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Eclectic aspects of cancer
Book Reviews 299
The loss of the need for this hormone appears to define the polycythemic cell. Thus the lessons learned in tissue culture are applicable to proliferative human disease. There is a treatment of the sensitivity of cells to radiotherapy. Cells in S phase are in general less sensitive to radiotherapy than cells in mitosis, Gl or G2 phases. The dose-response curve for cells at any phase has the same slope, but cells in early or late S phase have a pronounced shoulder reflecting repair processes. Unfortunately, the molecular basis of this DNA repair is not discussed. The book provides some interesting insights into the variables that affect the growth of freshly arising and transplantable tumors. Clearly, the increase in tumor mass is regulated by both cell replication and cell loss. Surprisingly, cell loss has a dominant role in the growth of many tumors. Carcinomas with a high mitotic index occasionally grow surprisingly slowly. Cell loss plays a particularly large role in regulating the mass of carcinomas, and also has an important role in the maintenance of certain normal epithelial surfaces (for example, the lining of the gastrointestinal tract). Loss and replication are, under normal circumstances, finely tuned. The book provides convincing evidence that the mechanism of cell loss in both normal tissues and cancers deserves further study. Charles D. Scher Division of Oncology Children’s Hospital of Philadelphia Department of Pediatrics University of Pennsylvania Philadelphia, Pennsylvania 19104
Eclectic
Aspects of Cancer
Cancer Biology Reviews, 3. Edited by J. J. Marchalonis and M. G. Hanna, Jr. New York: Marcel-Dekker. (1982). 224 pp. $39.50. The five chapters in this volume deal with diverse aspects of cancer biology-namely, peroxisomes and hepatocarcinogenesis, quantitative mutagenesis, oncogenic transformation, tumor immunobiology and differentiation and chemotherapy. Tsukada and Mochizuki express their views on peroxisomes in hepatomas and hepatocarcinogenesis, stressing that analysis of peroxisomes offers a means to study sequential events occurring in preneoplastic hepatocytes during hepatoma development. Fox gives a detailed analysis of quantitative mutagenesis with somatic cells derived from rodents and humans. She primarily uses the dose-response data of alkane sulfonates and alkylnitrosoureas to illustrate
her viewpoints on the quantitative nature of and the role of DNA repair in mammalian cell mutagenesis, and to discuss the relationship of mutation, cytotoxicity, carcinogenesis and transformation. In addition, she cautiously points out many problems, such as the relative sensitivities of rodent and human cells to induced mutations at the same or different loci, which makes it difficult to estimate risks of induced germinal or somatic mutation resulting from chemical exposure in humans. Naha discusses the use of temperature-sensitive mutants of mammalian cells in studies of the genetics of somatic cells, cellular regulatory mechanisms, clonal selection in malignant transformation and cell synchrony. Mainly on the basis of analysis of reversion, the author points out that the origin of some observed altered phenotypes could be non-Mendelian (epigenetic). Using documented examples, Naha emphasizes the use of temperature-sensitive mutants for studying the functions of normal and malignant cells. Olsson’s chapter emphasizes the relationship between malignant tumor growth and immune reactions, the importance of cytotoxic autoreactive immune mechanisms and the impact of the natural clonability of tumors. The author suggests that tumors may have a natural polyclonability, with antigenic heterogeneity of some clones being nonantigenic in autologous hosts, and that “self-directed” immune reactions contribute to the inhibition of tumor growth irrespective of the antigeneity of the tumor cells. Hozumi presents a new approach to cancer chemotherapy; the malignancy of tumor cells was controlled through induction of normal cell differentiation, using mouse myeloid leukemia Ml cell line as a model. From studies of induction of differentiation with a concomitant loss of leukemogenicity in vitro, the author discovered that differentiation of these cells in vivo can be achieved with various inducers that act through proteinaceous factor or factors (D factor). D factor and factors found in other similar systems may be of potential value in controlling myeloid leukemia. A unique feature of this book is that instead of compiling up-to-date published literature, as is most commonly done for review articles, all the authors have emphasized their own work and expressed their own viewpoints. Each article is of high quality, and Fox’s writing is most entertaining. I have no doubt this volume will be of value to every biomedical science library. Because of its broad spectrum, with each article unrelated to each other except in a very general sense, this book may not have many individual collectors; the authors may instead be swamped with reprint requests. Abraham W. Hsie Biology Division Oak Ridge National Laboratory P. 0. Box Y Oak Ridge, Tennessee 37830
The loss of the need for this hormone appears to define the polycythemic cell. Thus the lessons learned in tissue culture are applicable to proliferative human disease. There is a treatment of the sensitivity of cells to radiotherapy. Cells in S phase are in general less sensitive to radiotherapy than cells in mitosis, Gl or G2 phases. The dose-response curve for cells at any phase has the same slope, but cells in early or late S phase have a pronounced shoulder reflecting repair processes. Unfortunately, the molecular basis of this DNA repair is not discussed. The book provides some interesting insights into the variables that affect the growth of freshly arising and transplantable tumors. Clearly, the increase in tumor mass is regulated by both cell replication and cell loss. Surprisingly, cell loss has a dominant role in the growth of many tumors. Carcinomas with a high mitotic index occasionally grow surprisingly slowly. Cell loss plays a particularly large role in regulating the mass of carcinomas, and also has an important role in the maintenance of certain normal epithelial surfaces (for example, the lining of the gastrointestinal tract). Loss and replication are, under normal circumstances, finely tuned. The book provides convincing evidence that the mechanism of cell loss in both normal tissues and cancers deserves further study. Charles D. Scher Division of Oncology Children’s Hospital of Philadelphia Department of Pediatrics University of Pennsylvania Philadelphia, Pennsylvania 19104
Eclectic
Aspects of Cancer
Cancer Biology Reviews, 3. Edited by J. J. Marchalonis and M. G. Hanna, Jr. New York: Marcel-Dekker. (1982). 224 pp. $39.50. The five chapters in this volume deal with diverse aspects of cancer biology-namely, peroxisomes and hepatocarcinogenesis, quantitative mutagenesis, oncogenic transformation, tumor immunobiology and differentiation and chemotherapy. Tsukada and Mochizuki express their views on peroxisomes in hepatomas and hepatocarcinogenesis, stressing that analysis of peroxisomes offers a means to study sequential events occurring in preneoplastic hepatocytes during hepatoma development. Fox gives a detailed analysis of quantitative mutagenesis with somatic cells derived from rodents and humans. She primarily uses the dose-response data of alkane sulfonates and alkylnitrosoureas to illustrate
her viewpoints on the quantitative nature of and the role of DNA repair in mammalian cell mutagenesis, and to discuss the relationship of mutation, cytotoxicity, carcinogenesis and transformation. In addition, she cautiously points out many problems, such as the relative sensitivities of rodent and human cells to induced mutations at the same or different loci, which makes it difficult to estimate risks of induced germinal or somatic mutation resulting from chemical exposure in humans. Naha discusses the use of temperature-sensitive mutants of mammalian cells in studies of the genetics of somatic cells, cellular regulatory mechanisms, clonal selection in malignant transformation and cell synchrony. Mainly on the basis of analysis of reversion, the author points out that the origin of some observed altered phenotypes could be non-Mendelian (epigenetic). Using documented examples, Naha emphasizes the use of temperature-sensitive mutants for studying the functions of normal and malignant cells. Olsson’s chapter emphasizes the relationship between malignant tumor growth and immune reactions, the importance of cytotoxic autoreactive immune mechanisms and the impact of the natural clonability of tumors. The author suggests that tumors may have a natural polyclonability, with antigenic heterogeneity of some clones being nonantigenic in autologous hosts, and that “self-directed” immune reactions contribute to the inhibition of tumor growth irrespective of the antigeneity of the tumor cells. Hozumi presents a new approach to cancer chemotherapy; the malignancy of tumor cells was controlled through induction of normal cell differentiation, using mouse myeloid leukemia Ml cell line as a model. From studies of induction of differentiation with a concomitant loss of leukemogenicity in vitro, the author discovered that differentiation of these cells in vivo can be achieved with various inducers that act through proteinaceous factor or factors (D factor). D factor and factors found in other similar systems may be of potential value in controlling myeloid leukemia. A unique feature of this book is that instead of compiling up-to-date published literature, as is most commonly done for review articles, all the authors have emphasized their own work and expressed their own viewpoints. Each article is of high quality, and Fox’s writing is most entertaining. I have no doubt this volume will be of value to every biomedical science library. Because of its broad spectrum, with each article unrelated to each other except in a very general sense, this book may not have many individual collectors; the authors may instead be swamped with reprint requests. Abraham W. Hsie Biology Division Oak Ridge National Laboratory P. 0. Box Y Oak Ridge, Tennessee 37830