scholarly journals Oncogenes, tumor suppressor and differentiation genes represent the oldest human gene classes and evolve concurrently

2018 ◽  
Author(s):  
A. Makashov ◽  
S.V. Malov ◽  
A.P. Kozlov
Keyword(s):  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Human Gene ◽  
The Other ◽  
Human Lineage ◽  
Human Genes ◽  
Hereditary Tumors ◽  
Evolutionary Role ◽  
Predominant Expression

AbstractEarlier we showed that human genome contains many evolutionarily young or novel genes with tumor-specific or tumor-predominant expression. We suggested to call them TSEEN genes, i.e. Tumor Specifically Expressed, Evolutionarily New genes. In this paper we performed a study of the evolutionary ages of different classes of human genes, using homology searches in genomes of different taxa in human lineage. We discovered that different classes of human genes have different evolutionary ages and confirmed the existence of TSEEN gene classes. On the other hand, we found that oncogenes, tumor-suppressor genes and differentiation genes are among the oldest gene classes in humans and their evolution occurs concurrently. These findings confirm predictions made by our hypothesis of the possible evolutionary role of hereditary tumors.

scholarly journals Oncogenes, tumor suppressor and differentiation genes represent the oldest human gene classes and evolve concurrently

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
A. A. Makashov ◽  
S. V. Malov ◽  
A. P. Kozlov
Keyword(s):  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Human Gene ◽  
Tumor Biology ◽  
The Other ◽  
Human Genes ◽  
Hereditary Tumors ◽  
Evolutionary Role ◽  
Predominant Expression

Abstract Earlier we showed that human genome contains many evolutionarily young or novel genes with tumor-specific or tumor-predominant expression. We suggest calling such genes Tumor Specifically Expressed, Evolutionarily New (TSEEN) genes. In this paper we performed a study of the evolutionary ages of different classes of human genes, using homology searches in genomes of different taxa in human lineage. We discovered that different classes of human genes have different evolutionary ages and confirmed the existence of TSEEN gene classes. On the other hand, we found that oncogenes, tumor-suppressor genes and differentiation genes are among the oldest gene classes in humans and their evolution occurs concurrently. These findings confirm non-trivial predictions made by our hypothesis of the possible evolutionary role of hereditary tumors. The results may be important for better understanding of tumor biology. TSEEN genes may become the best tumor markers.

scholarly journals Evolutionarily novel genes are expressed in transgenic fish tumors and their orthologs are involved in development of progressive traits in humans

2019 ◽  
Vol 14 (1) ◽  
Author(s):  
E. A. Matyunina ◽  
A. V. Emelyanov ◽  
T. V. Kurbatova ◽  
A. A. Makashov ◽  
I. V. Mizgirev ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Transgenic Fish ◽  
Novel Genes ◽  
New Class ◽  
Human Genes ◽  
Human Orthologs ◽  
New Gene ◽  
Hereditary Tumors ◽  
Evolutionary Role

Abstract Earlier we suggested a new hypothesis of the possible evolutionary role of hereditary tumors (Kozlov, Evolution by tumor Neofunctionalization, 2014), and described a new class of genes – tumor specifically expressed, evolutionarily novel (TSEEN) genes - that are predicted by this hypothesis (Kozlov, Infect Agents Cancer 11:34, 2016). In this paper we studied evolutionarily novel genes expressed in fish tumors after regression, as a model of evolving organs. As evolutionarily novel genes may not yet have organismal functions, we studied the acquisition of new gene functions by comparing fish evolutionarily novel genes with their human orthologs. We found that many genes involved in development of progressive traits in humans (lung, mammary gland, placenta, ventricular septum, etc.) originated in fish and are expressed in fish tumors and tumors after regression. These findings support a possible evolutionary role of hereditary tumors, and in particular the hypothesis of evolution by tumor neofunctionalization. Research highlights Earlier we described a new class of genes that are tumor-specifically expressed and evolutionarily novel (TSEEN). As the functions of TSEEN genes are often uncertain, we decided to study TSEEN genes of fishes so that we could trace the appearance of their new functions in higher vertebrates. We found that many human genes which are involved in development of progressive traits (placenta development, mammary gland and lung development etc.,) originated in fishes and are expressed in fish tumors.

The functional role of tumor suppressor genes in gliomas: Clues for future therapeutic strategies

Neurology ◽  
1998 ◽  
Vol 51 (5) ◽  
pp. 1250-1255 ◽  
Author(s):  
J. Fueyo ◽  
C. Gomez-Manzano ◽  
W. K. Alfred Yung ◽  
A. P. Kyritsis
Keyword(s):  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Functional Role ◽  
Therapeutic Strategies ◽  
Suppressor Genes

scholarly journals BRN2 is a non-canonical melanoma tumor-suppressor

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Michael Hamm ◽  
Pierre Sohier ◽  
Valérie Petit ◽  
Jérémy H. Raymond ◽  
Véronique Delmas ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Transcription Factors ◽  
Tumor Suppressor ◽  
The Other ◽  
Pi3k Signaling ◽  
Melanoma Tumor ◽  
Temporal Regulation ◽  
Metastatic Colonization ◽  
Pou Domain

AbstractWhile the major drivers of melanoma initiation, including activation of NRAS/BRAF and loss of PTEN or CDKN2A, have been identified, the role of key transcription factors that impose altered transcriptional states in response to deregulated signaling is not well understood. The POU domain transcription factor BRN2 is a key regulator of melanoma invasion, yet its role in melanoma initiation remains unknown. Here, in a BrafV600EPtenF/+ context, we show that BRN2 haplo-insufficiency promotes melanoma initiation and metastasis. However, metastatic colonization is less efficient in the absence of Brn2. Mechanistically, BRN2 directly induces PTEN expression and in consequence represses PI3K signaling. Moreover, MITF, a BRN2 target, represses PTEN transcription. Collectively, our results suggest that on a PTEN heterozygous background somatic deletion of one BRN2 allele and temporal regulation of the other allele elicits melanoma initiation and progression.

scholarly journals The role of XPC protein deficiency in tobacco smoke-induced DNA hypermethylation of tumor suppressor genes

2013 ◽  
Vol 03 (04) ◽  
pp. 285-293 ◽  
Author(s):  
Gan Wang ◽  
Le Wang ◽  
Vanitha Bhoopalan ◽  
Yue Xi ◽  
Deepak K. Bhalla ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Tobacco Smoke ◽  
Tumor Suppressor Genes ◽  
Protein Deficiency ◽  
Dna Hypermethylation ◽  
Suppressor Genes

scholarly journals Loss of Heterozygosity at the Ink4a/ArfLocus Facilitates Abelson Virus Transformation of Pre-B Cells

2000 ◽  
Vol 74 (20) ◽  
pp. 9479-9487 ◽  
Author(s):  
Justin Mostecki ◽  
Anne Halgren ◽  
Arash Radfar ◽  
Zohar Sachs ◽  
James Ravitz ◽  
...  
Keyword(s):  
B Cells ◽  
Tumor Suppressor ◽  
Loss Of Heterozygosity ◽  
Cell Lines ◽  
Tumor Suppressor Genes ◽  
Single Copy ◽  
Transformation Process ◽  
Suppressor Genes ◽  
Abelson Virus

ABSTRACT In many tumor systems, analysis of cells for loss of heterozygosity (LOH) has helped to clarify the role of tumor suppressor genes in oncogenesis. Two important tumor suppressor genes, p53 and the Ink4a/Arf locus, play central roles in the multistep process of Abelson murine leukemia virus (Ab-MLV) transformation. p53 and the p53 regulatory protein, p19Arf, are required for the apoptotic crisis that characterizes the progression of primary transformed pre-B cells to fully malignant cell lines. To search for other tumor suppressor genes which may be involved in the Ab-MLV transformation process, we used endogenous proviral markers and simple-sequence length polymorphism analysis to screen Abelson virus-transformed pre-B cells for evidence of LOH. Our survey reinforces the role of the p53-p19 regulatory pathway in transformation; 6 of 58 cell lines tested had lost sequences on mouse chromosome 4, including theInk4a/Arf locus. Consistent with this pattern, a high frequency of primary pre-B-cell transformants derived fromInk4a/Arf +/− mice became established cell lines. In addition, half of them retained the single copy of the locus when the transformation process was complete. These data demonstrate that a single copy of the Ink4a/Arf locus is not sufficient to fully mediate the effects of these genes on transformation.

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