and surgery, has led to dramatic reductions in the mortality rates of certain types of cancer, even in their metastatic phases; complete cure is found frequently in over 60% of patients with embryonic tumors, in tumors in children, and in hematologic cancers.4, 5

There also have been significant changes in the increase of disease-free survival periods and the quality of life and increases in the percentage of remission in patients with breast, ovarian, prostatic, colorectal, esophageal, and pulmonary cancers and others, when the previously mentioned alternatives are used together with surgery, which is the best option today.14 It is true that these advances have not been reflected in an increase in the rate of remission of the more prevalent neoplasias, which makes it necessary to modify strategies and to continue trying to understand what cancer is at the intracellular level, integrating concepts constantly delivered by the vertiginous advances in molecular and cellular biology.48

The complexity of what cancer represents at the cellular and biomolecular level has not been an obstacle to achieve important improvements in the understanding of cellular function and particularly of the basic cellular processes that allow a normal cell to change into a neoplastic cell. This carcinogenic cascade is regulated by complex alterations of the genes that have only begun to be understand recently. Already partially defined concepts, such as oncogenes, tumor suppressor genes, cellular cycle regulatory genes, and so forth, have been complemented with newer ones, such as the identification of genes that play a role in programmed cellular death and apoptosis, cellular inmortality and its relationship to telomeres, metastatic cascade, cellular differentiation, and so forth.1, 7

This new knowledge allows us to postulate with optimism that the genetic paradigm of cancer is something that can be possibly understood; perhaps, in the near future, this new knowledge can be used in the logical design of new preventive and therapeutic strategies that will be more efficient, selective, and specific.50

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 Address reprint requests to Manuel G. Alvarez, MD, PhD, Department of Medicine, Pontificia Universidad Católica de Chile, Diagonal Paraguay 319, Santiago, Chile, e-mail: malvarez@med.puc.cl
This work was, in part, supported by a Grant No. 1960475 from Fondo Nacional de Ciencia y Tecnología (Fondecyt) of the Chilean Government.


© 2000  W. B. Saunders Company. Publié par Elsevier Masson SAS. Tous droits réservés.
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Vol 80 - N° 2

P. 443-457 - avril 2000 Retour au numéro
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