Table 1.

Association of clock genes and proteins with various forms of cancers.

Cancer type (and effect)	Trigger	Circadian genes/proteins	Reference
Sporadic and familiar breast tumors	Decreased expression levels	Per1, Per2	49
Familiar breast tumors (than sporadic)	Lower expression levels	Per1	49
Survival of breast cancer cells	Methylation of promoters	Per1, Cry1	50
Proliferation of breast cancer cells	Methylation of promoters	Per	118
Higher risk of breast cancer	Polymorphisms	Clock	51
Inhibits breast cancer cell proliferation and tumor growth	Expression	Per1	89
Breast cancer cell proliferation and tumor growth	Downregulation	Per2	91
ER/PR-negative cases of breast cancer	SNPs	Clock	150
Breast cancer	Histone acetyltransferase activity	CLOCK (protein)	154
Tumor apoptosis in breast cancer	Increased expression	Per2	153
Prostate cancer risk and hormone-related breast cancer	SNPs	NPAS2	53,151
Non–Hodgkin lymphoma and acute lymphocytic leukemia	Epigenetic inactivation (via CpG hypermethylation)	Bmal1	52
Non–Hodgkin lymphoma	Genetic variations, functional polymorphism	Cry2, NPAS2	53,54
Chronic myeloid leukemia	Methylation	Per3	55
Prostate cancer	Downregulation	Per1	57
Prostate cancer	Increased expression level	Per2, Clock	120
Prostate cancer	Decreased expression levels	Bmal1	120
Glioma	Lower expression rates	Per1, Per2	60,61
Suppression of proliferation in pancreatic cancer	Expression	Per1, Per2	62,63
Proliferation of human pancreatic cancer cell line	Knockdown	Per1	119
Epithelial ovarian cancer	Low expression levels	Cry1, Bmal1	66
Endometrial cancer	CpG methylation	Per1, Per2, Cry1	67
Colorectal cancer	Increased expression level	Tim	68
Colon cancer	Downregulation	Per2	106,107
Undifferentiated colorectal tumors	Decreased expression levels	Per1	114
Chronic myeloid leukemia	Downregulation	Per1, Per2, Per3, CRY1–2, TIM	70
Intestinal epithelial neoplastic transformation	PER2 protein degradation	Per2	72