Aspects of Endocrine Carcinogenesis

Bielschowsky, F; Es, Horning

doi:10.1093/oxfordjournals.bmb.a069651

Cited by 32 publications

(6 citation statements)

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“…This, in turn, stimulates proliferation of TSH secretory cells in the pituitary [169][170][171][172][173]. By the same principle, partial thyroidectomy of rats and mice can cause pituitary adenomas as well [174][175][176][177][178][179]. The tumors can be transplanted [180]; initially only to those mice treated with thiouracil or other goitrogenic compounds that induce TSH and then gradually to normal mice [181], which again shows the trajectory of "initial dependence and then autonomy".…”

Section: Hormone-induced Tumors In Animals Are Inducer-dependent Untimentioning

confidence: 99%

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: Hormone-induced Tumors In Animals Are Inducer-dependent Untimentioning

confidence: 99%

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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“…The height of the epithelium is controlled by androgens and the total amount of tubular tissue increased by androgens. Oestrogens cause a cystlike degeneration in the juxtamedullary layer of the cortex in rats and induce renal tumours in the male, but not the female golden hamster (Bielschowsky & Horning, 1958). The juxtaglomerular system which is implicated in the formation of renin, erythropoietin and the control of aldosterone and electrolyte secretion, does not respond to the administration of androgens, although the tubular tissue does.…”

Section: Sexual Dimorphism In Adult Mammalsmentioning

confidence: 99%

Sexual Dimorphism in Mammals

Glücksmann

1974

Biological Reviews

132

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Summary 1. Life expectancy and mortality rates from diseases arising in various organs vary with sex because of differential exposure to external hazards and because of essential differences between males and females in aspects not directly connected with reproduction. This review attempts to collate data about the structural and functional dimorphism of mammals exclusive of the genital organs and psychological aspects. 2. The primary sex ratio is not certain and like the secondary and tertiary may vary with species. In many mammals more males are aborted and born than females. Later a higher mortality of males, due to sex‐linked congenital diseases and greater exposure to external hazards, shifts the balance in favour of females at the time of sexual maturity. The average life span of females is longer than that of males, except in hamsters and in inbred strains of mice with a high incidence of mammary tumours. 3. Chromosomes as well as gonadal hormones are responsible for the development of male and female characteristics. The Y‐chromosome initiates the differentiation of the testis, but gonadal hormones control the subsequent differentiation of the genital tract and other organs. In embryos the testicular secretion precedes that of the ovary. The Y‐chromosome is devoid of, but the X‐chromosome retains structural genes. The random heterochromatization of a paternal or a maternal X‐chromosome in the somatic cells of female embryos equalizes the genetic information for both sexes and produces a mosaicism of female somatic cells except in the kangaroo where the paternal X‐chromosome is selectively inactivated. Deficient genes on the X‐chromosome become manifest in hemizygous males, in homozygous females and can be detected in heterozygous women in half of the somatic cell population in some conditions. 4. The testis grows faster than the ovary and starts to secrete earlier, but the maturation of female gonocytes precedes that of males. Spermatogenesis starts at puberty and is maintained throughout life, while multiplication of oogonia ceases in the perinatal period (except in lemurs), when the stage of the first meiotic division is reached. The stock of oocytes dwindles during life. 5. In many mammals the male grows faster than the female before and after birth, but is less mature. Puberty tends to start earlier in females and the associated growth spurt does not last as long as in males. Testosterone has a direct anabolic effect, promotes growth and delays differentiation. Oestrogens are considered katabolic, but promote growth indirectly by stimulating the production of growth hormone in the pituitary. Progesterone has an anabolic and slight androgenic effect. 6. A female pattern of differentiation of the hypothalamus, the pituitary and the pineal gland, manifested at puberty by cyclical activities of the reproductive organs requires the absence of androgens during a critical phase of ante‐ or perinatal development. Oestrogens given to males at that period produce effects similar to castration. Antiandrogens ind...

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“…In rats and mice, for example, squamous metaplasia, adenomyosis, fibroma, papilloma and even carcinoma have been induced, the changes being partially dependent on the hormone dosage (Miller and Pybus, 1942;Bonser, StickUmd and Connal, 1937;Zondek, 1936;Bielschowsky and Horning, 1958;Lacassagne, 1936). In the dog, however, stilboestrol injections frequently produce an effect on the uterus similar to that sometimes observed spontaneously in bitches bearing ovarian foUieular eysts; the alterations appear dependent on the dosage and length of time of hormone administration.…”

Section: Discussionmentioning

confidence: 98%

“…These include changes in the testicles (Purves and Griesbach, 1957;Mulligan, 1944Mulligan, , 1945Brouwers, Derivaux, Bienfit and Joarlette, 1956); prostate gland (Mulligan, 1944(Mulligan, , 1945Mulligan and Becker, 1947;Huggins and Clark, 1940;Huggins and Sommer, 1953;Gardner, 1939Gardner, , 1944Bielschowsky and Horning, 1958); adrenal glands (Mulligan, 1944Mulligan and Beeker, 1947); vagina (Mulligan, Longwell and Morrell, 1943;Mulhgan, 1947); liver (MacBryde, Castrodale, Helwig and Bierbaum, 1942;Mulligan ct al, 1943;Castrodale, Bierbaum, Helwig and MacBryde, 1941); kidneys (Mulligan and Becker, 1947;Kunde, D'Amour, Custavson and Carlson, 1930); haemopoietic tissue (Arnold, Hamper], Holtz, Junkmann and Marx, 1937;Arnold, 1939;Crafts, 1941;Castrodale et al, 1941;MacBryde, et al, 1942;Mulligan et al, 1943;Mulligan and Beeker, 1947;Tyslowitz and Dingemanse, 1941; •S a "B -s tc .E …”

Section: Introductionmentioning

confidence: 99%

Some Tissue Changes in the Dog Following Stilboestrol Administration

Jabara

1962

Aust J Exp Biol Med

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SUMMARY.Dogs (18 female, 4 male) receiving subcutaneous depot injections of diethylstilboestrol at intervals of 4-6 weeks developed alopecia after 11 months. All areas except the head and distal parts of the legs were affected and the denuded skin became dry, scaly and excoriated. Microscopic changes were observed in all elements of the skin and the hair follicles were atrophic. The hair grew again 3-7 months after injections were stopped, and at necropsy 11-14}^ months later the skin was histologically normal.Other findings included testicular atrophy, a high incidence of inguinal hernia, and endometrial hyperplasia which progressed to a cystic stage and eventually to pyometra. When injections were stopped the cndometrium regenerated after an interval the duration of which was independent of the duration of treatment or of total dose administered, but may have been related to the time taken to deplete the residual depot.Treated dogs also showed an increase of pituitary acidophils and a reduction in basophils and chromophobes; these changes were reversed on hormone withdrawal.Generalized or focal atrophy of the pancreas occurred in four of the longer surviving dogs; this was regarded as a toxic effect of stilboestrol.INTRODUCTION.

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Aspects of Endocrine Carcinogenesis

Cited by 32 publications

References 0 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

Sexual Dimorphism in Mammals

Some Tissue Changes in the Dog Following Stilboestrol Administration

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