SelTarbase, main

NEWS
release 201306.30, june 2013

SelTarbase TOOLS (→ Services)
· MNR_ensembl v2.2: [extended] search for human (mouse) coding, untranslated, non-coding, and intronic mononucleotide repeats (based on Ensembl rel. 66_37) including stratification by subcellular localization database LOCATE's information
· Predicted targets: genes with significantly altered mutation frequencies within MNRs compared to the background
· Submit data: upload your own new data and let the regression analysis recalculated including these data
· Register for free: use SelTarbase Tools and keep informed about recent changes
· Cancer Cell Line Infos: get detail information on human (MSI) cancer cell lines.

ABOUT SelTarbase
SelTarbase is a comprehensive mononucleotide repeat (MNR) mutation database. The primary data are derived from investigations of human microsatellite high-unstable (MSI-H) tumors of different organs. SelTarbase provides newest information of a very large, growing number of genes respectively the contained mononucleotide repeats. Additionally an up to date tissue specific regression analysis helps to decide which mutation frequencies seem to be elevated or reduced and could help focus direct investigation to promising candidate genes of MSI-H tumorigenesis. Furthermore, SelTarbase allows for upload of new (anonymized) data and recalculation of a regression analysis including these new data endowing the user with new aspects of his own research results. NAR 2010 Database Issue

ABOUT SelTarbase

SelTarbase is a comprehensive mononucleotide repeat (MNR) mutation database. The primary data are derived from investigations of human microsatellite high-unstable (MSI-H) tumors of different organs.

SelTarbase provides newest information of a very large, growing number of genes respectively the contained mononucleotide repeats. Additionally an up to date tissue specific regression analysis helps to decide which mutation frequencies seem to be elevated or reduced and could help focus direct investigation to promising candidate genes of MSI-H tumorigenesis. Furthermore, SelTarbase allows for upload of new (anonymized) data and recalculation of a regression analysis including these new data endowing the user with new aspects of his own research results.

NAR 2010 Database Issue

BACKGROUND
Deficient DNA mismatch repair (MMR deficiency) results in deletions or insertions in small repetitive DNA elements consisting of one, two or more nucleotides as single units, known as microsatellites. Microsatellite instability (MSI) occurs in more than 90% of human tumors in patients suffering from hereditary non-polyposis colorectal cancer (HNPCC/ Lynch syndrome, OMIM #120435) but also arises in sporadic carcinomas of the colon, endometrium, and stomach albeit at lower frequency (up to about 15%). The mutability of microsatellites mainly depends on their length and additionally on other biochemical and biological attributes, whose impact is not finally determined. Most of all genes respectively repeat tracts without physiologic relevance will show a similar mutation rate. However, some of the manifest mutations provide a positive or negative selection impact to affected cell clones leading to increased or reduced mutation frequencies. Therefore, the observed mutation rate may vary in a wide range. We have proposed a statistical model based on sigmoid regression analysis aiming at the identification of relevant genes of MSI driven carcinogenesis by their mutation frequency in regard to the repeat tract length. Extensive literature review leads to inclusion of datasets regarding a specific mononucleotide repeat tract (MNR) in the human genome as well as the number of analyzed MSI-H tumors of a certain tissue type (e. g. colon, stomach, and endometrium) and the number of tumors showing mutations within this MNR. Mutational data from the literature are collected and stored in a MySQL database. Tissue specific regression analyses are performed with R and nls2. All steps from database query and R calculation to complete web page presentation is done by a number of perl scripts.

BACKGROUND

Deficient DNA mismatch repair (MMR deficiency) results in deletions or insertions in small repetitive DNA elements consisting of one, two or more nucleotides as single units, known as microsatellites. Microsatellite instability (MSI) occurs in more than 90% of human tumors in patients suffering from hereditary non-polyposis colorectal cancer (HNPCC/ Lynch syndrome, OMIM #120435) but also arises in sporadic carcinomas of the colon, endometrium, and stomach albeit at lower frequency (up to about 15%). The mutability of microsatellites mainly depends on their length and additionally on other biochemical and biological attributes, whose impact is not finally determined. Most of all genes respectively repeat tracts without physiologic relevance will show a similar mutation rate. However, some of the manifest mutations provide a positive or negative selection impact to affected cell clones leading to increased or reduced mutation frequencies. Therefore, the observed mutation rate may vary in a wide range.

We have proposed a statistical model based on sigmoid regression analysis aiming at the identification of relevant genes of MSI driven carcinogenesis by their mutation frequency in regard to the repeat tract length. Extensive literature review leads to inclusion of datasets regarding a specific mononucleotide repeat tract (MNR) in the human genome as well as the number of analyzed MSI-H tumors of a certain tissue type (e. g. colon, stomach, and endometrium) and the number of tumors showing mutations within this MNR.

Mutational data from the literature are collected and stored in a MySQL database. Tissue specific regression analyses are performed with R and nls2. All steps from database query and R calculation to complete web page presentation is done by a number of perl scripts.

SUMMARY STATUS

The following table summarizes the contents of the selected and the previous release.

	release last	release latest
date	201210	201306

references analyzed	803	817
references included	604	611
colon	389	394
stomach	162	165
endometrium	93	96
colonculture	104	105
Genes analyzed	708	737
Genes included	669	696
colon	562	569
stomach	210	218
endometrium	102	105
colonculture	378	396
MNRs analyzed	5168	5266
MNRs included	4336 (3673 c., 637 nc.)	4428 (3756 c., 646 nc.)
colon	2276 (1789 c., 479 nc.)	2322 (1830 c., 484 nc.)
stomach	1050 (979 c., 64 nc.)	1097 (1021 c., 69 nc.)
endometrium	848 (814 c., 34 nc.)	1110 (1076 c., 34 nc.)
colonculture	2572 (2296 c., 276 nc.)	2590 (2310 c., 280 nc.)
observations included
colon	179917	182147
stomach	43845	45355
endometrium	30552	60263
colonculture	29575	29839