Further Evidence Favoring the Concept of the Stem Cell in Ascites Tumors of Rats

Makino, Sajiro

doi:10.1111/j.1749-6632.1956.tb50894.x

Cited by 117 publications

(36 citation statements)

References 9 publications

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“…Solid tumour transplantation work, conducted throughout the 1950's, intended primarily to answer the question of whether malignancy was a virally transmitted phenomenon. Retrospectively, these studies provided further evidence that although single-cell inoculation could initiate a malignancy in a recipient animal, this was achieved on only a minority of occasions (Ishibashi, 1950; Hewitt, 1953; Makino, 1956). …”

Section: The History Of Csc Researchmentioning

confidence: 95%

Understanding the cancer stem cell

et al. 2010

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The last 15 years has seen an explosion of interest in the cancer stem cell (CSC). Although it was initially believed that only a rare population of stem cells are able to undergo self-renewing divisions and differentiate to form all populations within a malignancy, a recent work has shown that these cells may not be as rare as thought first, at least in some malignancies. Improved experimental models are beginning to uncover a less rigid structure to CSC biology, in which the concepts of functional plasticity and clonal evolution must be incorporated into the traditional models. Slowly the genetic programmes and biological processes underlying stem cell biology are being elucidated, opening the door to the development of drugs targeting the CSC. The aim of ongoing research to understand CSCs is to develop novel stem cell-directed treatments, which will reduce therapy resistance, relapse and the toxicity associated with current, non-selective agents.

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Section: The History Of Csc Researchmentioning

confidence: 95%

Understanding the cancer stem cell

et al. 2010

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“…The cancer stem cell model was proposed more than 50 years ago, and refreshed a few years ago [28,29]. The "hypothesis of cancer stem cells" proposed that tumours originated from stem cells that were located in the wrong place during embryonic development.…”

Section: Cancer Stem Cellsmentioning

confidence: 99%

Heterogeneity of breast cancer: etiology and clinical relevance

Almendro

Fuster

2011

Clin Transl Oncol

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Cancer progression is a dynamic process of clonal adaptation to changing microenvironments. From the single founder cell until the clinical detection of tumours, there are consecutive clonal expansions and a constant acquisition of genetic and epigenetic alterations, events that contribute to the generation of intra-tumor heterogeneity. In breast cancer intra-tumor heterogeneity can arise from the differentiation of stem-like cells along with the clonal selection during tumor progression, and represents a major challenge for the design of effective therapies. To infer breast cancer progression and its response to particular treatments it is important to understand the origins of the inter- and intra-tumor heterogeneity and the forces that control tumor evolution. Insights about the evolution of breast cancer heterogeneity would contribute to the design of most effective therapeutic strategies to target the tumors at single clon level. This review is intended to give a general overview about the origins of breast cancer heterogeneity and its impact in the clinical management of the disease.

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“…Indeed, numerous investigators have described karyotypic differences (22,30,37,(51)(52)(53)(54)(55), as well as the presence of different marker chromosomes in different tumor subpopulations (37, 56). Using murine mammary tumor virus (MuMTV) DNA as a probe, cellular heterogeneity in the location and copy number of a specific gene has been demonstrated in strain GR mouse mammary tumors (33,35).…”

Section: Heterogeneity Of Experimental Tumorsmentioning

confidence: 99%

“…Similar observations have been made by more recent workers (21, 137). Makino showed that two different sarcomas could control each other's growth (138), and Cheshire noted that the growth rate of single, spontaneously arising C3H mouse mammary tumors was generally faster than were the rates of the first tumors appearing on mice which had developed multiple tumors (139).…”

Section: Tumor Cell Subpopulation Interactionsmentioning

confidence: 99%

Tumor heterogeneity: biological implications and therapeutic consequences

1983

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It is now appreciated that cancers can be composed of multiple clonal s~bpopulations of cancer cells which differ among themselves in many properties, including karyotype, growth rate, ability to metastasize, immunological characteristics, production and expression of markers, and sensitivity to therapeutic modalities. Such tumor heterogeneity has been demonstrated in a wide variety of animal tumors of differing etiology, tissue and cellular origin, and species. It has been shown in autochthonous, as well as transplanted, tumors. Similar results have been reported for human cancers, although much of the evidence that heterogeneity of human cancers, also reflects, at least in part, the existence of clonal subpopulations, is still indirect. Heterogeneity is not a unique property of malignancy. Preneoplastic tumors, as well as normal tissues, are also composed of cellular subpopulations.Proposed mechanisms for the origin of tumor heterogeneity include coalescence of multiple loci of cancer clones and the generation of diverse subpopulations from a single clone. This latter process could be due to genetic errors arising from classical genetic mechanisms or to the production of cellular variants as in normal tissue differentiation. Indeed, certain tumor subpopulations have been shown to produce variants at high frequency. In some cases this frequency can be modified by environmental circumstances. Nontumor cells may also contribute to production of cancer cell variants, perhaps, in the case of infiltrating phagocytic cells, by producing mutagens or by somatic hybridization with cancer cells. Production of tumor cell variants is a dynamic process which can occur at any time.Although tumors are mixed populations of cells, knowledge of the characteristics of individual components is not sufficient to predict the behavior of the whole. Individual cancer subpopulations can interact to affect each other's growth, immunogenicity, ability to metastasize, sensitivity to drugs, and clonal stability. The existence of multiple, interactive subpopulations provides a basis for the well-known phenomenon of 'tumor progression' in which tumors undergo qualitative changes in characteristics over the course of time. Selection of subpopulations better able to survive changing environmental circumstances allows for such changes as autonomy in regard to endogenous growth regulation, more "malignant' behavior, and loss of response to therapy. Tumor subpopulation interactions may play a regulatory role in this process.Tumor heterogeneity has obvious consequences to the design of effective therapy. It provides one rationale for combination therapies and suggests that initial treatment should be early and comprehensive. The continuing emergence of new clones suggests that treatment which is unsuccessful at one point might be effective later. Assays to predict effective therapy for individual patients need to address the multiplicity of tumor subpopulations and the ability of these subpopulations to influence each other. Subpopulation interacti...

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Further Evidence Favoring the Concept of the Stem Cell in Ascites Tumors of Rats

Cited by 117 publications

References 9 publications

Understanding the cancer stem cell

Understanding the cancer stem cell

Heterogeneity of breast cancer: etiology and clinical relevance

Tumor heterogeneity: biological implications and therapeutic consequences

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