Loss of Mitotic Antipairing

Loss of Mitotic Antipairing is a Conserved Characteristic in Primary and Secondary Renal Carcinoma

Presenter: Shayla Shahar

Co-Presenter(s):
Kayla Arce

Presenter Status: Undergraduate student

Academic Year: 20-21

Semester: Spring

Faculty Mentor: Lisa Hua

Department: Biology

Funding Source/Sponsor: Koret Scholars Program, LSAMP

Other Funding Source/Program: National Science Foundation

Screenshot URL: https://drive.google.com/uc?id=191TOdV64WOPF-b1eeeuGMqw1C4oBUMSS

Abstract:
Little is known for the mechanisms underlying metastatic progression in cancer. One possibility is that heterogeneous chromosome organization within the cancer may play a role in tumor metastases. It was found that a secondary renal tumor, Caki1, exhibited abnormal pairing of homologous chromosome 19. The abnormal pairing was correlated to genome instability. Although abnormal pairing has been observed in Caki1 cells, it is unknown whether it is conserved in the original/primary tumor. We employed chromosome painting, and high resolution confocal fluorescence microscopy to visualize homologous chromosome 19 to test whether primary Caki2 renal tumors also exhibit abnormal homologous pairing. Primary Caki2 renal tumors exhibit pairing of chromosome 19 at both metaphase and anaphase (binomial probability distribution, p=0.0039). This data supports that a loss of mitotic homologous chromosome antipairing is a defining characteristic preserved in both primary and secondary tumors. Our findings provide a new avenue to explore a shared characteristic for a loss of mitotic antipairing in primary and secondary tumors, supporting the phenomenon of mitotic antipairing and its importance in normal cell function and behavior.