methanol extract suppresses the phosphorylation of ETV6‑NTRK3.

ETS variant transcription factor 6 (ETV6)-neurotrophic receptor tyrosine kinase 3 (NTRK3) (EN) fusions are typically found in rare diseases, such as primary renal fibrosarcoma (only six cases have been reported), secretory carcinoma of the breast and salivary gland (1 case), and AML (4 cases). Few cases have been reported, and expression of the EN gene fusion requires additional clinical data and fundamental research to be supported. The aim of the present study was to determine the inhibitory effect of methanol extract (MeAP) on EN-related cell lines, IMS-M2 and BaF3/EN, as well as evaluate the mechanism of action.

Artemisia vulgaris inhibits BCR/ABL and promotes apoptosis in chronic myeloid leukemia cells.

In previous research, the authors demonstrated that the methanol extract of (AVM) has the ability to inhibit chronic myeloid leukemia (CML) cell proliferation. The aim of the present study was to determine and clarify the mechanism of action of AVM. BCR/ABL activation is present in >90% of CML cases.

(L.) Pruski (Asteraceae) Methanol Extract Induces Apoptosis in Leukemia Cells through Suppression of BCR/ABL.

We will study the effects of the methanol extract of (L.) Pruski (Asteraceae) (MeST) on the growth of leukemia cells that may contain the gene. This study also clarifies the mechanism of this effect on these cells.

Recurrent BRCA1 Mutation, but no BRCA2 Mutation, in Vietnamese Patients with Ovarian Carcinoma Detected with Next Generation Sequencing.

Background: Identification of germline and somatic BRCA1/2 mutations in ovarian cancer is important for genetic counseling and treatment decision making with poly ADP ribose polymerase inhibitors. Unfortunately, data on the frequency of BRCA1/2 mutations in Vietnamese patients are scare.

Methods: We aim to explore the occurrence of BRCA1/2 mutations in 101 Vietnamese patients with ovarian cancer including serous (n = 58), endometrioid (n = 14), mucinous (n = 24), and clear cell (n = 5) carcinomas.

Combined effect of (-)-epigallocatechin-3-gallate and all-trans retinoic acid in -mutated cell lines.

Patents diagnosed with acute promyelocytic leukemia were treated with Vesanoid [all-trans retinoic acid (ATRA)]. ATRA promotes the maturation and differentiation of leukemia cells and is therefore capable of reducing the symptoms of leukemia by preventing aggregation of myeloid cells. However, the clinical applications of ATRA are limited by its side effects, including acute retinoid resistance, hypertriglyceridemia, mucocutaneous dryness, nausea, brief recovery time relapse and drug resistance.

Effects of green tea epigallocatechin-3-gallate on transcription factors regulating expression of FLT3.

Purpose: In our previous paper we previously reported that epigallocatechin-3-gallate (EGCG) inhibits FLT3 expression in cell lines harboring FLT3 mutations. In this research, we carried on to investigate the influence of EGCG on FLT3 promoter activity and FLT3 transcription. Methods The effect of EGCG on the mRNA expression of flt3 and flt3-promoter activity was evaluated using semiquantitative reverse transcription-PCR and luciferase reporter assay.

ETV6/FLT3 Fusion Is a Novel Client Protein of Hsp90.

FMS-like tyrosine kinase-3 fragments from exon 14 to the end without any mutations or deletions have been reported to fuse to ETV6 (TEL) in a few cases of myeloid/lymphoid neoplasms with eosinophilia carrying a translocation t(12;13)(p13;q12). This fusion protein confers constitutive activation on the FLT3 fragment and induces factor-independent growth in transfected Ba/F3 cells, indicating that it is an oncoprotein. However, the mechanism controlling the stability of this oncoprotein is unknown.

Spectrum of Common α-Globin Deletion Mutations in the Southern Region of Vietnam.

The common deletion mutations of α-globin genes in the Vietnamese population is not well known. Here we report the presence of five deletional mutations of Southeast Asia in the southern region of Vietnam. The - -(SEA) (NG_000006.

Synergistic effect of all‑trans retinoic acid in combination with protein kinase C 412 in FMS-like tyrosine kinase 3-mutated acute myeloid leukemia cells.

Acute myeloid leukemia (AML) is a heterogeneous disease. Numerous molecular abnormalities have been identified in AML and, amongst these, FMS‑like tyrosine kinase 3 (FLT3) mutations are one of the most common somatic alterations detected. In the present study, an in vitro investigation was performed to evaluate the effects of all‑trans retinoic acid (ATRA) and PKC412, alone and in combination, in FLT3‑mutated AML cell lines.

Down-regulated expression of NPM1 in IMS-M2 cell line by (-)-epigallocatechin-3-gallate.

Objective: To investigate the inhibited effect of epigallocatechin-3-gallate (EGCG) on the expression of NPM1 in IMS-M2 cells harboring the NPM1 mutations.

Methods: Cell proliferation assay was performed to test the effects of EGCG on cell growth of IMS-M2 cells harboring the NPM1 mutations. Western blot analysis were performed to test the protein expression of NPM1, AKT, those associated with apoptosis.

Inhibition of FLT3 expression by green tea catechins in FLT3 mutated-AML cells.

Acute myeloid leukemia (AML) is a heterogeneous disease characterized by a block in differentiation and uncontrolled proliferation. FLT3 is a commonly mutated gene found in AML patients. In clinical trials, the presence of a FLT3-ITD mutation significantly correlates with an increased risk of relapse and dismal overall survival.

ETV6-NTRK3 as a therapeutic target of small molecule inhibitor PKC412.

The ETV6-NTRK3 (EN) fusion gene which encodes a chimeric tyrosine kinase was first identified by cloning of the t(12;15)(p13;q25) translocation in congenital fibrosarcoma (CFS). Since then, EN has been also found in congenital mesoblastic nephroma (CMN), secretory breast carcinoma (SBC) and acute myelogenous leukemia (AML). Using IMS-M2 and M0-91 cell lines harboring the EN fusion gene, and Ba/F3 cells stably transfected with EN, we demonstrated that PKC412, also known as midostaurin, is an inhibitor of EN.

Green tea epigallocatechin gallate exhibits anticancer effect in human pancreatic carcinoma cells via the inhibition of both focal adhesion kinase and insulin-like growth factor-I receptor.

The exact molecular mechanism by which epigallocatechin gallate (EGCG) suppresses human pancreatic cancer cell proliferation is unclear. We show here that EGCG-treated pancreatic cancer cells AsPC-1 and BxPC-3 decrease cell adhesion ability on micro-pattern dots, accompanied by dephosphorylations of both focal adhesion kinase (FAK) and insulin-like growth factor-1 receptor (IGF-1R) whereas retained the activations of mitogen-activated protein kinase and mammalian target of rapamycin. The growth of AsPC-1 and BxPC-3 cells can be significantly suppressed by EGCG treatment alone in a dose-dependent manner.

Detection of exon 12 type A mutation of NPM1 gene in IMS-M2 cell line.

Nucleophosmin 1 (NPM1), a protein that shuttles between the nucleus and cytoplasm, is mostly located in nucleoli. This is a multifunctional phosphoprotein to which both tumor-suppressor and oncogenic functions have been attributed. Here, we have found the cell line with the type A NPM1 mutation and with the other genetic alterations including ETV6-NTRC fusion.

Green tea (-)-epigalocatechin-3-gallate inhibits KIT activity and causes caspase-dependent cell death in gastrointestinal stromal tumor including imatinib-resistant cells.

Imatinib, a selective tyrosine kinase inhibitor, has been used as a standard first-line therapy for gastrointestinal stromal tumor (GIST) patients. Unfortunately, most patients responding to imatinib will eventually exhibit the resistance, the cause of which is not fully understood. The serious clinical problems of imatinib-resistance demand alternative treatment strategy.