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Commentary |
St. Joseph’s Hospital and Medical Center Phoenix, Arizona
In general, the development and biology of epithelial
tumors, carcinomas, and adenocarcinomas are associated with an array of
orchestrated genetic changes characterized by a successive process of
loss of heterozygosity. On the other hand, tumors of mesodermal origin
(bone and soft tissue tumors) are often associated with translocations
thought to be causally related to the development of the neoplasia.
Often, the translocation is the only cytogenetic change observed in
these tumors (Table 1)
. The occurrence of
translocations as a sole karyotypic event in carcinomas, as indicated
by the authors of the article by French et al,1
is
extremely rare.
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and
their associated molecular events are not only diagnostic of these
tumors, regardless of their site of origin and variability of the
histology, but also, as already mentioned, the genetic changes
resulting from these translocations are responsible for the genesis of
these tumors. Furthermore, therapeutic approaches, akin to those found
effective in leukemias associated with specific translocations, eg,
t(9;22) in chronic myelocytic leukemia and t(15;17) in acute
promyelocytic leukemia, hold much promise for the treatment of these
tumors. The present article by French et al1 points to the strong possibility that a somewhat heterogeneous group of rare carcinomas may be characterized by a t(15;19) and the molecular events associated with this translocation. The heterogeneity is related to the reported breakpoints on chromosome 15 (q11, q12, q13, q15, and p12) and the somewhat anatomical variability of the tumor sites, though the tumors appear to be mediastinal or thoracic in their location. However, these carcinomas as a group do share a poor prognosis and an apparently similar histology.
Although the studies of French et al1 have not yet revealed the presumptive oncogenic fusion product associated with the t(15;19), they have established that the BRD4 gene on chromosome 19 is interrupted by the translocation and that a 9 kb region containing the Nop10p gene on chromosome 15 is affected by the translocation break. Thus, it remains imperative to ascertain the exact gene affected on chromosome 15 and to determine the structure and transforming mechanisms of the fusion product of the t(15;19). It is equally important to evaluate further whether the above-mentioned variability in the breakpoints on chromosome 15 is real and thus raises concerns regarding the specificity of the t(15;19) in these tumors. Obviously, more carcinomas with t(15;19) will have to be studied to more firmly establish their cytogenetic and molecular aspects.
Footnotes
Address reprint requests to Avery A. Sandberg, M.D., Department of DNA Diagnostics, St. Joseph’s Hospital and Medical Center, 350 West Thomas Rd., Phoenix, AZ 85013.
Accepted for publication September 26, 2001.
References
This article has been cited by other articles:
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  H. Liu, X. Li, Z. Niu, L. Zhang, M. Zhou, H. Huang, J. He, W. Zhang, L. Xiao, Y. Tang, et al. Preparation of Polyclonal Antibody Specific for BRD7 and Detection of Its Expression Pattern in the Human Fetus J. Histochem. Cytochem., June 1, 2008; 56(6): 531 - 538. [Abstract] [Full Text] [PDF]
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