Disease relevance of CABLES1

• Breast and pancreatic cancers show strong Cables expression; however, loss of Cables expression was found in approximately 50-60% of primary colon and head and neck cancer specimens [1].
• This study was undertaken to analyze transcripts of Cables gene in endometrial and colon cancers [2].
• Loss of Cables expression was found in many human cancers, especially colon and endometrial cancer [2].
• Furthermore, nuclear immunostaining for Cables is lost in a high percentage of cases of human endometrial hyperplasia and adenocarcinoma, which are likely the product of unopposed estrogen [3].
• We hypothesize that loss of Cables expression is associated with ovarian cancer [4].

High impact information on CABLES1

• Expression of antisense Cables in primary cortical neurons inhibited neurite outgrowth [5].
• Active c-Abl kinase leads to Cdk5 tyrosine phosphorylation, and this phosphorylation is enhanced by Cables [5].
• Ectopic expression of Cables in human endometrial cells dramatically slows cell proliferation [3].
• The loss of Cables immunostaining in the human endometrial cancer samples correlates with a marked decrease in Cables mRNA [3].
• In vitro and in vivo studies demonstrate that levels of Cables mRNA in benign human endometrial epithelium are up-regulated by progesterone and down-regulated by estrogen [3].

Biological context of CABLES1

• Lack of Cables expression was associated with loss of heterozygosity on chromosome 18q11 [1].
• Conversely, loss of Cables may cause uncontrolled cell growth and enhance tumor formation [1].
• The relationship between tumor histology type and Cables expression appears to be statistically significant (P = 0.028) [6].
• A previous study found Cables is located on human chromosome 18q11-12 [7].
• Similarly, Cables(-/-) MEFs show a delayed onset of senescence and extension of lifespan, while the Cables(+/+) MEFs ceased proliferating after eight cumulative population doublings [8].

Anatomical context of CABLES1

• Expression of Cables in HeLa cells inhibited cell growth and colony formation [1].
• We found that Cables was strongly expressed in normal human epithelial cells including squamous and glandular mucosa [1].
• Overexpression of Cables in Hela and other cell lines inhibits cell proliferation and tumor formation [4].
• Hyperplastic endometrium and low and high grade endometrioid adenocarcinoma showed loss of Cables expression when compared to benign control secretory endometrium [9].
• Cultured cell lines that overexpress Cables show a reduction in cell proliferation and Cables(-/-) mice are viable with normal embryonic development [8].

Associations of CABLES1 with chemical compounds

• Cables-/- mice (n = 25) and the Cables+/+ littermates (n = 25) were treated with subcutaneous DMH injections over 20 weeks to initiate tumorigenesis [7].

Analytical, diagnostic and therapeutic context of CABLES1

• In proliferating cells, Cables was predominantly localized in the nucleus by cell fractionation and immunostaining [1].
• The analysis of RT-PCR products of the Cables gene revealed shortened products in each sample along with the product of the expected size [2].
• Sequence analysis indicated that these shortened products represented eight intragenic deletions in Cables mRNA transcripts [2].
• Rigid endoscopes. Part III. Cables, loops, sheaths, forceps, and scissors [10].

References