A Nexus model of cellular transition in cancer

Abstract The exact cause of cancer is one of the most immutable medical questions of the century. Cancer as an evolutionary disease must have a purpose and understanding the purpose is more important than decoding the cause. The model of cancer proposed herein, provides a link between the cellular b...

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Autores principales: Yadav,Mukesh, Chatterjee,Payal, Tolani,Simran, Kulkarni,Jaya, Mulye,Meenakshi, Chauhan,Namrata, Sakhi,Aditi, Gorey,Sakshi
Lenguaje:English
Publicado: Sociedad de Biología de Chile 2018
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Acceso en línea:http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602018000100502
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spelling oai:scielo:S0716-976020180001005022018-09-05A Nexus model of cellular transition in cancerYadav,MukeshChatterjee,PayalTolani,SimranKulkarni,JayaMulye,MeenakshiChauhan,NamrataSakhi,AditiGorey,Sakshi Cancer The Nexus model Biochemical stress Epigenetics Mutations Genetics Abstract The exact cause of cancer is one of the most immutable medical questions of the century. Cancer as an evolutionary disease must have a purpose and understanding the purpose is more important than decoding the cause. The model of cancer proposed herein, provides a link between the cellular biochemistry and cellular genetics of cancer evolution. We thus call this model as the “Nexus model” of cancer. The Nexus model is an effort to identify the most apparent route to the disease. We have tried to utilize existing cancer literature to identify the most plausible causes of cellular transition in cancer, where the primary cancer-causing agents (physical, chemical or biological) act as inducing factors to produce cellular impeders. These cellular impeders are further linked to the Nexus. The Nexus then generates codes for epigenetics and genetics in cancer development.info:eu-repo/semantics/openAccessSociedad de Biología de ChileBiological Research v.51 20182018-01-01text/htmlhttp://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602018000100502en10.1186/s40659-018-0173-8
institution Scielo Chile
collection Scielo Chile
language English
topic Cancer
The Nexus model
Biochemical stress
Epigenetics
Mutations
Genetics
spellingShingle Cancer
The Nexus model
Biochemical stress
Epigenetics
Mutations
Genetics
Yadav,Mukesh
Chatterjee,Payal
Tolani,Simran
Kulkarni,Jaya
Mulye,Meenakshi
Chauhan,Namrata
Sakhi,Aditi
Gorey,Sakshi
A Nexus model of cellular transition in cancer
description Abstract The exact cause of cancer is one of the most immutable medical questions of the century. Cancer as an evolutionary disease must have a purpose and understanding the purpose is more important than decoding the cause. The model of cancer proposed herein, provides a link between the cellular biochemistry and cellular genetics of cancer evolution. We thus call this model as the “Nexus model” of cancer. The Nexus model is an effort to identify the most apparent route to the disease. We have tried to utilize existing cancer literature to identify the most plausible causes of cellular transition in cancer, where the primary cancer-causing agents (physical, chemical or biological) act as inducing factors to produce cellular impeders. These cellular impeders are further linked to the Nexus. The Nexus then generates codes for epigenetics and genetics in cancer development.
author Yadav,Mukesh
Chatterjee,Payal
Tolani,Simran
Kulkarni,Jaya
Mulye,Meenakshi
Chauhan,Namrata
Sakhi,Aditi
Gorey,Sakshi
author_facet Yadav,Mukesh
Chatterjee,Payal
Tolani,Simran
Kulkarni,Jaya
Mulye,Meenakshi
Chauhan,Namrata
Sakhi,Aditi
Gorey,Sakshi
author_sort Yadav,Mukesh
title A Nexus model of cellular transition in cancer
title_short A Nexus model of cellular transition in cancer
title_full A Nexus model of cellular transition in cancer
title_fullStr A Nexus model of cellular transition in cancer
title_full_unstemmed A Nexus model of cellular transition in cancer
title_sort nexus model of cellular transition in cancer
publisher Sociedad de Biología de Chile
publishDate 2018
url http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602018000100502
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