Literature DB >> 31521747

The "life code": A theory that unifies the human life cycle and the origin of human tumors.

Jinsong Liu1.   

Abstract

Tumors arise from the transformation of normal stem cells or mature somatic cells. Intriguingly, two types of tumors have been observed by pathologists for centuries: well-differentiated tumors and undifferentiated tumors. Well-differentiated tumors are architecturally similar to the tissues from which they originate, whereas undifferentiated tumors exhibit high nuclear atypia and do not resemble their tissue of origin. The relationship between these two tumor types and the human life cycle has not been clear. Here I propose a unifying theory that explains the processes of transformation of both tumor types with our life cycle. Human life starts with fertilization of an egg by a sperm to form a zygote. The zygote undergoes successive rounds of cleavage division to form blastomeres within the zona pellucida, with progressive decreases in cell size, and the cleaved blastomeres then compact to form a 32-cell or a "64n" morula [n = 1 full set of chromosomes]. Thus early embryogenesis can be interpreted as a progressive increase in ploidy, and if the zona pellucida is considered a cell membrane and cleavage is interpreted as endomitosis, then the 32-cell morula can be considered a multinucleated giant cell (or 64n syncytium). The decrease in cell size is accompanied by an increase in the nuclear-to-cytoplasmic (N/C) ratio, which then selectively activates a combined set of embryonic transcription factors that dedifferentiate the parental genome to a zygotic genome. This process is associated with a morphologic transition from a morula to a blastocyst and formation of an inner cell mass that gives rise to a new embryonic life. If the subsequent differentiation proceeds to complete maturation, then a normal life results. However, if differentiation is blocked at any point along the continuum of primordial germ cell to embryonic maturation to fetal organ maturation, a well-differentiated tumor will develop. Depending on the level of developmental hierarchy at which the stem cell differentiation is blocked, the resulting tumor can range from highly malignant to benign. Undifferentiated tumors are derived from mature somatic cells through dedifferentiation via a recently described reprogramming mechanism named the giant cell life cycle or the giant cell cycle. This mechanism can initiate "somatic embryogenesis" via an increase in ploidy ranging from 4n to 64n or more, similar to that in normal embryogenesis. This dedifferentiation mechanism is initiated through an endocycle and is followed by endomitosis, which leads to the formation of mononucleated or multinucleated polyploid giant cancer cells (PGCCs), that is, cancer stem-like cells that mimic the blastomere-stage embryo. The giant cell life cycle leads to progressive increases in the N/C ratio and awakens the suppressed embryonic reprogram, resulting in mature somatic transformation into undifferentiated tumors. Thus, the increase in ploidy explains not only normal embryogenesis for well-differentiated tumors but also "somatic embryogenesis" for undifferentiated tumors. I refer to this ploidy increase as the 'life code". The concept of the "life code" may provide a simple theoretical framework to guide our immense efforts to understand cancer and fight this disease.
Copyright © 2019 The Author. Published by Elsevier Ltd.. All rights reserved.

Entities:  

Keywords:  Endoreplication; Germ cell life cycle; Giant cell life cycle; Life code; Nuclear to cytoplasmic ratio (N/C ratio)

Mesh:

Year:  2019        PMID: 31521747     DOI: 10.1016/j.semcancer.2019.09.005

Source DB:  PubMed          Journal:  Semin Cancer Biol        ISSN: 1044-579X            Impact factor:   15.707


  16 in total

Review 1.  Giants and monsters: Unexpected characters in the story of cancer recurrence.

Authors:  Shai White-Gilbertson; Christina Voelkel-Johnson
Journal:  Adv Cancer Res       Date:  2020-05-04       Impact factor: 6.242

Review 2.  The life cycle of polyploid giant cancer cells and dormancy in cancer: Opportunities for novel therapeutic interventions.

Authors:  Jinsong Liu; Na Niu; Xiaoran Li; Xudong Zhang; Anil K Sood
Journal:  Semin Cancer Biol       Date:  2021-10-17       Impact factor: 15.707

3.  Polyploid giant cancer cells, stemness and epithelial-mesenchymal plasticity elicited by human cytomegalovirus.

Authors:  Zeina Nehme; Sébastien Pasquereau; Sandy Haidar Ahmad; Alain Coaquette; Chloé Molimard; Franck Monnien; Marie-Paule Algros; Olivier Adotevi; Mona Diab Assaf; Jean-Paul Feugeas; Georges Herbein
Journal:  Oncogene       Date:  2021-03-25       Impact factor: 9.867

Review 4.  The foundational framework of tumors: Gametogenesis, p53, and cancer.

Authors:  Chunfang Liu; Asad Moten; Zhan Ma; Hui-Kuan Lin
Journal:  Semin Cancer Biol       Date:  2021-04-30       Impact factor: 17.012

Review 5.  Sphingolipids in embryonic development, cell cycle regulation, and stemness - Implications for polyploidy in tumors.

Authors:  Christina Voelkel-Johnson
Journal:  Semin Cancer Biol       Date:  2021-01-08       Impact factor: 17.012

6.  Tamoxifen is a candidate first-in-class inhibitor of acid ceramidase that reduces amitotic division in polyploid giant cancer cells-Unrecognized players in tumorigenesis.

Authors:  Shai White-Gilbertson; Ping Lu; Christian M Jones; Stephanie Chiodini; Deborah Hurley; Arabinda Das; Joe R Delaney; James S Norris; Christina Voelkel-Johnson
Journal:  Cancer Med       Date:  2020-03-05       Impact factor: 4.452

7.  Cancer recurrence and lethality are enabled by enhanced survival and reversible cell cycle arrest of polyaneuploid cells.

Authors:  K J Pienta; E U Hammarlund; J S Brown; S R Amend; R M Axelrod
Journal:  Proc Natl Acad Sci U S A       Date:  2021-02-16       Impact factor: 11.205

8.  Loss of Aurora Kinase Signaling Allows Lung Cancer Cells to Adopt Endoreplication and Form Polyploid Giant Cancer Cells That Resist Antimitotic Drugs.

Authors:  Vural Tagal; Michael G Roth
Journal:  Cancer Res       Date:  2020-11-10       Impact factor: 12.701

9.  Poly-aneuploid cancer cells promote evolvability, generating lethal cancer.

Authors:  Kenneth J Pienta; Emma U Hammarlund; Robert Axelrod; Joel S Brown; Sarah R Amend
Journal:  Evol Appl       Date:  2020-02-22       Impact factor: 5.183

10.  Improved Autophagic Flux in Escapers from Doxorubicin-Induced Senescence/Polyploidy of Breast Cancer Cells.

Authors:  Agnieszka Bojko; Karolina Staniak; Joanna Czarnecka-Herok; Piotr Sunderland; Magdalena Dudkowska; Małgorzata Alicja Śliwińska; Kristine Salmina; Ewa Sikora
Journal:  Int J Mol Sci       Date:  2020-08-24       Impact factor: 5.923

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