That's short for "human epidermal growth factor receptor 2."

Epidermal growth factor receptor has been shown to interact with:

The epidermal growth factor receptor system, as such, has been used as an intermediate example.

Both drugs aim to block a cancer-spurring protein called epidermal growth factor receptor.

The lack of understanding is shown in the case of drugs that block the epidermal growth factor receptor.

Cetuximab (marketed as Erbitux) targets the epidermal growth factor receptor.

Furthermore, epidermal growth factor receptor plays a crucial role in tumorigenesis, which is the production of a new tumor.

This endosomal protein regulates the cell-surface expression of epidermal growth factor receptor.

Erlotinib inhibits epidermal growth factor receptor, and works through a similar mechanism as gefitinib.

In the trial, epidermal growth factor receptor showed a rapid response to the inhibitor, as demonstrated by the improvement of the cancer symptoms.

GAPVD1 is also involved in the degradation of the epidermal growth factor receptor.

One of them was a gene called HER-2, human epidermal growth factor receptor No. 2.

The drug works by blocking activation of a molecule called epidermal growth factor receptor, which causes tumor cells to grow.

It suppresses the phosphorylation of the epidermal growth factor receptor in human colon carcinoma cells.

Paracrine activates epidermal growth factor receptor in endothelial cells of the tumor to do this.

For example, the insulin or epidermal growth factor receptors retain surface expression of oligosaccharides are present but incompletely processed.

Tykerb blocks not only Her-2 but also the epidermal growth factor receptor, another protein that spurs tumor growth.

A variety of cancers, such as breast and pancreatic caners over-express epidermal growth factor receptors.

He discovered this in studies of the epidermal growth factor receptor (EGFR).

Paracrine signalling mediates the response to epidermal growth factor receptor kinase inhibitors.

Mutations in the epidermal growth factor receptor activate signalling pathways that promote cell survival.

In each group, improvements were noted after a single week of epidermal growth factor receptor tyrosine kinase inhibitor treatment.

The expression of psoriasin is induced in skin wounds through activation of the epidermal growth factor receptor.

Also, a death occurred possibly due to epidermal growth factor receptor tyrosine kinase inhibitor treatment; however, the correlation is not exactly clear.

HER2 is named because it has a similar structure to human epidermal growth factor receptor, or HER1.