ArticleBMC cancer2018
Tracing the path of cancer initiation: the AA protein-based model for cancer genesis.
Article in BMC cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
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Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCancer 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.
resultsThis 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.
conclusionsAdaptation 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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.