<abstract xmlns="http://www.w3.org/1999/xhtml">

Biological systems exhibit unique phenotypes as the result of the expression of a genomic program. The regulation of this program is a complex phenomenon, wherein different regulatory mechanisms are involved. The deregulation of this program is at the centre of the emergence of diseases such as breast cancer. In particular, it has been observed that coregulation patterns between physically distant genes are lost in breast cancer.
In this work, we present a systematic study of chromosome-wide gene coregulation patterns in breast cancer as inferred by information theoretical measures over large (whole-genome expression in several hundred transcriptomes) experimental data corpora. We analyzed the chromosomal distance decay of correlations and found it to be with fat-tail distribution in breast cancer while being fundamentally constant in nontumour samples.
After model discrimination analyses, we concluded that the behaviour of the breast cancer distributions belongs to an intermediate regime between power law and Weibull distributions, with distinctive contributions corresponding to different chromosomes. This behaviour may have biological implications in terms of the organization of the gene regulatory program, and the changes found in this program between health and disease.</abstract>

Biological systems exhibit unique phenotypes as the result of the expression of a genomic program. The regulation of this program is a complex phenomenon, wherein different regulatory mechanisms are involved. The deregulation of this program is at the centre of the emergence of diseases such as breast cancer. In particular, it has been observed that coregulation patterns between physically distant genes are lost in breast cancer.
In this work, we present a systematic study of chromosome-wide gene coregulation patterns in breast cancer as inferred by information theoretical measures over large (whole-genome expression in several hundred transcriptomes) experimental data corpora. We analyzed the chromosomal distance decay of correlations and found it to be with fat-tail distribution in breast cancer while being fundamentally constant in nontumour samples.
After model discrimination analyses, we concluded that the behaviour of the breast cancer distributions belongs to an intermediate regime between power law and Weibull distributions, with distinctive contributions corresponding to different chromosomes. This behaviour may have biological implications in terms of the organization of the gene regulatory program, and the changes found in this program between health and disease.

Intrachromosomal regulation decay in breast cancer

Applied Mathematics and Nonlinear Sciences

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

{"article-title":"Intrachromosomal regulation decay in breast cancer"}

Biological systems exhibit unique phenotypes as the result of the expression of a genomic program. The regulation of this program is a complex phenomenon,...

Intrachromosomal regulation decay in breast cancer

Article Category: Papers dedicated to the memory of Valetnin Afraymovich (1945-2018)

Publié en ligne: 28 juin 2019

Pages: 223 - 230

Reçu: 13 août 2018

Accepté: 13 nov. 2018

DOI: https://doi.org/10.2478/AMNS.2019.1.00020

Mots clés
Genomic regulation, Information theory, Cancer, Decay of correlations

© 2019 Guillermo de Anda-Jáuregui et al., published by Sciendo

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

Intrachromosomal regulation decay in breast cancer

Article Category: Papers dedicated to the memory of Valetnin Afraymovich (1945-2018)

Publié en ligne: 28 juin 2019

Pages: 223 - 230

Reçu: 13 août 2018

Accepté: 13 nov. 2018

DOI: https://doi.org/10.2478/AMNS.2019.1.00020

Mots clésGenomic regulation, Information theory, Cancer, Decay of correlations

© 2019 Guillermo de Anda-Jáuregui et al., published by Sciendo

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

Mots clés
Genomic regulation, Information theory, Cancer, Decay of correlations