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We are analyzing https://link.springer.com/article/10.1007/s12253-017-0287-2.

Title:
Frameshift Mutations in Repeat Sequences of ANK3, HACD4, TCP10L, TP53BP1, MFN1, LCMT2, RNMT, TRMT6, METTL8 and METTL16 Genes in Colon Cancers | Pathology & Oncology Research
Description:
Diminished ANK3 contributes to cell survival by inhibiting detachment-induced apoptosis. TP53BP1 that interacts with p53 and MFN1 that encodes a mitochondrial membrane protein are considered to have tumor suppressor gene (TSG) functions. HACD4 involving fatty acid synthesis and TCPL10 with transcription regulation functions are considered TSGs. Many genes involved in DNA methylations such as LCMT2, RNMT, TRMT6, METTL8 and METTL16 are often perturbed in cancer. The aim of our study was to find whether these genes were mutated in colorectal cancer (CRC). In a genome database, we observed that each of these genes harbored mononucleotide repeats in the coding sequences, which could be mutated in cancers with high microsatellite instability (MSI-H). For this, we studied 124 CRCs for the frameshift mutations of these genes and their intratumoral heterogeneity (ITH). ANK3, HACD4, TCP10L, TP53BP1, MFN1, LCMT2, RNMT, TRMT6, METTL8 and METTL16 harbored 11 (13.9%), 3 (3.8%), 0 (0%), 5 (6.3%), 1 (1.3%), 2 (2.5%), 4 (5.1%), 3 (3.8%), 2 (2.5%) and 2 (2.5%) of 79 CRCs with MSI-H, respectively. However, we found no such mutations in microsatellite stable (MSS) cancers in the nucleotide repeats. There were ITH of the frameshift mutations of ANK3, MFN1 and TP53BP1 in 1 (6.3%), 1 (6.3%) and 1 (6.3%) cases, respectively. Our data exhibit that cancer-related genes ANK3, HACD4, TP53BP1, MFN1, LCMT2, RNMT, TRMT6, METTL8 and METTL16 harbor mutational ITH as well as the frameshift mutations in CRC with MSI-H. Also, the results suggest that frameshift mutations of these genes might play a role in tumorigenesis through their inactivation in CRC.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {πŸ“š}

  • Education
  • Science
  • Telecommunications

Content Management System {πŸ“}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {πŸ“ˆ}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 7,642,828 visitors per month in the current month.

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How Does Link.springer.com Make Money? {πŸ’Έ}

We find it hard to spot revenue streams.

Websites don't always need to be profitable; some serve as platforms for education or personal expression. Websites can serve multiple purposes. And this might be one of them. Link.springer.com might have a hidden revenue stream, but it's not something we can detect.

Keywords {πŸ”}

article, pubmed, google, scholar, cas, cancer, cell, mutations, mettl, cancers, genes, kim, lee, frameshift, microsatellite, colon, dna, instability, access, research, ank, tpbp, mfn, choi, yoo, tumor, gene, colorectal, zhang, mol, central, privacy, cookies, content, hacd, tcpl, lcmt, rnmt, trmt, yeon, pathol, analysis, data, publish, search, suppressor, msih, heterogeneity, repair, open,

Topics {βœ’οΈ}

month download article/chapter double-strand break repair tumor suppressor gene mismatch repair deficiency sug hyung lee high-grade serous carcinoma cancer-related genes ank3 inhibiting detachment-induced apoptosis korea research foundation full article pdf colon cancers correlates related subjects article yeon mutation profiling privacy choices/manage cookies high microsatellite instability microsatellite instability high exon dna methylation tumor suppressor yun sol jo microarray analysis identifies ascitic cancer cells check access instant access colon cancers mitochondrial membrane protein multifunctional proteins involved inhibiting cell proliferation eun ji choi european economic area guiding adjuvant chemotherapy acute monocytic leukemia keap1 gene clinico-pathological parameters ethics declarations conflicts common solid cancers article log intra-tumour heterogeneity yoo nj intraindividual genomic heterogeneity conditions privacy policy ankyrin-based pathways control mitochondrial morphology accepting optional cookies transcription regulation functions article cite min sung kim microsatellite instability intratumoral genetic heterogeneity author information authors

Questions {❓}

  • Marusyk A, Almendro V, Polyak K (2012) Intra-tumour heterogeneity: a looking glass for cancer?

Schema {πŸ—ΊοΈ}

WebPage:
      mainEntity:
         headline:Frameshift Mutations in Repeat Sequences of ANK3, HACD4, TCP10L, TP53BP1, MFN1, LCMT2, RNMT, TRMT6, METTL8 and METTL16 Genes in Colon Cancers
         description:Diminished ANK3 contributes to cell survival by inhibiting detachment-induced apoptosis. TP53BP1 that interacts with p53 and MFN1 that encodes a mitochondrial membrane protein are considered to have tumor suppressor gene (TSG) functions. HACD4 involving fatty acid synthesis and TCPL10 with transcription regulation functions are considered TSGs. Many genes involved in DNA methylations such as LCMT2, RNMT, TRMT6, METTL8 and METTL16 are often perturbed in cancer. The aim of our study was to find whether these genes were mutated in colorectal cancer (CRC). In a genome database, we observed that each of these genes harbored mononucleotide repeats in the coding sequences, which could be mutated in cancers with high microsatellite instability (MSI-H). For this, we studied 124 CRCs for the frameshift mutations of these genes and their intratumoral heterogeneity (ITH). ANK3, HACD4, TCP10L, TP53BP1, MFN1, LCMT2, RNMT, TRMT6, METTL8 and METTL16 harbored 11 (13.9%), 3 (3.8%), 0 (0%), 5 (6.3%), 1 (1.3%), 2 (2.5%), 4 (5.1%), 3 (3.8%), 2 (2.5%) and 2 (2.5%) of 79 CRCs with MSI-H, respectively. However, we found no such mutations in microsatellite stable (MSS) cancers in the nucleotide repeats. There were ITH of the frameshift mutations of ANK3, MFN1 and TP53BP1 in 1 (6.3%), 1 (6.3%) and 1 (6.3%) cases, respectively. Our data exhibit that cancer-related genes ANK3, HACD4, TP53BP1, MFN1, LCMT2, RNMT, TRMT6, METTL8 and METTL16 harbor mutational ITH as well as the frameshift mutations in CRC with MSI-H. Also, the results suggest that frameshift mutations of these genes might play a role in tumorigenesis through their inactivation in CRC.
         datePublished:2017-08-12T00:00:00Z
         dateModified:2017-08-12T00:00:00Z
         pageStart:617
         pageEnd:622
         sameAs:https://doi.org/10.1007/s12253-017-0287-2
         keywords:
            Tumor suppressor gene
            Frameshift mutation
            Colon cancer
            Microsatellite instability
            Cancer Research
            Oncology
            Pathology
            Immunology
            Biomedicine
            general
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                        type:PostalAddress
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               name:Yun Sol Jo
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                     name:The Catholic University of Korea
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                        name:Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul, South Korea
                        type:PostalAddress
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               name:Eun Ji Choi
               affiliation:
                     name:The Catholic University of Korea
                     address:
                        name:Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul, South Korea
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Min Sung Kim
               affiliation:
                     name:The Catholic University of Korea
                     address:
                        name:Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul, South Korea
                        type:PostalAddress
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               type:Person
               name:Nam Jin Yoo
               affiliation:
                     name:The Catholic University of Korea
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                        name:Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul, South Korea
                        type:PostalAddress
                     type:Organization
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               name:Sug Hyung Lee
               affiliation:
                     name:The Catholic University of Korea
                     address:
                        name:Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul, South Korea
                        type:PostalAddress
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      headline:Frameshift Mutations in Repeat Sequences of ANK3, HACD4, TCP10L, TP53BP1, MFN1, LCMT2, RNMT, TRMT6, METTL8 and METTL16 Genes in Colon Cancers
      description:Diminished ANK3 contributes to cell survival by inhibiting detachment-induced apoptosis. TP53BP1 that interacts with p53 and MFN1 that encodes a mitochondrial membrane protein are considered to have tumor suppressor gene (TSG) functions. HACD4 involving fatty acid synthesis and TCPL10 with transcription regulation functions are considered TSGs. Many genes involved in DNA methylations such as LCMT2, RNMT, TRMT6, METTL8 and METTL16 are often perturbed in cancer. The aim of our study was to find whether these genes were mutated in colorectal cancer (CRC). In a genome database, we observed that each of these genes harbored mononucleotide repeats in the coding sequences, which could be mutated in cancers with high microsatellite instability (MSI-H). For this, we studied 124 CRCs for the frameshift mutations of these genes and their intratumoral heterogeneity (ITH). ANK3, HACD4, TCP10L, TP53BP1, MFN1, LCMT2, RNMT, TRMT6, METTL8 and METTL16 harbored 11 (13.9%), 3 (3.8%), 0 (0%), 5 (6.3%), 1 (1.3%), 2 (2.5%), 4 (5.1%), 3 (3.8%), 2 (2.5%) and 2 (2.5%) of 79 CRCs with MSI-H, respectively. However, we found no such mutations in microsatellite stable (MSS) cancers in the nucleotide repeats. There were ITH of the frameshift mutations of ANK3, MFN1 and TP53BP1 in 1 (6.3%), 1 (6.3%) and 1 (6.3%) cases, respectively. Our data exhibit that cancer-related genes ANK3, HACD4, TP53BP1, MFN1, LCMT2, RNMT, TRMT6, METTL8 and METTL16 harbor mutational ITH as well as the frameshift mutations in CRC with MSI-H. Also, the results suggest that frameshift mutations of these genes might play a role in tumorigenesis through their inactivation in CRC.
      datePublished:2017-08-12T00:00:00Z
      dateModified:2017-08-12T00:00:00Z
      pageStart:617
      pageEnd:622
      sameAs:https://doi.org/10.1007/s12253-017-0287-2
      keywords:
         Tumor suppressor gene
         Frameshift mutation
         Colon cancer
         Microsatellite instability
         Cancer Research
         Oncology
         Pathology
         Immunology
         Biomedicine
         general
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         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12253-017-0287-2/MediaObjects/12253_2017_287_Fig2_HTML.gif
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            name:Su Yeon Yeon
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                  address:
                     name:Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul, South Korea
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Yun Sol Jo
            affiliation:
                  name:The Catholic University of Korea
                  address:
                     name:Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul, South Korea
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Eun Ji Choi
            affiliation:
                  name:The Catholic University of Korea
                  address:
                     name:Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul, South Korea
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Min Sung Kim
            affiliation:
                  name:The Catholic University of Korea
                  address:
                     name:Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul, South Korea
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Nam Jin Yoo
            affiliation:
                  name:The Catholic University of Korea
                  address:
                     name:Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul, South Korea
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Sug Hyung Lee
            affiliation:
                  name:The Catholic University of Korea
                  address:
                     name:Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul, South Korea
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      name:Springer Netherlands
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      name:The Catholic University of Korea
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         name:Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul, South Korea
         type:PostalAddress
      name:The Catholic University of Korea
      address:
         name:Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul, South Korea
         type:PostalAddress
      name:The Catholic University of Korea
      address:
         name:Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul, South Korea
         type:PostalAddress
      name:The Catholic University of Korea
      address:
         name:Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul, South Korea
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      name:Su Yeon Yeon
      affiliation:
            name:The Catholic University of Korea
            address:
               name:Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul, South Korea
               type:PostalAddress
            type:Organization
      name:Yun Sol Jo
      affiliation:
            name:The Catholic University of Korea
            address:
               name:Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul, South Korea
               type:PostalAddress
            type:Organization
      name:Eun Ji Choi
      affiliation:
            name:The Catholic University of Korea
            address:
               name:Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul, South Korea
               type:PostalAddress
            type:Organization
      name:Min Sung Kim
      affiliation:
            name:The Catholic University of Korea
            address:
               name:Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul, South Korea
               type:PostalAddress
            type:Organization
      name:Nam Jin Yoo
      affiliation:
            name:The Catholic University of Korea
            address:
               name:Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul, South Korea
               type:PostalAddress
            type:Organization
      name:Sug Hyung Lee
      affiliation:
            name:The Catholic University of Korea
            address:
               name:Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul, South Korea
               type:PostalAddress
            type:Organization
      email:[email protected]
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      name:Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul, South Korea
      name:Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul, South Korea
      name:Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul, South Korea
      name:Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul, South Korea
      name:Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul, South Korea
      name:Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul, South Korea
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