Evolution-adjusted Tumor Pathophysiology:: The Novel Language of Tumor Biology

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Tumour heterogeneity

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Evolution as fact and theory Social effects Creation—evolution controversy Objections to evolution Level of support. Adipose tissue in human infants [28] Arthritis and other chronic inflammatory diseases [29] [30] [31] Ageing [6] [32] Alzheimer disease [33] Childhood [34] Menarche [35] Menopause [36] Menstruation [37] [38] [39] Morning sickness [40] [41]. Evolutionary psychology and Evolutionary approaches to depression.

This section duplicates the scope of other sections , specifically, Evolutionary psychology Abnormal psychology.

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Radiology Interventional radiology Nuclear medicine Pathology Anatomical pathology Clinical pathology Clinical chemistry Clinical immunology Cytopathology Medical microbiology Transfusion medicine. Psychological development Morality Religion Depression Educational psychology Evolutionary aesthetics Music Darwinian literary studies Evolution of emotion. Joseph Carroll Denis Dutton. Simon Baron-Cohen Justin L. Barrett Jay Belsky David F. Kirby Robert Kurzban Michael T. This active phosphorylation may serve as a biomarker in clear-cell carcinoma.

Mechanochemical heterogeneity is a hallmark of living eukaryotic cells. It has an impact on epigenetic gene regulation. The heterogeneous dynamic mechanochemical processes regulate interrelationships within the group of cellular surfaces through adhesion.

Heterogeneity between tumour cells can be further increased due to heterogeneity in the tumour microenvironment. Regional differences in the tumour e. The influence of microenvironment on clonal dominance is also a likely reason for the heterogeneity between primary and metastatic tumours seen in many patients, as well as the inter-tumour heterogeneity observed between patients with the same tumour type. Heterogeneic tumours may exhibit different sensitivities to cytotoxic drugs among different clonal populations.

This is attributed to clonal interactions that may inhibit or alter therapeutic efficacy, posing a challenge for successful therapies in heterogeneic tumours and their heterogeneic metastases.

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Drug administration in heterogeneic tumours will seldom kill all tumour cells. The initial heterogeneic tumour population may bottleneck , such that few drug resistant cells if any will survive. This allows resistant tumour populations to replicate and grow a new tumour through the branching evolution mechanism see above. The resulting repopulated tumour is heterogeneic and resistant to the initial drug therapy used.

The repopulated tumour may also return in a more aggressive manner. The administration of cytotoxic drugs often results in initial tumour shrinkage. This represents the destruction of initial non-resistant subclonal populations within a heterogeneic tumour, leaving only resistant clones. These resistant clones now contain a selective advantage and can replicate to repopulate the tumour. Replication will likely occur through branching evolution, contributing to tumour heterogeneity. The repopulated tumour may appear to be more aggressive. This is attributed to the drug-resistant selective advantage of the tumour cells.

Due to the genetic differences within and between tumours, biomarkers that may predict treatment response or prognosis may not be widely applicable.

Tumour heterogeneity - Wikipedia

However, it has been suggested that the level of heterogeneity can itself be used as a biomarker since more heterogeneous tumours may be more likely to contain treatment-resistant subclones. Current model systems typically lack the heterogeneity seen in human cancers. One such model, the patient derived tumour xenograft , has shown excellent utility in preserving tumour heterogeneity whilst allowing detailed study of the drivers of clonal fitness. While the problem of identifying, characterizing, and treating tumour heterogeneity is still under active research, some effective strategies have been proposed, including both experimental and computational solutions.

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