Simultaneous demonstration of lens regeneration from dorsal iris and tumour production from ventral iris in the same newt eye after carcinogen administration

Okamoto, Mitsumasa

doi:10.1046/j.1432-0436.1997.6150285.x

Cited by 45 publications

(34 citation statements)

References 12 publications

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“…Thus, for the present observation, that is, enhancement of lens regeneration in vitamin A treated animals, it may be true that vitamin A injection in lentectomized mice could enhanced RNA synthetic activity and hence induction of lens regeneration. This hypothesis is also supported by previous finding of Jangir et al (1995, 1997) andShekhawat et al (2001. The work of Harreno Saenz et al (1994) on lens regeneration in adult newt also supports the present observations.…”

Section: Discussionsupporting

confidence: 89%

“…Workers from the same laboratory also observed that vitamin A induced and accelerated lens regeneration in amphibian tadpoles, froglets and chick embryos, swiss albino mice, guinea pigs, rabbits and pigs (Shekhawat et al, 2001;Swami, 1992;Swami and Jangir, 1997, 2000, 1997Garg, 1993). The exact mechanism of Vitamin A action is still not well known.…”

Section: Discussionmentioning

confidence: 96%

“…Urodele amphibians are unique among vertebrates in their strong ability to regenerate lost part/ parts of body throughout their lives (Ferretti and Geraudie 1998;Wolpert et al, 1998) and in their striking resistance to tumor occurrence (Okamoto, 1987(Okamoto, , 1988(Okamoto, , 1997Brockes, 1998). After lens removals through the pupil of the newt's eye, pigmented dorsal iris epithelial cells begin to dedifferentiate, proliferate and transdifferentiate into lens cells (Wolff, 1895;Kodama and Eguchi, 1995).…”

Section: Introductionmentioning

confidence: 99%

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In vivo study of lens regeneration in Rana cyanophlyctis under influence of vitamin A and ascorbic acid

Singh¹,

Jangir²

2014

Afr. J. Biotechnol.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 99%

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In vivo study of lens regeneration in Rana cyanophlyctis under influence of vitamin A and ascorbic acid

Singh¹,

Jangir²

2014

Afr. J. Biotechnol.

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“…induced tumors, whereas the non-regenerative ventral iris is susceptible (Okamoto, 1997). These findings suggest that regenerating tissues can resist or suppress carcinogen-induced malignant transformation and/or propagation of tumor cells within them.…”

Section: Introductionmentioning

confidence: 86%

Tumor suppressors: enhancers or suppressors of regeneration?

Pomerantz

Blau

2013

Development

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SummaryTumor suppressors are so named because cancers occur in their absence, but these genes also have important functions in development, metabolism and tissue homeostasis. Here, we discuss known and potential functions of tumor suppressor genes during tissue regeneration, focusing on the evolutionarily conserved tumor suppressors pRb1, p53, Pten and Hippo. We propose that their activity is essential for tissue regeneration. This is in contrast to suggestions that tumor suppression is a trade-off for regenerative capacity. We also hypothesize that certain aspects of tumor suppressor pathways inhibit regenerative processes in mammals, and that transient targeted modification of these pathways could be fruitfully exploited to enhance processes that are important to regenerative medicine.

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“…Highly-regenerative organisms are resistant to carcinogenesis and indeed activating regenerative response (figure 1(D)) can normalize existing tumors [147][148][149][150][152][153][154][155][156], although this does not always occur [157]. The inverse relationship between regeneration and cancer susceptibility [72,158] is more compatible with the importance of morphogenetic field guidance than with cancer risk associated with the presence of highly-active, undifferentiated cells [68].…”

Section: Cancer As a Disease Of Anatomical Homeostasismentioning

confidence: 99%

Cancer as a disorder of patterning information: computational and biophysical perspectives on the cancer problem

Moore

Walker

Levin

2017

Converg. Sci. Phys. Oncol.

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TOPICAL REVIEWCancer as a disorder of patterning information: computational and biophysical perspectives on the cancer problem IntroductionCancer is well-recognized not only as an extremely pernicious medical problem, but also as a group of phenomena deeply connected to the fundamental questions of evolution, multicellularity, pattern (disregulation, and the interplay between the genome and the environment [1,2]. Two fundamental paradigms currently divide the field. One is that cancer results from disorders of genetics: cancer cells are fundamentally broken due to genomic mutation or instability, and their clonal progeny form tumors and metastases. This view is sometimes called the SMT, somatic mutation theory [3][4][5]. A competing perspective is that of cancer as a circuit disease-a disorder of the complex biophysical, transcriptional, and epigenetic dynamics that regulate cellular state and the ability of cells to cooperate in vivo [6][7][8]. Under this view (sometimes called the tissue organization field theory or TOFT, [9,10]), cancer is akin to a traffic jam [11]-the problem is not a permanent discrete alteration within a founder cell and all of its clonal descendants, but an undesirable stable attractor in the complex network of controls that normally guides anatomical homeostasis [12].The relative merits of the two models have been discussed extensively [10,[13][14][15][16][17] AbstractThe current paradigm views cancer as arising clonally from a degradation of genetic information in single cells. A complementary perspective, originating at the dawn of modern developmental biology, is that cancer is the result of a system disorder of algorithms that normally orchestrate individual cell activities toward specific anatomical structures and away from tumorigenesis. A view of cancer as a disease of geometry focuses on the pathways that allow cells to cooperate to build and maintain large-scale anatomical patterning. Cancer may result when cells stop maintaining higher-order structures and reduce the boundary of their computational selves to a single-cell level, reverting to a unicellular lifestyle in which the rest of the organism is merely part of the environment at the expense of which all living things survive. While this view has been widely discussed, little progress has been made in providing a quantitative, mechanistic framework within which this perspective's specific and unique implications for treatment strategies can be tested and biomedically exploited. Here, we highlight two recent areas of progress which may facilitate much-needed progress on the cancer problem. First, we review the roles that endogenous bioelectrical networks, operating across many tissues in vivo, play as a medium of information processing in tumor suppression, progression, and reprogramming. Second, we provide a primer to the development of computational theory and tools for quantifying the information and causal control structures in cancer and other complex biological systems. Rigorous mathematical formalisms now exist to...

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Simultaneous demonstration of lens regeneration from dorsal iris and tumour production from ventral iris in the same newt eye after carcinogen administration

Cited by 45 publications

References 12 publications

In vivo study of lens regeneration in Rana cyanophlyctis under influence of vitamin A and ascorbic acid

In vivo study of lens regeneration in Rana cyanophlyctis under influence of vitamin A and ascorbic acid

Tumor suppressors: enhancers or suppressors of regeneration?

Cancer as a disorder of patterning information: computational and biophysical perspectives on the cancer problem

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