Acute erythroleukemia - Evaluation of 48 cases with reference to classification, cell proliferation, cytogenetics, and prognosis

被引:45
作者
Mazzella, FM
Kowal-Vern, A
Shrit, MA
Wibowo, AL
Rector, JT
Cotelingam, JD
Collier, J
Mikhael, A
Cualing, H
Schumacher, HR
机构
[1] Univ Cincinnati, Med Ctr, Dept Pathol & Lab Med, Cincinnati, OH 45267 USA
[2] Loyola Univ, Ctr Med, Dept Pathol & Lab Med, Maywood, IL USA
[3] Miami Valley Hosp, Dept Pathol, Dayton, OH USA
[4] USN, Natl Med Ctr, Dept Navy, Bethesda, MD USA
关键词
erythroleukemia; M6a (FAB-MG); M6b (pure erythroleukemia); cell proliferation;
D O I
10.1093/ajcp/110.5.590
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
We evaluated 48 archival cases of acute erythroleukemia and divided them into 3 groups: M6a, corresponding to the traditional French-American-British M6 category; M6b, which is pure erythroleukemia; and M6c, in which myeloblasts and pronormoblasts each account for more than 30% of cells by the French-American-British exclusion criteria. No significant differences were noted among the subtypes for ratio of males to females; age; or exposure to toxins, alcohol, or both. However, compared with the patients in the M6a group, patients in the M6b and M6c groups demonstrated a statistically significant increase in cytogenetic aberrations, proliferation markers (proliferating cell nuclear antigen and Ki67), and ringed (type III) sideroblasts. Marked survival differences were noted between the M6a (30.1 +/- 29.5 months) and M6b (3.15 +/- 4.2 months) groups, with patients in the M6c group demonstrating an intermediate prognosis (10.5 +/- 12.7 months). Chemotherapeutic regimens induced remission in all treated patients in the M6a and M6c groups but did not appear to affect the M6b group. However; the patients in the M6c group remained in remission for a significantly shorter period of time than did patients in the M6a group. Overall, survival appeared to depend on the ratio of pronormoblasts to myeloblasts at diagnosis and demonstrated a rapid decline with increasing pronormoblast and decreasing myeloblast counts. We must, therefore, devise chemotherapeutic regimens that target both blastic components of this disease.
引用
收藏
页码:590 / 598
页数:9
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