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1.
A C Braun 《In vitro》1980,16(1):38-48
Four neoplastic diseases of plants: crown gall, which is caused by Ti plasmid DNA; Black's wound tumor disease by an RNA virus; the Kostoff genetic tumors by chromosomal imbalance; and habituation, which results from a spontaneous activation of select biosynthetic systems, have been analyzed and compared. It has been found that both the development of a capacity for autonomous growth and the nature of the heritable cellular change that underlies tumorigenesis are similar in the four instances. All develop a capacity for autonomous growth as a result of the persistent activation of select biosynthetic systems, the products of which are concerned with cell growth and division. That the persistent activation of these biosynthetic systems does not involve heritable changes of an irreversible type is indicated by the finding that a reversal of the neoplastic state occurred in three of the test systems. Since the tumor cells in these instances were found to remain totipotent the results suggest that whether the normal or tumor phenotype is expressed is determined by how the genetic information is regulated in a cell. Regulation appears to be accomplished in part through positive feedback control mechanisms. Foreign genetic information could act either in a regulatory manner to persistently activate normal biosynthetic systems or it could code for one or more essential but normally limiting substance(s) and thus replace a substance(s) that in the case of the Kostoff tumors or habituation is specified by host cell genes, or it could do both. In either case, the foreign genetic information can be regulated in much the same manner as are the host cell genes to give rise to either the normal or tumor phenotype. 相似文献
2.
Peltomäki P 《Experimental cell research》2012,318(4):299-310
Cancer is traditionally viewed as a disease of abnormal cell proliferation controlled by a series of mutations. Mutations typically affect oncogenes or tumor suppressor genes thereby conferring growth advantage. Genomic instability facilitates mutation accumulation. Recent findings demonstrate that activation of oncogenes and inactivation of tumor suppressor genes, as well as genomic instability, can be achieved by epigenetic mechanisms as well. Unlike genetic mutations, epimutations do not change the base sequence of DNA and are potentially reversible. Similar to genetic mutations, epimutations are associated with specific patterns of gene expression that are heritable through cell divisions. Knudson's hypothesis postulates that inactivation of tumor suppressor genes requires two hits, with the first hit occurring either in somatic cells (sporadic cancer) or in the germline (hereditary cancer) and the second one always being somatic. Studies on hereditary and sporadic forms of colorectal carcinoma have made it evident that, apart from genetic mutations, epimutations may serve as either hit or both. Furthermore, recent next-generation sequencing studies show that epigenetic genes, such as those encoding histone modifying enzymes and subunits for chromatin remodeling systems, are themselves frequent targets of somatic mutations in cancer and can act like tumor suppressor genes or oncogenes. This review discusses genetic vs. epigenetic origin of cancer, including cancer susceptibility, in light of recent discoveries. Situations in which mutations and epimutations occur to serve analogous purposes are highlighted. 相似文献
3.
Tatsuhiko Ikeda Qi-fu Liu David Danielpour Jefferson B. Officer Masayoshi Iio Frances E. Leland David A. Sirbasku 《In vitro cellular & developmental biology. Plant》1982,18(12):961-979
Summary The role of polypeptide growth factors (estromedins) as mediators of estrogen-responsive mammary tumor growth is studied in
this report. Three possible new mechanisms were investigated that include endocrine, autocrine, and paracrine related growth
factors. The first hypothesis being tested is whether estrogens interact with target tissues and cause the biosynthesis and
secretion of polypeptide growth factors, which then act as mitogens for normal and neoplastic mammary tissues. Data presented
suggest that this mechanism involves estrogen interaction with uterus, kidney, and pituitary gland causing production of growth
factors, which then enter the general circulation and promote growth of distant target tissues. This is an endocrine type
mechanism. Another type of estromedin control (autocrine control) may be exerted in an autostimulatory way in which the target
tissue produces the polypeptide factors for its own growth in response to estrogen stimulation. A variation of the autocrine
mechanism may be a paracrine mechanism in which some cells of an estrogen-responsive normal or neoplastic tissue produce growth
factors that act on adjacent or neighboring cells. From the data available, all three possible types of growth factors could
be functioning synergistically to yield the final result of continuous estrogen responsive tumor growth in vivo.
Presented in the symposium on Plant and Animal Physiology in Vitro at the 33rd Annual Meeting of the Tissue Culture Association,
San Diego, California, June 6–10, 1982.
This work was supported by American Cancer Society Grant BC-255; D. A. S. is the recipient of an American Cancer Society Faculty
Research Award, FRA-212. D. D. is supported by a Rosalie B. Hite predoctoral fellowship from the Rosalie B. Hite Foundation,
Houston, Texas.
This symposium was supported in part by the following organizations: Bellco Glass, Inc., California Branch of the Tissue Culture
Association, Collaborative Research, Hana Media, Hybridtech, K C Biological, Inc., and Millipore Corporation. 相似文献
4.
E. Sidebottom 《In vitro cellular & developmental biology. Plant》1980,16(1):77-86
Summary The lecture reviews some aspects of the work on the analysis of malignancy that have been, and are now being, pursued in the
Dunn School. A brief outline of the early experiments that first demonstrated that the malignancy of mouse tumor cells can
be suppressed by the fusion with normal cells is given, and then two areas of current interest in the laboratory are described.
The first is an attempt to analyze the clinically important property of tumors to metastasize and the second is the work on
the isolation and identification of an abnormal membrane glycoprotein present in tumor cells. In addition the value of cell
fusion methods as a general test of hypotheses of malignancy is emphasized.
Presented in the symposium on Gene Transfer, Differentiation and Neoplasia in Plant and Animal Cells at the 30th Annual Meeting
of the Tissue Culture Association, Seattle, Washington, June 10–14, 1979. This symposium was supported in part by Grant CA
26748 from the National Cancer Institute, DHEW, and Grant RD-67 from the American Cancer Society. 相似文献
5.
Thomas B. Shows Alan Y. Sakaguchi 《In vitro cellular & developmental biology. Plant》1980,16(1):55-76
Summary The ability to transfer mammalian genes parasexually has opened new possibilities for gene mapping and fine structure mapping
and offers great potential for contributing to several aspects of mammalian biology, including gene expression and genetic
engineering. The DNA transferred has ranged from whole genomes to single genes and smaller segments of DNA. The transfer of
whole genomes by cell fusion forms cell hybrids, which has promoted the extensive mapping of human and mouse genes. Transfer,
by cell fusion, of rearranged chromosomes has contributed significantly to determining close linkage and the assignment of
genes to specific chromosomal regions. Transfer of single chromosomes has been achieved utilizing microcells fused to recipient
cells. Metaphase chromosomes have been isolated and used to transfer single-to-multigenic DNA segments. DNA-mediated gene
transfer, simulating bacterial transformation, has achieved transfer of single-copy genes. By utilizing DNA cleaved with restriction
endonucleases, gene transfer is being employed as a bioassay for the purification of genes. Gene mapping and the fate of transferred
genes can be examined now at the molecular level using sequence-specific probes. Recently, single genes have been clones into
eucaryotic and procaryotic vectors for transfer into mammalian cells. Moreover, recombinant libraries in which entire mammalian
genomes are represented collectively are a rich new source of transferable genes. Methodology for transferring mammalian genetic
information and applications for mapping mammalian genes is presented and prospects for the future discussed.
Presented in the symposium on Gene Transfer, Differentiation and Neoplasia in Plant and Animal Cells at the 30th Annual Meeting
of the Tissue Culture Association, Seattle, Washington, June 10–14, 1979. This symposium was supported in part by Grant CA
26748 from the National Cancer Institute, DHEW, and Grant RD-67 from the American Cancer Society.
Supported by NIH grants HD 05196 and GM 20454 and by MOD grants 1-485 and 1-692. 相似文献
6.
G. Barry Pierce Lewis D. Johnson 《In vitro cellular & developmental biology. Plant》1971,7(3):140-145
Summary Cancer is discussed from a standpoint of a postembryonic differentiation. A differentiation requires the interaction of an
exogenous inductive stimulus with competent precursor cell, which then evolve a new tissue with unique, stable heritable properties
distinguishable from the progenitor. Evidence is cited pinpointing the normal stem cells of tissues as the competent target
precursor cells in carcinogenesis. The resultant phenotype differs from its progenitor and has stable and unique characteristics.
All of the characteristics associated with malignancy are expressed during some stage of development, suggesting that the
normal genome contains the information necessary for malignant expression, and that the mechanism of malignancy is probably
an alteration of control of genomic expression.
Malignant tissue, like normal tissue, maintains itself by proliferation and differentiation of its stem cells; at least, that
is what was observed in two tumors examined. In each of these tumors the differentiated progeny of the malignant stem cells
proved to be benign.
A third tumor was adapted to growth in vitro and under the conditions of the experiments could be modulated by altering the
in vitro conditions. These data suggest that direction of the naturally occurring differentiation that occurs in tumors may
be a suitable therapeutic alternative to cytotoxic chemotherapy.
Presented in the Symposium on Regulation in Tumor Cells at the 22nd Annual Meeting of the Tissue Culture Association, Lake
Placid, New York.
Supported in part by Grant E105 from the American Cancer Society and Grant AM 13112 from the United States Public Health Service.
Supported by a Traineeship from National Institutes of Health Training Grant GM 00977. 相似文献
7.
R. Tchao 《In vitro cellular & developmental biology. Plant》1980,16(5):407-414
Summary The terminal differentiation, keratinization, of a rat bladder tumor cell line, NBT II, occurred in multicellular aggregates.
After aggregation, these cells did not undergo a round of mitosis before keratinization. 5-Bromodeoxyuridine added to the
monolayer cell culture 2 days before aggregation completely prevented this differentiation; it was ineffective when added
at the time of cell aggregation. Vitamin A prevented the keratinization of NBT II cells in aggregates but did not inhibit
aggregate formation; it enhanced the number of cells engaged in DNA synthesis. This model appears to be very useful for analyzing
the mechanisms of terminal differentiation and its modulation by vitamin A in tumor cells.
This research was supported by Institutional Research Grant 731-01-E from the American Cancer Society and in part by Research
Grant CA 14137 from the National Cancer Institute to Dr. J. Leighton. 相似文献
8.
John Donahoe Inge Noyes George E. Milo Steven E. Weisbrode 《In vitro cellular & developmental biology. Plant》1982,18(5):429-434
Summary Human foreskin fibroblasts transformed by representative chemicals from five different classes of chemical carcinogens, some
requiring enzymatic activation and direct acting carcinogens, produced cell populations that exhibited anchorage-independent
growth and expression of neoplastic potential in either nude mice or chick-embryonic skin (CES). There is a high degree of
correlation between tumor incidence and invasiveness of CES. The unique feature of CES is the rapidity of expression of cellular
neoplasia and interpretation of the simulated tumor in 4 d as a simulated fibrosarcoma. This method represents a system that
can be used to evaluate human carcinogens in vitro in 6 to 10 wk.
This work was supported in part by AFSOR, F49620-80 and the National Cancer Institute, Bethesda, MD, R01-CA-25907. 相似文献
9.
Etienne Y. Lasfargues Jennie C. Lasfargues 《In vitro cellular & developmental biology. Plant》1981,17(9):805-810
Summary Out of three attempts to induce neoplasia in normal C57B1 mammary epithelial cells with the mouse mammary tumor virus (MuMTV)
only one presented signs of tumorigenicity. Immunofluorescence showed that virus synthesis took place in all three sublines
but tumorigenicity as detected by cell aggregation viability (CAV) and transplantation into syngeneic mice failed to occur
in two of them. By comparison, cells from a BALB/c spontaneous mammary tumor that do not express MuMTV were 100% tumorigenic,
whereas cells from a BALB/cfC3H tumor with a 95% virus-producing cell population had a normal CAV and were tumorigenic only
in 60% of the test animals. This lack of correlation suggested that many of the virus-producing cells were not neoplastic
and that neoplasia might occur under virus stimulation only if a restricted population of genetic cell variants existed. Accelerated
tissue culture passages of virus-free C57B1 and BALB/c normal mammary cells resulted in their spontaneous neoplasia at Passages
23 and 50 respectively; when duplicated cells cryopreserved in early passages were revived and cultivated in the same manner,
neoplasia occurred at Passages 27 and 58. The similarity of the passage numbers appears to confirm the existence of genetic
cell variants among the normal cell population.
This investigation was supported by U.S. Public Health Service Grant R01-CA-08515 from the National Cancer Institute. 相似文献
10.
Harald H. Rossi 《Radiation and environmental biophysics》1981,20(1):1-9
Summary Although extension of the time period during which a given dose of radiation is administered commonly reduces effectiveness, there are well established instances where the reverse is true. Theoretical considerations are presented which relate reduction or enhancement to the shape of the dose-effect curve. While in many instances these changes of sensitivity may be due to intracellular processes it appears that in the case of carcinogenesis by low doses of neutrons, time dependent intercellular action must be involved.This investigation was supported by Contract DE-AC02-78EV04733 from the Department of Energy and by Grant Nos. CA 12536 and CA 15307 to the Radiological Research Laboratory/Department of Radiology, and by Grant No. CA 13696 to the Cancer Center/Institute of Cancer Research, awarded by the National Cancer Institute, DHHS 相似文献