Reviewing cancer’s biology: an eclectic approach

Abstract Background Cancer refers to a group of some of the worldwide most diagnosed and deadliest pathophysiological conditions that conquered researchers’ attention for decades and yet begs for more questions for a full comprehension of its complex cellular and molecular pathology. Main body The d...

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Autores principales: Ibrahim Diori Karidio, Senay Hamarat Sanlier
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Lenguaje:EN
Publicado: SpringerOpen 2021
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Acceso en línea:https://doaj.org/article/ac62069bbfac42a1bd1f257bdf7e2a8d
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spelling oai:doaj.org-article:ac62069bbfac42a1bd1f257bdf7e2a8d2021-11-07T12:12:04ZReviewing cancer’s biology: an eclectic approach10.1186/s43046-021-00088-y2589-0409https://doaj.org/article/ac62069bbfac42a1bd1f257bdf7e2a8d2021-11-01T00:00:00Zhttps://doi.org/10.1186/s43046-021-00088-yhttps://doaj.org/toc/2589-0409Abstract Background Cancer refers to a group of some of the worldwide most diagnosed and deadliest pathophysiological conditions that conquered researchers’ attention for decades and yet begs for more questions for a full comprehension of its complex cellular and molecular pathology. Main body The disease conditions are commonly characterized by unrestricted cell proliferation and dysfunctional replicative senescence pathways. In fact, the cell cycle operates under the rigorous control of complex signaling pathways involving cyclins and cyclin-dependent kinases assumed to be specific to each phase of the cycle. At each of these checkpoints, the cell is checked essentially for its DNA integrity. Genetic defects observed in these molecules (i.e., cyclins, cyclin-dependent kinases) are common features of cancer cells. Nevertheless, each cancer is different concerning its molecular and cellular etiology. These could range from the genetic defects mechanisms and/or the environmental conditions favoring epigenetically harbored homeostasis driving tumorigenesis alongside with the intratumoral heterogeneity with respect to the model that the tumor follows. Conclusions This review is not meant to be an exhaustive interpretation of carcinogenesis but to summarize some basic features of the molecular etiology of cancer and the intratumoral heterogeneity models that eventually bolster anticancer drug resistance for a more efficient design of drug targeting the pitfalls of the models.Ibrahim Diori KaridioSenay Hamarat SanlierSpringerOpenarticleLonal evolution modelCancer stem cellCancer stem cell plasticityEpithelial-mesenchymal transition (EMT)Cancer epigeneticsMicrobiotaNeoplasms. Tumors. Oncology. Including cancer and carcinogensRC254-282ENJournal of the Egyptian National Cancer Institute, Vol 33, Iss 1, Pp 1-17 (2021)
institution DOAJ
collection DOAJ
language EN
topic Lonal evolution model
Cancer stem cell
Cancer stem cell plasticity
Epithelial-mesenchymal transition (EMT)
Cancer epigenetics
Microbiota
Neoplasms. Tumors. Oncology. Including cancer and carcinogens
RC254-282
spellingShingle Lonal evolution model
Cancer stem cell
Cancer stem cell plasticity
Epithelial-mesenchymal transition (EMT)
Cancer epigenetics
Microbiota
Neoplasms. Tumors. Oncology. Including cancer and carcinogens
RC254-282
Ibrahim Diori Karidio
Senay Hamarat Sanlier
Reviewing cancer’s biology: an eclectic approach
description Abstract Background Cancer refers to a group of some of the worldwide most diagnosed and deadliest pathophysiological conditions that conquered researchers’ attention for decades and yet begs for more questions for a full comprehension of its complex cellular and molecular pathology. Main body The disease conditions are commonly characterized by unrestricted cell proliferation and dysfunctional replicative senescence pathways. In fact, the cell cycle operates under the rigorous control of complex signaling pathways involving cyclins and cyclin-dependent kinases assumed to be specific to each phase of the cycle. At each of these checkpoints, the cell is checked essentially for its DNA integrity. Genetic defects observed in these molecules (i.e., cyclins, cyclin-dependent kinases) are common features of cancer cells. Nevertheless, each cancer is different concerning its molecular and cellular etiology. These could range from the genetic defects mechanisms and/or the environmental conditions favoring epigenetically harbored homeostasis driving tumorigenesis alongside with the intratumoral heterogeneity with respect to the model that the tumor follows. Conclusions This review is not meant to be an exhaustive interpretation of carcinogenesis but to summarize some basic features of the molecular etiology of cancer and the intratumoral heterogeneity models that eventually bolster anticancer drug resistance for a more efficient design of drug targeting the pitfalls of the models.
format article
author Ibrahim Diori Karidio
Senay Hamarat Sanlier
author_facet Ibrahim Diori Karidio
Senay Hamarat Sanlier
author_sort Ibrahim Diori Karidio
title Reviewing cancer’s biology: an eclectic approach
title_short Reviewing cancer’s biology: an eclectic approach
title_full Reviewing cancer’s biology: an eclectic approach
title_fullStr Reviewing cancer’s biology: an eclectic approach
title_full_unstemmed Reviewing cancer’s biology: an eclectic approach
title_sort reviewing cancer’s biology: an eclectic approach
publisher SpringerOpen
publishDate 2021
url https://doaj.org/article/ac62069bbfac42a1bd1f257bdf7e2a8d
work_keys_str_mv AT ibrahimdiorikaridio reviewingcancersbiologyaneclecticapproach
AT senayhamaratsanlier reviewingcancersbiologyaneclecticapproach
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