Cyclin B1-Cdk1 is involved in the early events of mitosis, such as chromosome condensation, nuclear envelope breakdown, and spindle pole assembly.

Phosphorylation of the lamins by cyclin B1-Cdk1 causes them to dissociate,[8] compromising the structural integrity of the nuclear envelope so that it breaks down.

Just prior to mitosis, a large amount of cyclin B1 is present in the cell, but it is inactive due to phosphorylation of Cdk1 by the Wee1 kinase.

Binding of Cdks can lead to phosphorylation of other substrates at inappropriate time and unregulated proliferation.

[20][21] Previous work has shown that high cyclin B1 expression levels are found in variety of cancers such as breast, cervical, gastric, colorectal, head and neck squamous cell, non-small-cell lung cancer, colon, prostate, oral and esophageal.

[19][22][23][24][25] High expression levels are usually seen before the tumor cells become immortalized and aneuploid which can contribute to the chromosomal instability and the aggressive nature of certain cancers.

A possible treatment option for tumor suppression is to deliver gene or protein to target the degradation of cyclin B1.

Therefore the delivery of a therapeutic gene to correct these mutations is a viable treatment option for tumor suppression.

[19] In early stages of cancer when the cyclin B1 concentration is high, it is recognized by the immune system, leading to the production of antibodies and T cells.

[26] Studies in non-small cell lung cancer demonstrated that high levels of cyclin B1 are associated with poorer prognosis.

This finding indicates the possibility of using cyclin B1 expression as a prognostic marker for patients with early stage non-small cell lung cancer.