Allografts of tumor nuclear transplantation embryos: differentiation competence.

Lust, J M; Carlson, Debra L.; Kowles, Richard; Rollins‐Smith, Louise A.; Williams, John W; McKinnell, Robert G.

doi:10.1073/pnas.88.15.6883

Cited by 14 publications

(8 citation statements)

References 26 publications

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“…More convincingly, injection of the nuclei isolated from the Lucké renal cancer cells of the frog origin into enucleated frog eggs allows the eggs to hatch out tadpoles that are normal without any trace of cancer (Fig. 4) [285,[662][663][664][665][666][667][668]. Similar conversion back to a normal state by an embryonic microenvironment has also been shown for a few other cancer cell types [448, 669-673, 673, 674].…”

Section: Actually Whether Mutation Is Needed or Not For Tumor Formatmentioning

confidence: 81%

Evidence for immortality and autonomy in animal cancer models is often not provided, which causes confusion on key issues of cancer biology

Dou¹,

Tong²,

Huang³

et al. 2020

J. Cancer

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Modern research into carcinogenesis has undergone three phases. Surgeons and pathologists started the first phase roughly 250 years ago, establishing morphological traits of tumors for pathologic diagnosis, and setting immortality and autonomy as indispensable criteria for neoplasms. A century ago, medical doctors, biologists and chemists started to enhance "experimental cancer research" by establishing many animal models of chemical-induced carcinogenesis for studies of cellular mechanisms. In this second phase, the two-hit theory and stepwise carcinogenesis of "initiation-promotion" or "initiation-promotion-progression" were established, with an illustrious finding that outgrowths induced in animals depend on the inducers, and thus are not authentically neoplastic, until late stages. The last 40 years are the third incarnation, molecular biologists have gradually dominated the carcinogenesis research fraternity and have established numerous genetically-modified animal models of carcinogenesis. However, evidence has not been provided for immortality and autonomy of the lesions from most of these models. Probably, many lesions had already been collected from animals for analyses of molecular mechanisms of "cancer" before the lesions became autonomous. We herein review the monumental work of many predecessors to reinforce that evidence for immortality and autonomy is essential for confirming a neoplastic nature. We extrapolate that immortality and autonomy are established early during sporadic human carcinogenesis, unlike the late establishment in most animal models. It is imperative to resume many forerunners' work by determining the genetic bases for initiation, promotion and progression, the genetic bases for immortality and autonomy, and which animal models are, in fact, good for identifying such genetic bases.

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Section: Actually Whether Mutation Is Needed or Not For Tumor Formatmentioning

confidence: 81%

Evidence for immortality and autonomy in animal cancer models is often not provided, which causes confusion on key issues of cancer biology

Dou¹,

Tong²,

Huang³

et al. 2020

J. Cancer

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show abstract

“…The Lucké cancer nucleus after transplantation into enucleated eggs directed, in the best cases, the formation of swimming tadpoles (King and DiBerardino, 1965; McKinnell et al, 1969). More recently, Lust et al (1991) reported that allografts from tumor nuclear transplants on normal hosts differentiated into a variety of tissues equivalent to that in the 50‐day old hosts that were about two‐thirds of the way toward metamorphosis. These studies demonstrated that the normal genes in a cancer genome responded to the “differentiation inducers” in an embryonic system and their “cancer genes” were repressed.…”

Section: Other Applications and Genetic Modificationsmentioning

confidence: 99%

Animal Cloning – the route to new genomics in agriculture and medicine

Berardino

2001

Differentiation

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“…Significant concerns arose in the 1960s as transplanted nuclei containing the genetic information from frog renal cancer cells into enucleated eggs resulted in various normal tissue without cancer [28] and that this was not due to primary "irreversible changes that prevent them from responding to the host environment" [29]. The weakness in the SMT was pointed out some 40 years ago and again more recently [30,31].…”

Section: Somatic Mutation Theory (Smt)mentioning

confidence: 99%

Prelude and premise to the special issue: disruption of homeostasis-induced signaling and crosstalk in the carcinogenesis paradigm “Epistemology of the origin of cancer”

Brücher

Jamall

2019

4open

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The vast majority of anticancer strategies are symptomatic but in order to achieve some tangible progress, we need to identify the cause(s) of the majority of cancers. There is a kind of zeitgeist that findings in genetics, namely somatic mutations, are reflexively viewed as being causative for carcinogenesis, although some 80% of all cancers are presently termed “sporadic” (i.e., with no proven cause). The observation that one inch of cancerous liver tissue can have more than 100 000 000 mutations and an identical mutation can result in different phenotypes, depending on the environment surrounding that mutation, makes it very unlikely that mutations by themselves are causative of most cancers. 4open debuts its Special Issue series with papers that provide strong evidence that carcinogenesis consists of a 6-step sequence (1) a pathogenic stimulus followed by (2) chronic inflammation from which develops (3) fibrosis with associated remodeling of the extracellular microenvironment, and from these changes a (4) precancerous niche (PCN), a product of fibrosis with remodeling by persistent inflammation develops which triggers the deployment of (5) a chronic stress escape strategy and when this fails to be resolved it results in (6) the normal cell to cancerous cell transition. This Special Issue contains separate papers discussing undervalued ubiquitous proteins, chronic inflammation, eicosanoids, microbiome and morbid obesity, PCN, cell transition, followed by altered signaling induced by Metformin, NF-κB signaling and crosstalk during carcinogenesis, and a brief synopsis. In essence, the available evidence, both in vitro and in vivo, lends credence to the proposition that the majority of cancers occur from a disruption of homeostasis-induced signaling and crosstalk in the carcinogenesis paradigm “Epistemology of the origin of cancer”.

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Allografts of tumor nuclear transplantation embryos: differentiation competence.

Abstract: The developmental potential of nuclei can be studied by nuclear transplantation.

Cited by 14 publications

References 26 publications

Evidence for immortality and autonomy in animal cancer models is often not provided, which causes confusion on key issues of cancer biology

Evidence for immortality and autonomy in animal cancer models is often not provided, which causes confusion on key issues of cancer biology

Animal Cloning – the route to new genomics in agriculture and medicine

Prelude and premise to the special issue: disruption of homeostasis-induced signaling and crosstalk in the carcinogenesis paradigm “Epistemology of the origin of cancer”

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