Shivani Golem
Dr. Golem is the medical director of Cytogenetics at the University of Kansas Medical Center and the University of Kansas Health System. She is dual boarded in Laboratory Genetics and Genomics, and Clinical Cytogenetics and Genomics. She authored/co-authored in more than 50 peer-reviewed publications, presentations, and book chapter on a wide variety of constitutional and cancer fields.
Abstract
Shivani Golema, Venkata Rakesh Sethapatib, George Kostanianc, Kamilla Isakovac, Harsh Pathakc
aUniversity of Kansas Medical Center, Lenexa, KS, USA; bCity of Hope, Los Angeles, CA, USA; cUniversity of Kansas Medical Center, Kansas City, KS, USA
Background: The t(11;14)(q13;q32) rearrangement is the most common genetic abnormality in Multiple myeloma (MM). The myeloma overexpressed (MYEOV) gene maps very close to the CCND1 gene on chromosome 11. In vitro studies have shown role of MYEOV in cancer proliferation and invasion. The aim of this study was to investigate the prognostic significance of MYEOV deregulation in a series of primary MM cases.
Methods: 58 MM cases (21 with t(11;14), 26 with polysomy 11, 6 with complex cytogenetics not involving chromosome 11 and 5 controls) were included in the study. RNA was extracted from CD138 positive plasma cells from bone marrow samples and analyzed with QRT-PCR.
Results: Fold changes in cyclin D1 mRNA levels in MM with t(11;14) ranged from 3.8 to 1106.7, median 110.41, MM with polysomy 11 ranged from 0.01-52.46, median 7.37, MM without chromosome 11 abnormalities ranged from 0.06 to 4.12, median 1.23 and control cases ranged from 0.30 to 2.52. 21/21 (100%) of t(11;14) cases and 17/26 (65.4%) cases with polysomy 11 had significant increase in CCND1 levels. Significant fold changes in MYEOV mRNA levels were seen in 7/21 (33.3%) cases with t(11;14), 15/26 (57.7%) cases with polysomy 11, 1/6 (16.6%) cases with no chromosome 11 abnormalities and 0/5 control cases.
Conclusions: High levels of CCND1 is seen in all MM cases with t(11;14) unlike with polysomy 11. MYEOV levels are significantly increased in both polysomy 11 and t(11;14). This study shows preliminary evidence of MYEOV overexpression in MM with chromosome 11 aberrations.