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Multiple Myeloma FISH Probes


Copy number variations in both the p and q arms of chromosome 1 are recurrent in multiple myeloma, and both contribute to disease progression. On the p arm, loss of the tumor suppressor CDKN2C aids in tumor growth; on the q arm, amplification of CDKN2C causes genomic breakdown.


BIRC3 is often inactivated by copy number loss or by nonsense/frameshift mutations in multiple myeloma. These abnormalities likely contribute to oncogenesis through activation of the NF-kB signaling pathway.


BRD4 has been implicated in several solid tumor and blood cancers, including MM. As a transcriptional elongation regulator, it interacts with MYC and other oncogenes to facilitate malignant cell survival.


CCND1, which helps regulate cell cycle progression through the G1 phase, is found fused to IGH in approximately 20% of MM cases. As with other oncogenic IGH fusions, CCND1/IGH results in overexpression of CCND1, leading to abnormal cell development and survival.


CCND1, which helps regulate cell cycle progression through the G1 phase, is found fused to IGH in approximately 20% of MM cases. As with other oncogenic IGH fusions, CCND1/IGH results in overexpression of CCND1, leading to abnormal cell development and survival.


The t(4;14) translocation, which fuses FGFR3 to IGH, is found in approximately 15-20% of MM patients. The abnormality upregulates FGFR3 and the myeloma SET domain protein. Most patients with the fusion also harbor deletion of chromosome 13q.


The t(4;14) translocation, which fuses FGFR3 to IGH, is found in approximately 15-20% of MM patients. The abnormality upregulates FGFR3 and the myeloma SET domain protein. Most patients with the fusion also harbor deletion of chromosome 13q.


IGH translocations are found in about 60% of myeloma patients. These rearrangements result in fusions with partner genes that are upregulated by IGH enhancers. Frequency of IGH fusions increases with disease stage: 50% in MGUS, 60-65% in intramedullarly MM, and 70-80% in extramedullary MM.


MAF/IGH fusions are rare but recurrent in multiple myeloma, found in around 5% of patients. Beyond MAF upregulation, the fusion also triggers transactivation of the cell cycle regulator CCND2, enhancing proliferation of myeloma cells.


MAF/IGH fusions are rare but recurrent in multiple myeloma, found in around 5% of patients. Beyond MAF upregulation, the fusion also triggers transactivation of the cell cycle regulator CCND2, enhancing proliferation of myeloma cells.


RB1 is altered in approximately 6% of MM. Abnormalities in the cell cycle regulator are mainly homozygous losses, interrupting cell progression through the G1/S phase to spur increased proliferation.


Hemizygous loss of TP53 is found in just under 10% of newly diagnosed MM patients. These typically monoallelic deletions result in haploinsufficiency of this important tumor suppressor, resulting in defective P53 transcription and consequent apoptotic resistance in tumor cells, among other oncogenic effects.


TRAF3, a recently identified tumor suppressor, undergoes biallelic deletion/inactivation in several lymphoproliferative malignancies, including MM. Inactivation of the gene results in constitutive activation of the NF-kB2 pathway, abnormally extending B-cell survival.