Cancer. A Comprehensive Treatise: Volume 1. Etiology: by Peter C. Nowell (auth.), Frederick F. Becker (eds.)

By Peter C. Nowell (auth.), Frederick F. Becker (eds.)

This sequence of books makes an attempt to provide, in a accomplished demeanour, the sector of oncology divided into 3 significant parts; etiology, biology, and remedy. those books should still function landmarks within the swiftly increasing experimental and medical "universe" of this box. to a few, they are going to be introductory; to others, a precis; for all, serious reviews at the futuI'e of analysis. In l'ecognition of the problems inherent in trying to pause and replicate whereas experimental information emerge with ever-increasing rapidity, the displays take the shape of overviews instead of stories. the place attainable, an historic viewpoint on observations and experimentation which ended in our current knowing is gifted, the cutting-edge in approach and method is reviewed, and the gaps in wisdom and in strategy are indicated. the purpose all through is integration-using the findings from one procedure for comparability with others. The great growth of curiosity in oncology as a medical-biological self-discipline inspired the booklet of those volumes. This enlargement, good warranted by way of the effect of oncology on human morbidity, has been characterised by means of at the least 3 phenomena. First, there was a tremendous bring up in funds and manpower dedicated to the research and therapy of malignancy. That the examine has turn into a growing number of "directed" or program-oriented signs the curiosity of these past the medical group within the administration of the eHort. moment, expanding numbers of scholars are getting into the sphere of oncology as their significant education program.

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Additional resources for Cancer. A Comprehensive Treatise: Volume 1. Etiology: Chemical and Physical Carcinogenesis

Example text

Ionizing radiation has long been known to produce chromosome breakage in many different organisms, and it has even become possible recently, by enumerating chromosome lesions in cultured lymphocytes from the peripheral blood, to make rough estimates of radiation dose in some exposed humans. Ionizing radiation is also a potent carcinogen, and it has been suggested that in some instances tumor induction may be mediated through direct damage to the genome, as indicated by visible chromosome lesions.

1965, Abnormal length of the small acrocentric chromosomes in chronic lymphocytic leukemia, Cancer Res. 25:1094 FITZGERALD, P. , CROSSEN, P. , ADAMS, A. , SHARMAN,C. , AND GUNZ, F. , 1966, Chromosome studies in familial leukemia, J. Med. Genet. 3:96. FITZGERALD, P. , CROSSEN, P. , AND HAMER, J. , 1973, Abnormal karyotypic clones in human acute leukemia: Their nature and significance, Cancer 31:1069. FORD, C. , 1966, The use of chromosome markers, in: Tissue Grafting and Radiation (H. Micklem and J.

In some cases, very stable chromosome patterns have emerged after a number of passages and subsequently persisted for years; in other tumor lines, variants have continued to appear. These phenomena have been well illustrated in cytogenetic studies of the Morris hepatomas, a series of transplantable rat liver tumors induced by chemical agents and generally selected for their high degree of differentiation and slow growth. In a few of these neoplasms, the cells were diploid when first studied, and the development of predominant aneuploid clones was not observed until later generations.

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