Disease relevance of GAS7

• GAS7 is a new partner gene of MLL in treatment-related acute myeloid leukemia [1].
• MLL-GAS7 transforms multipotent hematopoietic progenitors and induces mixed lineage leukemias in mice [2].
• However in the present study, the expression of GAS7 was detected in 20 of 29 childhood medulloblastoma samples regardless of the presence of i(17q) [3].
• MLL/GAS7 fusion in a pediatric case of t(11;17)(q23;p13)-positive precursor B-cell acute lymphoblastic leukemia [4].

High impact information on GAS7

• Two different MLL-GAS7 fusion transcripts were expressed [1].
• Association of endogenous Gas7 protein with microfilaments was verified by F-actin affinity chromatography; direct binding of purified His-Gas7 to actin also was demonstrated and shown to be mediated by the Gas7 C-terminal domain [5].
• 2. Seven OSs showed copy number gain or amplification of 17p between the loci bounded by GAS7 and PMI (17p11.2-17p12), and three of these tumors also showed small losses at 17p13, including the region containing TP53 [6].
• Human Gas7 isoforms homologous to mouse transcripts differentially induce neurite outgrowth [7].
• Analysis of the human Gas7 sequences using the DNA database revealed that the two forms resulted from the canonical alternative splicing of a Gas7 genomic sequence [7].

Biological context of GAS7

• GAS7, a growth arrest-specific gene at chromosome band 17p13, was the partner gene of MLL [1].
• Therefore, GAS7 is not likely to be a tumor suppressor gene in medulloblastoma development [3].
• Human GAS7 is located on chromosome 17p11.3 close to or within the putative breakpoint of isochromosome 17q (i(17q)) in medulloblastoma, indicating a potential role as a tumor suppressor gene, lost by formation of i(17q) [3].
• The molecular genetic features of MLL/GAS7 and the clinical impact of t(11;17) are discussed [4].
• Screening of an autologous tumor cell cDNA library using transferred TILs resulted in the identification of novel mutated growth arrest-specific gene 7 (GAS7) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) gene transcripts [8].

Anatomical context of GAS7

• The persistent T cells recognized both the mutated GAS7 and GAPDH [8].

Analytical, diagnostic and therapeutic context of GAS7

• Fluorescent in situ hybridization and reverse transcriptase polymerase chain reaction analyses revealed an MLL/GAS7 chimera identical to the one previously described in AML [4].
• Western blot and ELISA results showed a progressive increase in growth arrest-specific protein (Gas7) from early postmolt stage to a maximum at late postmolt stage [9].

References