What is CDKN2A loss?

CDKN2A Loss is an inclusion criterion in 1 clinical trial for B-cell non-hodgkin lymphoma, of which 1 is open and 0 are closed. Of the trial that contains CDKN2A Loss and B-cell non-hodgkin lymphoma as inclusion criteria, 1 is phase 2 (1 open) [5].

Is CDKN2A a tumor suppressor gene?

CDKN2A is one of the most studied tumor suppressor genes. It encodes the p16-INK4a protein that plays a critical role in the cell cycle progression, differentiation, senescence, and apoptosis. Mutations in CDKN2A or dysregulation of its functional activity are frequently associated with various types of human cancer.

How common is CDKN2A mutation?

Germline CDKN2A mutations are rare in the whole population (<0.1%) with clusters seen in familial melanoma probands [1]. The function of CDK2A gene is that it codes for a number of proteins; among them tumour suppressors p16(INK4A) and unrelated p14(ARF) proteins.

Is p16 hereditary?

These mutations, classified as germline mutations, are typically inherited and are present in essentially all of the body’s cells. The CDKN2A gene mutations found in melanoma result in a nonfunctional p16(INK4A) protein. In many cases, a second, somatic mutation occurs in the normal copy of the gene in melanocytes.

What are the effects of loss of CDKN2B?

The tumor-promoting effects are generally attributed to loss of CDKN2A -encoded p16 and p14ARF tumor suppressors. The degree to which the associated CDKN2B -encoded p15 loss contributes to human tumorigenesis is unclear.

What kind of cancer can CDKN2A mutations cause?

Somatic CDKN2A gene mutations have been found in some people with brain tumors and in children with a blood cancer called acute lymphoblastic leukemia. Other Names for This Gene ARF

Which is a strong adverse prognosis factor for CDKN2A?

Here we showed in a large cohort of 428 malignant IDH -mutant gliomas lacking 1p/19q codeletion that CDKN2A homozygous deletion was a strong adverse prognosis factor. The same results were recorded in 483 anaplastic oligodendrogliomas, IDH -mutant + 1p/19q codeleted.

Is the presence of CDKN2A homozygous deletion a negative prognosis?

In both groups, the presence of microvascular proliferation and/or necrosis remained of prognostic value only in cases lacking CDKN2A homozygous deletion. CDKN2A homozygous deletion was not recorded in grade II gliomas.