Table 2.

Studies reporting HERV expression in cancer.

Cancer	HERV	Study Setting	Study Main Findings	Reference
Colorectal cancer	HERV	Preclinical	DNA-demethylating agents act by inducing endogenous dsRNAs that activate an interferon response pathway. This anti-viral response reduces proliferation of colorectal cancer-initiating cells.	[26]
Ovarian cancer	HERV families	Preclinical/Clinical	DNA methyltransferase inhibitors upregulate endogenous retroviruses in tumor cells to induce a growth-inhibiting immune response.	[27]
Ovarian cancer	HERV families	Preclinical	Dual inhibition of DNA and histone methyltransferases in ovarian cancer cell lines induces synergistic anti-tumor effects by upregulation of endogenous retroviruses, and activation of the viral defense response.	[15]
Breast cancer	HERV-K	Clinincal	HERV-K env protein products are able of acting as tumor associated antigens, activating both T cell and B cell responses in breast cancer patients.	[28]
Ovarian cancer	HERV-K	Clinincal	Ovarian cancer cells in primary tumors express HERV transcripts, including HERV-K env protein. Ovarian cancer patient sera contain HERV-K immunoreactive antibodies.	[29]
Melanoma	HERV-K	Preclinical/Clinical	HERV-K env protein is expressed on melanoma but not in normal tissues.	[30]
Renal cell carcinoma	HERV families	Clinincal	Abnormal expression of ERVs is associated with ccRCC, and ERV3-2 expression is associated with response to ICB in ccRCC.	[31]
Hepatoblastoma	HERV-K (HML-2)	Clinical	HERV-K is expressed from multiple loci in hepatoblastoma. Expression is increased for several proviruses compared to normal liver controls.	[32]
Hepatocellular carcinoma	HERV-K (HML-2)	Clinical	Upregulation of HERV-K (HML-2) in HCC patients is significantly correlated to cancer progression and poor outcome.	[33]