Genomic imbalances in human leukemia and lymphoma detected by comparative genomic hybridization (Review)

Abstract

A large number and variety of neoplasias of the hematopoietic system have been successfully subjected to CGH analysis. The obtained data shed light on genomic alterations beyond the basic rearrangements known as 'causative aberrations' in many of these diseases. Some of these alterations seem to play an important role in disease progression and specificity of the disease. They can also be associated with clinical parameters like response to therapy and survival. The patterns of genomic alterations found by CGH can characterize certain disease entities and differentiate them from others. If the chromosomal segments affected in > 10% of the cases of each basic disease entity [acute myeloblastic leukemia (AML), acute lymphoblastic leukemia (ALL), chronic lymphocytic leukemia (CLL) and multiple myeloma (MM)] are compared, most of the frequently involved chromosomal regions differ from entity to entity in the leukemias. The only exception are losses on 13q which are common to CLL and multiple myeloma. However, these patterns can also deduce chromosomal locations basically involved in the processes of hematopoietic oncogenesis, which is particularly evident in lymphomas. For instance, gain of 18q is shared by all lymphoma entities presented, and gain of 3q, 7q and 12q is commonly found in three of the differentiated classes. It is also of practical interest to control the differences and consistencies of imbalances found in nodular and in organ-confined lymphomas. Besides aneuploidies, which can also be readily detected by chromosome banding, CGH defines imbalances of chromosomal segments, which can become the basis for searching for neoplasia-related genes. With respect to their clinical significance, the presence of genomic imbalances is associated with disease progression and, therefore, poorer prognosis.