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Bakaric, R.

Publications and source records attributed to Bakaric, R..

2 recordsLinked to original sources

Parallelism between phylogeny and ontogeny

Haeckels biogenetic law, or the recapitulation theory remains a controversial subject to this day. Currently, the modern version of biogenetic law is the hourglass model with its phylotypic period. Importantly, the hourglass model is nothing more than a model of development, and it does not provide any evidence that ontogeny recapitulates phylogeny. However, the hourglass model and biogenetic law are not mutually exclusive, and there are several examples of recapitulation-like processes observable after the phylotypic period of ontogeny. At the level of transcriptomics, all attempts to demonstrate recapitulation failed. Using a novel approach, combining transcriptomics with phylostratigraphy, we demonstrate that recapitulation, or parallelism between phylogeny and ontogeny, exists. We show that the mean indispensability of genes decreases for phylogenetically younger genes, as well as genes expressed during later stages of ontogeny. We also define the ontotypic period of phylogeny, an analog to the phylotypic period of ontogeny. Since it starts from the beginning of phylogeny, it is reasonable to hypothesize that recapitulation starts from the phylotypic period. We conclude that parallelism, or recapitulation, is explainable by the fact that genes that emerged later in phylogeny have tendencies to be expressed during later stages of ontogeny.

evolutionary biology↗

Comparable genomic copy number aberrations differ across astrocytoma malignancy grades

Malignancy grades of astrocytomas were analyzed for copy number aberrations by aCGH. Altogether 1438 CNA were found of which losses prevailed. We searched for regions that are more likely to drive cancer pathogenesis with Bioconductor package and Genomic Identification of Significant Targets in Cancer. On our total sample significant deletions affected 14 chromosomal regions, out of which deletions at 17p13.2, 9p21.3, 13q12.11, 22q12.3 remained significant even at 0.05 q-value. When divided to malignancy groups, the regions identified as significantly deleted in high grades were: 9p21.3; 17p13.2; 10q24.2; 14q21.3; 1p36.11 and 13q12.11, while amplified were: 3q28; 12q13.3 and 21q22.3. Low grades comprised significant deletions at 3p14.3; 11p15.4; 15q15.1; 16q22.1; 20q11.22 and 22q12.3 indicating their involvement in early stages of tumorigenesis. Significantly enriched pathways brought by DAVID software were PI3K-Akt, Cytokine-cytokine receptor, NODlike receptor, Jak-STAT, RIG-II-like receptor and Toll-like receptor pathways. HPV and herpex simplex infection and inflammation pathways were also represented. Present study brings new data to astrocytoma research amplifying the wide spectrum of changes which could help us identify the regions critical for tumorigenesis.

cancer biology↗