Abstract
We measured histone deacetylase (HDAC) activity in 17 patients with primary myelofibrosis (PMF); 19 with other myeloproliferative neoplasm (MPN) and 16 normal volunteers. Significantly elevated HDAC levels were shown in patients with PMF compared with other MPN patients and normal volunteers (p < 0.05). Sixteen patients with PMF were also studied for correlation between JAK2 mutation status and HDAC levels; no significant correlation was found. We further correlated HDAC levels with clinical features in PMF: there was no correlation with WBC, platelet counts, Hb levels or degree of bone marrow fibrosis, but HDAC levels were correlated to the degree of splenomegaly. This suggests that HDAC may be recruited as essential thrombocythemia or polycythemia vera progresses into myelofibrosis or PMF progresses into more advanced stage. We then used the qRT-PCR cycle threshold (CT) method to study which HDACs were elevated in PMF. The results showed that, in general, Class 1 HDACs were elevated (HDAC1,2,8) except HDAC3, Class II HDACs were depressed (HDAC4,5) except HDAC6 and 10, and Class III HDACs were generally elevated. The current study may form the basis for using HDAC inhibitor in the treatment of patients with PMF and may implicate a possible role of HDAC in the association of pathogenesis of PMF.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 2321-2327 |
| Number of pages | 7 |
| Journal | Leukemia and Lymphoma |
| Volume | 49 |
| Issue number | 12 |
| DOIs | |
| State | Published - Dec 16 2008 |
Fingerprint
All Science Journal Classification (ASJC) codes
- Hematology
- Oncology
- Cancer Research
Cite this
}
Enhanced histone deacetylase enzyme activity in primary myelofibrosis. / Wang, Jen Chin; Chen, Chi; Dumlao, Theresa; Naik, Seema; Chang, Thong; Xiao, Ying Yi; Sominsky, Inna; Burton, Jack.
In: Leukemia and Lymphoma, Vol. 49, No. 12, 16.12.2008, p. 2321-2327.Research output: Contribution to journal › Article
TY - JOUR
T1 - Enhanced histone deacetylase enzyme activity in primary myelofibrosis
AU - Wang, Jen Chin
AU - Chen, Chi
AU - Dumlao, Theresa
AU - Naik, Seema
AU - Chang, Thong
AU - Xiao, Ying Yi
AU - Sominsky, Inna
AU - Burton, Jack
PY - 2008/12/16
Y1 - 2008/12/16
N2 - We measured histone deacetylase (HDAC) activity in 17 patients with primary myelofibrosis (PMF); 19 with other myeloproliferative neoplasm (MPN) and 16 normal volunteers. Significantly elevated HDAC levels were shown in patients with PMF compared with other MPN patients and normal volunteers (p < 0.05). Sixteen patients with PMF were also studied for correlation between JAK2 mutation status and HDAC levels; no significant correlation was found. We further correlated HDAC levels with clinical features in PMF: there was no correlation with WBC, platelet counts, Hb levels or degree of bone marrow fibrosis, but HDAC levels were correlated to the degree of splenomegaly. This suggests that HDAC may be recruited as essential thrombocythemia or polycythemia vera progresses into myelofibrosis or PMF progresses into more advanced stage. We then used the qRT-PCR cycle threshold (CT) method to study which HDACs were elevated in PMF. The results showed that, in general, Class 1 HDACs were elevated (HDAC1,2,8) except HDAC3, Class II HDACs were depressed (HDAC4,5) except HDAC6 and 10, and Class III HDACs were generally elevated. The current study may form the basis for using HDAC inhibitor in the treatment of patients with PMF and may implicate a possible role of HDAC in the association of pathogenesis of PMF.
AB - We measured histone deacetylase (HDAC) activity in 17 patients with primary myelofibrosis (PMF); 19 with other myeloproliferative neoplasm (MPN) and 16 normal volunteers. Significantly elevated HDAC levels were shown in patients with PMF compared with other MPN patients and normal volunteers (p < 0.05). Sixteen patients with PMF were also studied for correlation between JAK2 mutation status and HDAC levels; no significant correlation was found. We further correlated HDAC levels with clinical features in PMF: there was no correlation with WBC, platelet counts, Hb levels or degree of bone marrow fibrosis, but HDAC levels were correlated to the degree of splenomegaly. This suggests that HDAC may be recruited as essential thrombocythemia or polycythemia vera progresses into myelofibrosis or PMF progresses into more advanced stage. We then used the qRT-PCR cycle threshold (CT) method to study which HDACs were elevated in PMF. The results showed that, in general, Class 1 HDACs were elevated (HDAC1,2,8) except HDAC3, Class II HDACs were depressed (HDAC4,5) except HDAC6 and 10, and Class III HDACs were generally elevated. The current study may form the basis for using HDAC inhibitor in the treatment of patients with PMF and may implicate a possible role of HDAC in the association of pathogenesis of PMF.
UR - http://www.scopus.com/inward/record.url?scp=57449114002&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=57449114002&partnerID=8YFLogxK
U2 - 10.1080/10428190802527699
DO - 10.1080/10428190802527699
M3 - Article
C2 - 19052980
AN - SCOPUS:57449114002
VL - 49
SP - 2321
EP - 2327
JO - Leukemia and Lymphoma
JF - Leukemia and Lymphoma
SN - 1042-8194
IS - 12
ER -