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A parthenogenetic quasi-program causes teratoma-like tumors during aging in wild-type C. elegans

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A parthenogenetic quasi-program causes teratoma-like tumors during aging in wild-type C. elegans. / Wang, Hongyuan; Zhao, Yuan; Ezcurra, Marina; Benedetto, Alexandre; Gilliat, Ann F.; Hellberg, Josephine; Ren, Ziyu; Galimov, Evgeniy R.; Athigapanich, Trin; Girstmair, Johannes; Telford, Maximilian J.; Dolphin, Colin T.; Zhang, Zhizhou; Gems, David.

In: npj Aging and Mechanisms of Disease, Vol. 4, No. 1, 6, 13.06.2018.

Research output: Contribution to Journal/MagazineJournal articlepeer-review

Harvard

Wang, H, Zhao, Y, Ezcurra, M, Benedetto, A, Gilliat, AF, Hellberg, J, Ren, Z, Galimov, ER, Athigapanich, T, Girstmair, J, Telford, MJ, Dolphin, CT, Zhang, Z & Gems, D 2018, 'A parthenogenetic quasi-program causes teratoma-like tumors during aging in wild-type C. elegans', npj Aging and Mechanisms of Disease, vol. 4, no. 1, 6. https://doi.org/10.1038/s41514-018-0025-3

APA

Wang, H., Zhao, Y., Ezcurra, M., Benedetto, A., Gilliat, A. F., Hellberg, J., Ren, Z., Galimov, E. R., Athigapanich, T., Girstmair, J., Telford, M. J., Dolphin, C. T., Zhang, Z., & Gems, D. (2018). A parthenogenetic quasi-program causes teratoma-like tumors during aging in wild-type C. elegans. npj Aging and Mechanisms of Disease, 4(1), [6]. https://doi.org/10.1038/s41514-018-0025-3

Vancouver

Wang H, Zhao Y, Ezcurra M, Benedetto A, Gilliat AF, Hellberg J et al. A parthenogenetic quasi-program causes teratoma-like tumors during aging in wild-type C. elegans. npj Aging and Mechanisms of Disease. 2018 Jun 13;4(1). 6. https://doi.org/10.1038/s41514-018-0025-3

Author

Wang, Hongyuan ; Zhao, Yuan ; Ezcurra, Marina ; Benedetto, Alexandre ; Gilliat, Ann F. ; Hellberg, Josephine ; Ren, Ziyu ; Galimov, Evgeniy R. ; Athigapanich, Trin ; Girstmair, Johannes ; Telford, Maximilian J. ; Dolphin, Colin T. ; Zhang, Zhizhou ; Gems, David. / A parthenogenetic quasi-program causes teratoma-like tumors during aging in wild-type C. elegans. In: npj Aging and Mechanisms of Disease. 2018 ; Vol. 4, No. 1.

Bibtex

@article{79c0f4f917624d0fadd8d905fc29b584,
title = "A parthenogenetic quasi-program causes teratoma-like tumors during aging in wild-type C. elegans",
abstract = "Many diseases whose frequency increases with advancing age are caused by aging (senescence), but the mechanisms of senescence remain poorly understood. According to G.C. Williams and M.V. Blagosklonny, a major etiological determinant of senescence is late-life, wild-type gene action and non-adaptive execution of biological programs (or quasi-programs). These generate a wide range of senescent pathologies causing illness and death. Here we investigate the etiology of a prominent senescent pathology in the nematode C. elegans, uterine tumors, in the light of the Williams Blagosklonny theory. Uterine tumors develop from unfertilized, immature oocytes which execute incomplete embryogenetic programs. This includes extensive endomitosis, leading to formation of chromatin masses and cellular hypertrophy. The starting point of pathogenesis is exhaustion of sperm stocks. The timing of this transition between program and quasi-program can be altered by blocking sperm production (causing earlier tumors) or supplying additional sperm by mating (delaying tumor onset). Other pathophysiological determinants are yolk consumption by tumors, and bacterial proliferation within tumors. Uterine tumors resemble mammalian ovarian teratomas (tera, Greek: monster) in that both develop from oocytes that fail to mature after meiosis I, and both are the result of quasi-programs. Moreover, older but not younger uterine tumors show expression of markers of later embryogenesis, i.e. are teratoma-like. These results show how uterine tumors in C. elegans form as the result of run-on of embryogenetic quasi-programs. They also suggest fundamental etiological equivalence between teratoma and some forms of senescent pathology, insofar as both are caused by quasi-programs.",
author = "Hongyuan Wang and Yuan Zhao and Marina Ezcurra and Alexandre Benedetto and Gilliat, {Ann F.} and Josephine Hellberg and Ziyu Ren and Galimov, {Evgeniy R.} and Trin Athigapanich and Johannes Girstmair and Telford, {Maximilian J.} and Dolphin, {Colin T.} and Zhizhou Zhang and David Gems",
year = "2018",
month = jun,
day = "13",
doi = "10.1038/s41514-018-0025-3",
language = "English",
volume = "4",
journal = "npj Aging and Mechanisms of Disease",
issn = "2056-3973",
publisher = "Nature Publishing Group",
number = "1",

}

RIS

TY - JOUR

T1 - A parthenogenetic quasi-program causes teratoma-like tumors during aging in wild-type C. elegans

AU - Wang, Hongyuan

AU - Zhao, Yuan

AU - Ezcurra, Marina

AU - Benedetto, Alexandre

AU - Gilliat, Ann F.

AU - Hellberg, Josephine

AU - Ren, Ziyu

AU - Galimov, Evgeniy R.

AU - Athigapanich, Trin

AU - Girstmair, Johannes

AU - Telford, Maximilian J.

AU - Dolphin, Colin T.

AU - Zhang, Zhizhou

AU - Gems, David

PY - 2018/6/13

Y1 - 2018/6/13

N2 - Many diseases whose frequency increases with advancing age are caused by aging (senescence), but the mechanisms of senescence remain poorly understood. According to G.C. Williams and M.V. Blagosklonny, a major etiological determinant of senescence is late-life, wild-type gene action and non-adaptive execution of biological programs (or quasi-programs). These generate a wide range of senescent pathologies causing illness and death. Here we investigate the etiology of a prominent senescent pathology in the nematode C. elegans, uterine tumors, in the light of the Williams Blagosklonny theory. Uterine tumors develop from unfertilized, immature oocytes which execute incomplete embryogenetic programs. This includes extensive endomitosis, leading to formation of chromatin masses and cellular hypertrophy. The starting point of pathogenesis is exhaustion of sperm stocks. The timing of this transition between program and quasi-program can be altered by blocking sperm production (causing earlier tumors) or supplying additional sperm by mating (delaying tumor onset). Other pathophysiological determinants are yolk consumption by tumors, and bacterial proliferation within tumors. Uterine tumors resemble mammalian ovarian teratomas (tera, Greek: monster) in that both develop from oocytes that fail to mature after meiosis I, and both are the result of quasi-programs. Moreover, older but not younger uterine tumors show expression of markers of later embryogenesis, i.e. are teratoma-like. These results show how uterine tumors in C. elegans form as the result of run-on of embryogenetic quasi-programs. They also suggest fundamental etiological equivalence between teratoma and some forms of senescent pathology, insofar as both are caused by quasi-programs.

AB - Many diseases whose frequency increases with advancing age are caused by aging (senescence), but the mechanisms of senescence remain poorly understood. According to G.C. Williams and M.V. Blagosklonny, a major etiological determinant of senescence is late-life, wild-type gene action and non-adaptive execution of biological programs (or quasi-programs). These generate a wide range of senescent pathologies causing illness and death. Here we investigate the etiology of a prominent senescent pathology in the nematode C. elegans, uterine tumors, in the light of the Williams Blagosklonny theory. Uterine tumors develop from unfertilized, immature oocytes which execute incomplete embryogenetic programs. This includes extensive endomitosis, leading to formation of chromatin masses and cellular hypertrophy. The starting point of pathogenesis is exhaustion of sperm stocks. The timing of this transition between program and quasi-program can be altered by blocking sperm production (causing earlier tumors) or supplying additional sperm by mating (delaying tumor onset). Other pathophysiological determinants are yolk consumption by tumors, and bacterial proliferation within tumors. Uterine tumors resemble mammalian ovarian teratomas (tera, Greek: monster) in that both develop from oocytes that fail to mature after meiosis I, and both are the result of quasi-programs. Moreover, older but not younger uterine tumors show expression of markers of later embryogenesis, i.e. are teratoma-like. These results show how uterine tumors in C. elegans form as the result of run-on of embryogenetic quasi-programs. They also suggest fundamental etiological equivalence between teratoma and some forms of senescent pathology, insofar as both are caused by quasi-programs.

U2 - 10.1038/s41514-018-0025-3

DO - 10.1038/s41514-018-0025-3

M3 - Journal article

VL - 4

JO - npj Aging and Mechanisms of Disease

JF - npj Aging and Mechanisms of Disease

SN - 2056-3973

IS - 1

M1 - 6

ER -