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Tracing the path of cancer initiation: the AA protein-based model for cancer genesis
BACKGROUND: Cancer is a defiant disease which cure is still far from being attained besides the colossal efforts and financial means deployed towards that end. The continuing setbacks encountered with today’s arsenal of anti-cancer drugs and cancer therapy modalities; show the need for a radical app...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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BioMed Central
2018
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6098654/ https://www.ncbi.nlm.nih.gov/pubmed/30119662 http://dx.doi.org/10.1186/s12885-018-4739-1 |
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author | Adjiri, Adouda |
author_facet | Adjiri, Adouda |
author_sort | Adjiri, Adouda |
collection | PubMed |
description | BACKGROUND: Cancer is a defiant disease which cure is still far from being attained besides the colossal efforts and financial means deployed towards that end. The continuing setbacks encountered with today’s arsenal of anti-cancer drugs and cancer therapy modalities; show the need for a radical approach in order to get to the root of the problem. And getting to the root of cancer initiation and development leads us to challenge the present dogmas surrounding the pathogenesis of this disease. RESULTS: This comprehensive analysis brings to light the following points: (i) Cancer with its plethora of genetic and cellular symptoms could originate from one major event switching a cell from normalcy-to-malignancy; (ii) The switching event is postulated to involve a pathological breakup of a non-mutated protein, called here AA protein, resulting in the acquisition of new cellular functions present only in cancer cells; (iii) Following this event, DNA mutations begin to accumulate as secondary events to ensure perpetuity of cancer. Supporting arguments for this protein-based model come mainly from these observations: (i) The AA protein-based model reconciles together the clonal-and-stem cell theories into one inclusive model; (ii) The breakup of a normal protein could be behind the cancer-linked inflammation symptom; (iii) Cancer hallmarks are but adaptive traits, earned as a result of the switch from normalcy-to-malignancy. CONCLUSIONS: Adaptation of cancer cells to their microenvironment and to different anti-cancer drugs is deemed here as the ultimate cancer hallmark, that needs to be understood and controlled. This adaptive power of cancer cells parallels that of bacteria also known with their resistance to a large range of substances in nature and in the laboratory. Consequently, cancer development could be viewed as a backward walk on the line of Evolution. Finally this unprecedented analysis demystifies cancer and puts the finger on the core problem of malignancy while offering ideas for its control with the ultimate goal of leading to its cure. |
format | Online Article Text |
id | pubmed-6098654 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-60986542018-08-23 Tracing the path of cancer initiation: the AA protein-based model for cancer genesis Adjiri, Adouda BMC Cancer Debate BACKGROUND: Cancer is a defiant disease which cure is still far from being attained besides the colossal efforts and financial means deployed towards that end. The continuing setbacks encountered with today’s arsenal of anti-cancer drugs and cancer therapy modalities; show the need for a radical approach in order to get to the root of the problem. And getting to the root of cancer initiation and development leads us to challenge the present dogmas surrounding the pathogenesis of this disease. RESULTS: This comprehensive analysis brings to light the following points: (i) Cancer with its plethora of genetic and cellular symptoms could originate from one major event switching a cell from normalcy-to-malignancy; (ii) The switching event is postulated to involve a pathological breakup of a non-mutated protein, called here AA protein, resulting in the acquisition of new cellular functions present only in cancer cells; (iii) Following this event, DNA mutations begin to accumulate as secondary events to ensure perpetuity of cancer. Supporting arguments for this protein-based model come mainly from these observations: (i) The AA protein-based model reconciles together the clonal-and-stem cell theories into one inclusive model; (ii) The breakup of a normal protein could be behind the cancer-linked inflammation symptom; (iii) Cancer hallmarks are but adaptive traits, earned as a result of the switch from normalcy-to-malignancy. CONCLUSIONS: Adaptation of cancer cells to their microenvironment and to different anti-cancer drugs is deemed here as the ultimate cancer hallmark, that needs to be understood and controlled. This adaptive power of cancer cells parallels that of bacteria also known with their resistance to a large range of substances in nature and in the laboratory. Consequently, cancer development could be viewed as a backward walk on the line of Evolution. Finally this unprecedented analysis demystifies cancer and puts the finger on the core problem of malignancy while offering ideas for its control with the ultimate goal of leading to its cure. BioMed Central 2018-08-17 /pmc/articles/PMC6098654/ /pubmed/30119662 http://dx.doi.org/10.1186/s12885-018-4739-1 Text en © The Author(s). 2018 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Debate Adjiri, Adouda Tracing the path of cancer initiation: the AA protein-based model for cancer genesis |
title | Tracing the path of cancer initiation: the AA protein-based model for cancer genesis |
title_full | Tracing the path of cancer initiation: the AA protein-based model for cancer genesis |
title_fullStr | Tracing the path of cancer initiation: the AA protein-based model for cancer genesis |
title_full_unstemmed | Tracing the path of cancer initiation: the AA protein-based model for cancer genesis |
title_short | Tracing the path of cancer initiation: the AA protein-based model for cancer genesis |
title_sort | tracing the path of cancer initiation: the aa protein-based model for cancer genesis |
topic | Debate |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6098654/ https://www.ncbi.nlm.nih.gov/pubmed/30119662 http://dx.doi.org/10.1186/s12885-018-4739-1 |
work_keys_str_mv | AT adjiriadouda tracingthepathofcancerinitiationtheaaproteinbasedmodelforcancergenesis |