JQDN

General

Human Ret Proto-Oncogene Mapped To Chromosome 10Q11.2

Di: Stella

The RET proto-oncogene, located on chromosome subband 10q11.2, encodes a receptor tyrosine kinase expressed in tissues and tumors derived from neural crest. Germline (present in every cell of the body) mutations in RET cause multiple endocrine neoplasia type 2 (MEN 2), an inherited cancer syndrome characterized by medullary thyroid carcinoma The RET (re arranged during t ransfectio141414148) gene was originally isolated as an oncogenic fusion protein in cell transformation assays (1). The RET proto-oncogene (2), on human chromosome 10q11.2, encodes a receptor tyrosine kinase (RTK) 4 (3, 4, 5) activated by members of the glial cell line-derived neurotrophic factor (GDNF) ligand family (GDNF, Oncogene 5: 1291-1296 6 Ishizaka Y, Itoh F, Tahira T, Ikeda I, Sugimura T, Tucker J, Fertitta A, Carrano AV, Nagao M (1989) Human ret proto­oncogene mapped to chromosome 10ql1.2.

A TaqI RFLP in the human ret proto-oncogene

Finally the orientation of RET on chromosome 10q11.2 made it possible to orientate three other genes rearranged with RET in papillary thyroid carcinomas, namely H4/D10S170 on 10q21, R1 alpha on 17q23 and RFG2/Ele1 on 10q11.2. Article „Human ret proto-oncogene mapped to chromosome 10q11.2.“ Detailed information of the J-GLOBAL is an information service managed by the Japan Science and Technology Agency (hereinafter referred to as „JST“). It provides free access to secondary information on researchers, articles, patents, etc., in science and technology, medicine and pharmacy. The search results

RET gene mutations (genotype and phenotype) of multiple endocrine ...

In 1989, RET was mapped to the long arm of chromosome 10 (10q11.2)5, a milestone that indicated RET in agreement with our as a candidate gene for multiple endocrine neoplasia type 2 (MEN2) syndrome (Box 1), which had

Alterations in the RET proto-oncogene have been found in various human cancers and developmental disorders, including thyroid cancer, non-small cell lung cancer, multiple endocrine neoplasia type 2 (MEN2), and Hirschsprung disease (HSCR) [3]. Mutations in the RET proto-oncogene are also associated with some familial forms of Hirschsprung’s disease. 4,5 In the case of MEN-2, the RET mutations are activating — that is, they enhance the

In 1989, RET was mapped to the long arm of chromosome 10 (10q11.2)5, a milestone that indicated RET as a candidate gene for multiple endocrine neoplasia type 2 (MEN2) syndrome orientate three other (Box 1), which had also been mapped to that chromosomal region6. Also in 1989, RET was demon-strated to encode a transmembrane receptor with tyrosine kinase (RTK) activity7.

  • Inherited cancers associated with the RET proto-oncogene
  • Molecular Mechanisms of Disease: The RET Proto-oncogene
  • Human ret proto-oncogene mapped to chromosome 10q11.2.
  • A novel polymorphism in the coding sequence of the human RET proto-oncogene

RET is a proto-oncogene located on chromosome 10q11.2. It encodes a transmembrane glycoprotein receptor tyrosine kinase which interacts with ligands from the family of glial-derived neurotrophic factors (GDNF) (Fig. 1 -1 and 1 -2). ELEI was localized to band 10q11.2, the subband where RET also maps, at a minimum distance of more than 500 kb from the proto-oncogene. The fusion event corresponding to the rearrangement reciprocal to that leading to the formation Ishizaka Y, Itoh F, Tahira T, Ikeda I, Sugimura T, Tucker J, Fertitta A, Carrano AV, Nagao M. Human ret proto-oncogene mapped to chromosome 10q11.2. Oncogene. 1989 Dec;4(12):1519–1521.

Ishizaka, Y., Itoh, F., Tahira, T., Ikeda, I., Sugimura, T., Tucker, J., Fertitta, A., Carrano, A.V. & Nagao, M. Human RET proto-oncogene mapped to chromosome 10q11.2. (1989) Oncogene, 4, 1519-1521. A new highly polymorphic CA repeat sequence was identified within intron 5 of RET (RET-INT5). Finally the orientation of RET on chromosome 10q11.2 made it possible to orientate three other genes rearranged with RET in papillary thyroid carcinomas, namely H4/D10S170 on 10q21, R1 alpha on 17q23 and RFG2/Ele1 on 10q11.2. Ishizaka Y, Itoh F, Tahira T, Ikeda I, Sugimura T, Tucker J, Fertitta A, Carrano AV, Nagao M. Human ret proto-oncogene mapped to chromosome 10q11.2. Oncogene. 1989 Dec;4(12):1519–1521.

A novel polymorphism in the coding sequence of the human RET proto-oncogene

Abstract A novel polymorphism in the coding sequence of the human RET proto-oncogene is described. The RET proto-oncogene maps to chromosome 10q11.2, and is involved in multiple endocrine neoplasia (MEN 2A, MEN 2B), familial medullary The RET proto-oncogene lies in the pericentromeric region of chromosome 10q11.2 (Ref. 1). The expression of RET is regulated by DNA-binding factors that modulate basal MTC develops in either transcription (such as SPI Medullary thyroid carcinoma is a rare malignant tumor originating in parafollicular C cells. It accounts for 5 to 8% of all thyroid cancers. MTC develops in either sporadic (75%) or hereditary form (25%). Genetic and molecular studies have demonstrated the involvement of the RET proto-oncogene in hereditary MTC and, less often, in its sporadic form. Although a strong

We recently identified transcripts of the RET proto-oncogene in human prostate cancer xenografts and prostate cancer cell lines by means of reverse Ikeda I transcription-polymerase chain reaction analyses. The purpose of this study was to investigate Ret protein expression in human prostate tissue.

Activation of REarranged during Transfection (RET) proto-oncogene is responsible for various human cancers such as papillary and medullary thyroid carcinomas and non-small cell lung carcinomas. RET activation in these tumors is caused by point mutations or gene rearrangements, resulting in constitutive activation of RET tyrosine kinase.

The RET proto-oncogene, located on chromosome subband 10q11.2, encodes a receptor tyrosine kinase expressed in tissues and tumors derived from neural crest. Germline (present in every cell of the body) mutations in RET cause multiple endocrine neoplasia In 1989, RET was mapped to the long arm of chromosome 10 (10q11.2) 5, a milestone that indicated RET as a candidate gene for multiple endocrine was mapped to the long neoplasia type 2 (MEN2) syndrome (Box 1), which had RET proto-oncogene is the cause of MEN2. (A) The proto-oncogene RET is composed of 21 exons located on chromosome 10 (10q11.2) and encodes for a transmembrane receptor tyrosine kinase. (B) The RET protein is composed of 3 functional domains,including an extracellular ligand-binding domain, a transmembrane domain, and a cytoplasmic tyrosine

While the receptor tyrosine kinase RET is involved in the fetal development of nervous, hematopoietic, gastrointestinal, and genitourinary systems, activating RET aberration is a potent oncogenic driver in many cancer types [2–7]. RET proto-oncogene can be activated aberrantly by two major mechanisms: gene fusion and point mutation. We aimed to provide an updated narrative review with respect to the RET pathogenic variants and their implications at the clinical and molecular level in the diagnosis of medullary thyroid cancer (MTC)/multiple endocrine Note Added in Proof During the publication of this paper the chromosomal localization of the ret proto-oncogene to 10q11.2 has been published by ishizaka et al. (Oncogene 4, 1519-1521, 1989). This report is in agreement with our preliminary observations (Sozzi et al., unpublished data). es a fused protein. Mol. Cell. Blot. 7, 1226-1232.

Specific mutations of the RET proto-oncogene are related to

We have recently reported the activation of a new oncogene in human papillary thyroid carcinomas. This oncogene, papillary thyroid carcinoma (PTC), is a novel rearranged version of the ret tyrosine-kinase protooncogene. Thyroid neoplasms include a

RET was originally identified as an oncogene activated by DNA rearrangement in 1985 [1–3]. The RET proto-oncogene encodes a receptor tyrosine kinase with a cadherin-related motif and a cysteine-rich domain in the extracellular domain and is located on chromosome 10q11.2. [4–7]. So far, three isoforms (short, middle and long isoforms) that are generated by alternative splicing

The RET proto-oncogene is located on the long arm of chromosome 10 (10q11.2) and encodes a 150-kD recep-tor tyrosine kinase.5 RET is relatively well conserved among species, and RET homologs have been identified in several vertebrates as well as in Drosophila mela-nogaster.6,7 RET is encoded by 21 exons, and several RET messenger RNA (mRNA O carcinoma medular de tireóide (CMT) é uma neoplasia maligna rara, ocorrendo na forma esporádica ou hereditária. Mutações germinativas no proto-oncogene RET são responsáveis pelo CMT hereditário. No entanto, a maioria dos casos de CMT ocorre em indivíduos sem história familiar, na qual a patogênese da doença ainda é pouco compreendida. Os polimorfismos do

Genetic linkage analyses have mapped the loci for MEN 2A, MEN 2B and FMTC to an interval on chromosome 10q11.2 (refs 3-5). This region encompasses the RET proto-oncogene6•7, a receptor tyrosine The rearranged during transfection (RET) proto-oncogene was identified in 1985 and, very soon thereafter, a rearrangement named RET/PTC was discovered in papillary thyroid carcinoma (PTC). Ishizaka Y, Itoh F, Tahira T, Ikeda I, Sugimura T, Tucker J, Fertitta A, Carrano AV, Nagao M. Human ret proto-oncogene mapped to chromosome 10q11.2. Oncogene. 1989 Dec;4(12):1519–1521.