A new hot spot for mutations in the ret protooncogene causing familial medullary thyroid carcinoma and multiple endocrine neoplasia type 2A. 1998

I Berndt, and M Reuter, and B Saller, and K Frank-Raue, and P Groth, and M Grussendorf, and F Raue, and M M Ritter, and W Höppner
Institute for Hormone and Fertility Research, University of Hamburg, Germany.

One hundred and eighty-one families with multiple endocrine neoplasia type 2A (MEN-2A) or familial medullary thyroid carcinoma (FMTC) have been investigated for mutations in the ret protooncogene in Germany. In 8 families with FMTC or MEN-2A, no mutation could be detected in the cysteine-rich domain encoded in exons 10 and 11 of the ret protooncogene. DNA sequencing of additional exons (no. 13-15) revealed rare noncysteine mutations in 3 families (codons 631, 768, and 844). In contrast to these rare events, heterozygous missense mutations in exon 13, codons 790 and 791, were found in 5 families (4 with MTC only; 1 family with MTC and pheochromocytoma) and 11 patients with apparently sporadic tumors. Two different mutations in codon 790 (TTG-->TTT, TTG-->TTC; Leu790Phe) and one mutation in codon 791 (TAT-->TTT; Tyr791Phe) created a phenylalanine residue. We conclude that codons 790 and 791 of the ret protooncogene represent a new hot spot for FMTC/MEN-2A causing mutations. With the discovery of these considerably common mutations in codons 790 and 791 and the identification of some rare mutations, 100% of the German FMTC/MEN-2A families could be characterized by a mutation in the ret protooncogene.

UI MeSH Term Description Entries
D008297 Male Males
D008875 Middle Aged An adult aged 45 - 64 years. Middle Age
D009154 Mutation Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations. Mutations
D010375 Pedigree The record of descent or ancestry, particularly of a particular condition or trait, indicating individual family members, their relationships, and their status with respect to the trait or condition. Family Tree,Genealogical Tree,Genealogic Tree,Genetic Identity,Identity, Genetic,Family Trees,Genealogic Trees,Genealogical Trees,Genetic Identities,Identities, Genetic,Tree, Family,Tree, Genealogic,Tree, Genealogical,Trees, Family,Trees, Genealogic,Trees, Genealogical
D011518 Proto-Oncogene Proteins Products of proto-oncogenes. Normally they do not have oncogenic or transforming properties, but are involved in the regulation or differentiation of cell growth. They often have protein kinase activity. Cellular Proto-Oncogene Proteins,c-onc Proteins,Proto Oncogene Proteins, Cellular,Proto-Oncogene Products, Cellular,Cellular Proto Oncogene Proteins,Cellular Proto-Oncogene Products,Proto Oncogene Products, Cellular,Proto Oncogene Proteins,Proto-Oncogene Proteins, Cellular,c onc Proteins
D003062 Codon A set of three nucleotides in a protein coding sequence that specifies individual amino acids or a termination signal (CODON, TERMINATOR). Most codons are universal, but some organisms do not produce the transfer RNAs (RNA, TRANSFER) complementary to all codons. These codons are referred to as unassigned codons (CODONS, NONSENSE). Codon, Sense,Sense Codon,Codons,Codons, Sense,Sense Codons
D004273 DNA, Neoplasm DNA present in neoplastic tissue. Neoplasm DNA
D005091 Exons The parts of a transcript of a split GENE remaining after the INTRONS are removed. They are spliced together to become a MESSENGER RNA or other functional RNA. Mini-Exon,Exon,Mini Exon,Mini-Exons
D005260 Female Females
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man

Related Publications

I Berndt, and M Reuter, and B Saller, and K Frank-Raue, and P Groth, and M Grussendorf, and F Raue, and M M Ritter, and W Höppner
August 1994, The Journal of clinical endocrinology and metabolism,
I Berndt, and M Reuter, and B Saller, and K Frank-Raue, and P Groth, and M Grussendorf, and F Raue, and M M Ritter, and W Höppner
June 2005, The Journal of clinical endocrinology and metabolism,
I Berndt, and M Reuter, and B Saller, and K Frank-Raue, and P Groth, and M Grussendorf, and F Raue, and M M Ritter, and W Höppner
January 2013, Annals of Saudi medicine,
I Berndt, and M Reuter, and B Saller, and K Frank-Raue, and P Groth, and M Grussendorf, and F Raue, and M M Ritter, and W Höppner
May 2005, Surgery,
I Berndt, and M Reuter, and B Saller, and K Frank-Raue, and P Groth, and M Grussendorf, and F Raue, and M M Ritter, and W Höppner
January 2011, PloS one,
I Berndt, and M Reuter, and B Saller, and K Frank-Raue, and P Groth, and M Grussendorf, and F Raue, and M M Ritter, and W Höppner
January 1996, Human mutation,
I Berndt, and M Reuter, and B Saller, and K Frank-Raue, and P Groth, and M Grussendorf, and F Raue, and M M Ritter, and W Höppner
May 1998, Advances in anatomic pathology,
I Berndt, and M Reuter, and B Saller, and K Frank-Raue, and P Groth, and M Grussendorf, and F Raue, and M M Ritter, and W Höppner
November 1995, Nihon rinsho. Japanese journal of clinical medicine,
I Berndt, and M Reuter, and B Saller, and K Frank-Raue, and P Groth, and M Grussendorf, and F Raue, and M M Ritter, and W Höppner
April 1997, Proceedings of the National Academy of Sciences of the United States of America,
I Berndt, and M Reuter, and B Saller, and K Frank-Raue, and P Groth, and M Grussendorf, and F Raue, and M M Ritter, and W Höppner
July 2014, Cancer,
Copied contents to your clipboard!