Disease relevance of MYCL1

• Southern and Northern blot analyses of DNAs and RNAs from small cell lung carcinomas confirmed its MYCL1 homology [1].
• We propose that the neuroblastoma susceptibility gene is located distal to MYCL1 and that there is another gene which is linked to MYCL1 that may be involved in this neoplasm [2].
• Exclusion of the familial melanoma locus (MLM) from the PND/D1S47 and MYCL1 regions of chromosome arm 1p in 7 Australian pedigrees [3].
• Coexisting amplifications of the chromosome 1p32 genes (PTPRF and MYCL1) encoding protein tyrosine phosphatase LAR and L-myc in a small cell lung cancer line [4].
• While loss of heterozygosity at SRO1, between D1S2797 and MYCL1, showed no relationship with the pathological stage, it was more frequently observed in squamous cell carcinoma than adenocarcinoma (P=0.019), and associated with high telomerase activity (P=0.046), an indicator of cellular immortality [5].

High impact information on MYCL1

• No significant increase in metastasis was observed in the lung adenocarcinomas that contained one or more 6-kilobase EcoRI alleles of the LMYC gene [6].
• We identified one novel amplicon on chromosome 11q22, in addition to previously reported amplicons that include oncogenes MYCC, MYCL1 and previously identified amplification of chromosomal regions 6q21 and 3q26-27 [7].
• Seven markers between D1S2843 (1p36.12) and MYCL1 (1p34.1), and 1 each at D1S484 (1q24.1), IGF2R-3 (6q26), and TP53 (17p13.1) were used [8].
• In HCCs, LOH was detected most frequently at loci D1S2843 (1p36.1) (28.6%), D1S513 (1p34.3) (29.2%), and MYCL1 (1p34.1) (28.6%) [8].
• Losses of MYCL and RB1 alleles were more pronounced in patients having concomitant field disease because 11 of 14 informative cases showed losses compared with 3 of 8 cases without field disease [9].

Biological context of MYCL1

• Mapping and characterization of an X-linked processed gene related to MYCL1 [1].
• A DNA sequence with homology to the myc family of proto-oncogenes has been characterized and found to be a processed gene related to L-MYC (MYCL1) [1].
• Sequence analysis of MYCL2 revealed an open reading frame of 1194 bp with no intervening sequences and strong homology to the recently published DNA sequence of MYCL1 [1].
• Antisense transcripts were found spanning regions of MYCL2 corresponding to all three exons of MYCL1 [10].
• We have characterized the expression of MYCL2, an intronless X-linked gene related to MYCL1 [10].

Anatomical context of MYCL1

• In addition, using restriction fragment length polymorphisms, it was determined that in at least three of the five cell lines in which MYCL1 was deleted from a chromosome 1, the gene was translocated to another chromosome thus retaining the diploid complement [2].
• PATIENTS AND METHODS: The eight microsatellites BAT25, BAT26, D2S123, D3S1029, D5S346, D17S588, D17S261, MYCL1 were used to screen 25 tumors from seven patients with eight upper and 17 lower urinary tract carcinomas and compare them to DNA from normal tissue [11].
• Northern blot analysis of RNA samples derived from 11 non-malignant reactive lymphoid tissues and 33 NHL was used to investigate expression of MYC, MYCL and MYCN [12].

Other interactions of MYCL1

• Among our findings, we identified sets of genes whose expression correlated with MYC, MYCN or MYCL1 amplification, with surprisingly little overlap among gene sets [13].
• We found a significant difference in the numbers of gene loci hit by deletions muscle-invasive versus noninvasive tumors (P = 0.0000002), with the genes most often hit by deletions in muscle-invasive tumors being TP53, RB1, and MYCL [9].
• Ten out of 40 (25%) samples showed MSI at a minimum of one locus using five different tetranucleotide repeat primers (HPRT1, HPRTII, MYCL1, RB, REN) [14].
• Novel amplifications were identified, some encompassing oncogenes MYCL1, PDGFRA, KIT, and MYB not previously reported to show amplification in these tumors [15].
• In metastatic tumours, amplification of ERBB gene was detected in three metastatic tumours (9.4%), and all of them had allelic deletion of the LMYC gene [16].

Analytical, diagnostic and therapeutic context of MYCL1

• Reassignment of MYCL1 to human chromosome 1p34.3 by fluorescence in situ hybridization [17].
• Complementary microsatellites (BAT40, D10S197, D13S153, D18S58, MYCL1) were investigated by PCR and fragment analysis to find other instabilities which might hint to the MIN-pathway of the tumors [18].

References