Gene Function Methylation State in GBC Remarks
SHP1 Cell growth, differentiation and mitotic cycle. Hypermethylated No significant difference in methylation between CC and GBC [2]
p15 Cell cycle regulator Hypermethylated Poor survival rates[8]
3OST-2 Encodes an O-sulfotransferase Hypermethylated Altered expression in breast cancers as well[21]
CDH13 Promotes cell-cell adhesion Hypermethylated Causes cancer infiltration to serosa[8]
RUNX3 Role in TGF-beta signal pathway Hypermethylated Helicobacter pylori can accelerate its methylation status[1]
APC Negative regulator controlling beta-catenin and thus involved in adhesion and apoptosis Hypermethylated Poor survival rates[8]
p16 Cyclin dependent kinase Hypermethylated Significant prognostic factor; better survival rate without its methylation[1]
HPP1 Involved in TGF- beta signaliing pathway Methylation status not checked in normal gall bladder cells  
MGMT Methyltransferase Hypermethylated Significant correlation between survival rate and methylation status[8];favourable prognosis with alkylating agents[8]
RIZ1 Retinoblastoma protein-interacting zinc finger gene, a putative TSG Hypermethylated Associated with increasing depth of invasion and tumor-node-metastasis (TNM) [2]
CDH1 Cellular adhesion;loss leads to metastasis and invasion Hypermethylated No significant difference between methylated and non-methylated cases[1]
DLC1 GTPase activating protein Hypermethylated Poor survival rates[8];higher methylation through cancer progression[8]
Reprimo Cell cycle regulator Hypermethylated  
SEMA3B Induces apoptosis Hypermethylated  
FHIT Role in apoptosis and DNA replication Hypermethylated No correlation between survival rate and methylation status[7]
p73 Involved in apoptosis and cell cycle regulation Hypermethylated Low methylation frequency[2]
SOCS 1 Involved in JAK STAT pathway; also takes part in a negative feedback loop to attenuate cytokine signaling Hypermethylated Low methylation frequency[2]
RAR 2 Role in cell signalling Hypermethylated Higher methylation through cancer progression[8]
DAPK Serine throenine Kinase; positive mediator of gamma-interferon induced programmed cell death Hypermethylated Higher methylation through cancer progression[8]
DcR2 TNF-receptor superfamily Hypermethylated 4% methylation in CC[2]
RASSF1A Inhibits the expression of the RAS oncogene, acting as a tumor suppressor gene Hypermethylated Methylation in exon 1 of this gene was 36.4% in carcinoma samples, 25.0% in adenoma and 8.0% in normal epithelium [5,24]
UCHL1 Belongs topeptidase C12 family Hypomethylated Methylation frequency decreases from normal epithelium to adenoma to carcinoma[1]
TIMP3 Encodes inhibitors of the matrix metalloproteinases, a group of peptidases involved in degradation of the extracellular matrix Hypermethylated Higher methylation through cancer progression[8]
p14 Regulates cell cycle Hypermethylated High methylation frequency[4]
DUTT 1 Role in metastasis and migration Hypermethylated  
BLU Role in cell cycle Hypermethylated  
MLH1 Mismatch repair   GBC due to MSI[1]
GSTP1 Involved in detoxification by catalyzing the conjugation of hydrophobic
and electrophilic compounds
   
DrC 1 Key component of the nexin-dynein regulatory complex (N-DRC), essential for N-DRC integrity   Low methylation frequency[2]
HIN1 Inhibits cell growth(mainly secreted in Breast epithelium) Hypermethylated Low methylation frequency[2]
CHFR Cell cycle regulator; provides a checkpoint that delays entry into metaphase   Low methylation frequency[2]
Table 1: Methylation pattern of some of the significant genes in gallbladder cancer.
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