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GAEC1 (gene amplified in oesophageal cancer 1) is located at 7q22.1, first identified in oesophageal cancer.1 Initial work indicated that GAEC1 can act as an oncogene.2 Our pilot study found ∼80% of colorectal cancers showing amplification of GAEC1.3 In this research, we will study GAEC1 copy number in colon cancer cell lines and colorectal tissues, and its prognostic significance.
Two human colon cancer cell lines (SW480 and SW48) and one normal colonic epithelial cell line (FHC) were obtained from American Type Culture Collection. Culturing conditions for these cell lines were as published previously.4 Tissues were collected from 283 patients (213 Australian; 70 Japanese) diagnosed with colorectal cancers. Ninety surgically removed non-cancer colorectal tissues (diverticular diseases, hyperplastic polyps and volvulus) were used as controls. H&E stained sections from each cancer were checked to select a block with sufficient cancer tissue and representative morphological features for each patient for DNA extraction.
Cancers were staged according to the Union for International Cancer Control (UICC) for TNM (tumour, node and metastasis) classification.5 Only primary adenocarcinomas were included. Actuarial survival rates of patients were calculated from the date of surgical resection of the colorectal cancers to the date of death or last follow-up. DNA extraction and PCR reactions for GAEC1 copy number were performed as in our previous studies.3 ,4 A ΔCt of <−1 was considered as gain of GAEC1 copies, Ct value >1 was considered as reduced GAEC1 copies and a Ct between these ranges was defined as normal/no change in GAEC1 …
Footnotes
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Contributors VG: preparation of manuscript and laboratory works. KY: laboratory works and clinical data for Japanese samples. SP: laboratory works. TT: laboratory works. ML: data management. C-TL: clinical management and follow-up data. JC-oT: supervision of the laboratory works. RAS: co-supervision of the project and proof reading of the manuscript. AK-YL: preparation of manuscript and overall supervision.
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Funding The project was supported by grants from Griffith Health Institute and General Research Fund from Hong Kong.
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Competing interests None.
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Ethics approval Obtained from Griffith University with GU Ref Numbers—MED/05/06/HREC and MED/19/08/HREC.
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Provenance and peer review Not commissioned; externally peer reviewed.