Quiz: Understanding Epigenetics and Genomics of Multiple Myeloma

Question 1

Answer

B.False

Despite a range of recently approved treatment options and a near doubling of 5-year survival rates from 1980, multiple myeloma remains largely incurable.

Question 2

Answer

D.All of the above

Multiple myeloma is a disease of bone marrow–dwelling, antigen-producing plasma cells. Gene mutations, gene copy number variation, microenvironmental cellular interactions, methylation, and other epigenetic modifications of gene expression are now all believed to play a role in multiple myeloma initiation and progression.

Question 3

Answer

C.Hyperdiploidy

Karyotyping and fluorescent in situ hybridization are used to categorize myeloma as either hyperdiploid or non-hyperdiploid. Hyperdiploidy is associated with better prognosis, and non-hyperdiploid myeloma tends to carry a poor prognosis.

Question 4

Answer

D.All of the above

Secondary gene mutations and translocations acquired by myeloma clones in the course of disease progression can change disease aggressiveness and treatment efficacy. These secondary aberrations commonly include MYC translocations; gain-of-function gene mutations in the oncogenes NRAS, KRAS, BRAF, and CCNDI; and loss-of-function mutations in the tumor suppressor genes P53, RB1, DIS3, CDKN2A, and CDKN2C.

Question 5

Answer

D.All of the above

Aberrant DNA methylation, histone methylation, microRNA expression, histone modification, and mutations in epigenetic regulation genes are all suspected to play a role in disease initiation, progression, and drug resistance. Epigenetic inhibitors appear to possess pleiotropic effects on several myeloma disease processes, including clone proliferation, apoptosis, DNA repair and genomic stability, and slowing or counteracting acquired drug resistance.