This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Leppilampi, M. Articles by Rajaniemi, H. Search for Related Content PubMed PubMed Citation Articles by Leppilampi, M. Articles by Rajaniemi, H.

The Expression of Carbonic Anhydrase II in Hematological Malignancies¹

Departments of Anatomy and Cell Biology [M. L., S. Par., H. R.], Clinical Chemistry [M. L., E-R. S., J. H., O. N., S. Par.], and Internal Medicine [P. K.], University of Oulu, 90220 Oulu, Finland; EP Central Hospital, Laboratory, 60220 Seinäjoki, Finland [O. N.]; Institute of Virology, Slovak Academy of Sciences, 84245 Bratislava, Slovak Republic [S. Pas., J. P.]; Edward A. Doisy Department of Biochemistry and Molecular Biology, Saint Louis University School of Medicine, St. Louis, Missouri 63104 [A. W., W. S. S.]; and Institute of Medical Technology [S. Par.] and Department of Neurology [A-K. P.], University of Tampere and Tampere University Hospital, 33014 Tampere, Finland

Purpose: Carbonic anhydrases (CAs) are key enzymes that regulate acid-base homeostasis in both normal and pathological conditions. Recent studies have shown that they are functionally involved in the growth and invasion of cancer cells. However, there are only a few publications on CAs in hematological malignancies.

Experimental Design: Here we investigated the presence of CA isozymes in six malignant hematopoietic cell lines and malignant blast cells of bone marrow samples collected from patients with acute myeloid leukemia, acute lymphoblastic leukemia, or chronic myelomonocytic leukemia.

Results: Because three of the malignant hematopoietic cell lines expressed CA II, we also set out to examine its expression in a series of bone marrow samples. Positive reactions were found in 16 of 26 cases (62%) of acute myeloid leukemia, 11 of 15 cases (73%) of acute lymphoblastic leukemia, and 1 of 2 cases (50%) of chronic myelomonocytic leukemia.

Conclusions: The results indicate that CA II expression is not restricted to only one cell lineage but may result from a genetic aberration that occurs in both myeloid and lymphatic lineages or in their progenitor cell. Because CA II is expressed in most patients with leukemic blast cells, CA inhibitors may prove to be of value as an adjunct to chemotherapy for such cancers.

This article has been cited by other articles:

				F. Kassie, L. B. Anderson, L. Higgins, Y. Pan, I. Matise, M. Negia, P. Upadhyaya, M. Wang, and S. S. Hecht Chemopreventive agents modulate the protein expression profile of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone plus benzo[a]pyrene-induced lung tumors in A/J mice Carcinogenesis, March 1, 2008; 29(3): 610 - 619. [Abstract] [Full Text] [PDF]

				J. Haapasalo, K. Nordfors, S. Jarvela, H. Bragge, I. Rantala, A.-K. Parkkila, H. Haapasalo, and S. Parkkila Carbonic anhydrase II in the endothelium of glial tumors: A potential target for therapy Neuro-oncol, July 1, 2007; 9(3): 308 - 313. [Abstract] [Full Text] [PDF]

				K. Yoshiura, T. Nakaoka, T. Nishishita, K. Sato, A. Yamamoto, S. Shimada, T. Saida, Y. Kawakami, T. A. Takahashi, H. Fukuda, et al. Carbonic Anhydrase II Is a Tumor Vessel Endothelium-Associated Antigen Targeted by Dendritic Cell Therapy Clin. Cancer Res., November 15, 2005; 11(22): 8201 - 8207. [Abstract] [Full Text] [PDF]

				C.-G. Liu, L. Zhang, Y. Jiang, D. Chatterjee, C. M. Croce, K. Huebner, and L. Y.Y. Fong Modulation of Gene Expression in Precancerous Rat Esophagus by Dietary Zinc Deficit and Replenishment Cancer Res., September 1, 2005; 65(17): 7790 - 7799. [Abstract] [Full Text] [PDF]