Correction to: Pin1 inhibition exerts potent activity against acute myeloid leukemia through blocking multiple cancer-driving pathways.

The original article [1] contained minor typesetting errors affecting the following authors: Ziang Jeff Gao, Xiao Zhen Zhou, and Kun Ping Lu.

Pin1 inhibition exerts potent activity against acute myeloid leukemia through blocking multiple cancer-driving pathways.

Background: The increasing genomic complexity of acute myeloid leukemia (AML), the most common form of acute leukemia, poses a major challenge to its therapy. To identify potent therapeutic targets with the ability to block multiple cancer-driving pathways is thus imperative. The unique peptidyl-prolyl cis-trans isomerase Pin1 has been reported to promote tumorigenesis through upregulation of numerous cancer-driving pathways.

[Preparation of recombinant polypeptide of N-terminal heparin-binding domain of fibronectin and its effect on disseminated intravascular coagulation in rats].

This study was aimed to prepare the polypeptide of N-terminal heparin-binding domain of fibronectin(rhFNHN-29 polypeptide) with pichia expression system, to detect biological activity of recombinant polypeptide and investigate its effect on disseminated intravascular coagulation (DIC) in rats. The sequence of N-terminal heparin-binding domain of fibronectin was amplified from FNcDNA by PCR. The aim gene was cloned into T vector for selection.

[Recombinant polypeptide of N-terminal heparin-binding domain of fibronectin antagonizes hepatic failure induced by endotoxin in mice].

Objective: To study the preventive effect of recombinant polypeptide of N-terminal heparin-binding domain of fibronectin on hepatic failure induced by endotoxin in mice.

Methods: The 40 hepatic failure Balb/C mice were established by intraperitoneal injection of lipopolysaccharide (LPS) and d-galactosamine (GalN). The mice were randomly divided into two groups, one for polypeptide treatment, the othe for saline treatment.

[Calcium ionophore induces the differentiation of chronic myeloid leukemia cells into dendritic cells].

The aim of this study was to investigate the ability of calcium ionophore (CI ) to induce the differentiation of CML cells into dendritic cells (DC), to analyze the P210 expression in DCs and to evaluate the stimulatory effect of CML-DC on production of cytotoxic activity against CML cells via activating the autologous T cells. The mononuclear cells were isolated from bone marrow of CML patients whose WBC counts were more than 30x10(9)/L when samples were collected, then the lymphocytes and monocytes were discarded by pouring out supernatant twice at different culture time point. Slightly adherent cells were cultured in RPMI 1640 containing 10% FCS, with or without CI (375 ng/ml) and GM-CSF (200 ng/ml) at 37 degrees C, 5% CO2, fully humidified atmosphere for 96 hours.

[Effects of recombinant human tumor necrosis factor-alpha on HL-60 cells in vitro and in vivo].

To study the effects of recombinant human tumor necrosis factor-alpha (rhTNF-alpha) on HL-60 cells in vitro and in vivo, MTT and colony forming assay were used to examine the effects of rhTNF-alpha on proliferation of HL-60 cells; AO/EB (acridine orange-ethidium bromide) staining, Annexin-V flow cytometry analysis and TUNEL assay were used to detect apoptotic cells. The effect of rhTNF-alpha on xenograft growth of HL-60 cells was evaluated by tumor inhibition rate, histology, ultrastructure and TUNEL assay. The results showed that rhTNF-alpha inhibited the proliferation of HL-60 cells in a dose-dependent manner.

[The potential prognostic influence of granulocyte-colony stimulating factor in acute leukemia].

Objective: To investigate the potential influence of granulocyte-colony stimulating factor (G-CSF) on the prognosis of patients with acute leukemia(AL).

Methods: In 171 evaluable cases with AL, the complete remission (CR) rate post first course of chemotherapy, CR rate, effective rate, duration of leucopenia post chemotherapy, CR duration, lifespan and the relationship between the dosage of G-CSF and CR duration or lifespan were retrospectively analyzed with Chi-square test, paired t-test, Cox regression, Kaplan-Meier and rank correlation method. For remission induction and postremission therapy, the cases with acute myeloid leukemia (AML) received chemotherapy regimes based on daunorubicin + ara-C (DA), homoharringtonine + ara-C (HA) or mitoxantrone + ara-C (MA).