7 results match your criteria: "Guizhou Provincial Laboratory of Hematopoietic Stem Cell Transplantation Center[Affiliation]"

Article Synopsis
  • Sirt1 is a protein that is linked to aging cells and a type of cancer called DLBCL, but researchers want to learn more about how it works.
  • They found that when Sirt1 levels are higher, DLBCL cells can resist a cancer drug called Adriamycin, making it harder to treat the cancer.
  • Using special technology, they discovered that Sirt1's effect on drug resistance is connected to a pathway in cells that helps make energy, and blocking Sirt1 can make DLBCL cells more sensitive to the drug.
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Imatinib mesylate (IM) resistance has become a major clinical problem for chronic myeloid leukaemia (CML). It is known that Bcl-x splicing is deregulated and is involved in multiple malignant cancer initiation and chemotherapy resistance, including CML. The aim of the present study was to correct the abnormal splicing of Bcl-x in CML and investigate the subsequent malignant phenotype changes, especially response to IM.

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Deletion of HO-1 blocks development of B lymphocytes in mice.

Cell Signal

November 2019

Department of Hematology, Affiliated Hospital of Guizhou Medical University, Guiyang 550004, China; Key Laboratory of Hematological Disease Diagnostic and Treat Centre of Guizhou Province, Guiyang 550004, China; Department of Hematology, Guizhou Provincial Laboratory of Hematopoietic Stem Cell Transplantation Center, Guiyang 550004, China. Electronic address:

B lymphocytes, a key cluster of cells composing the immune system, can protect against abnormal biological factors. Heme oxygenase-1 (HO-1) plays important roles in cell proliferation and immune regulation, but its effects on the development and growth of B lymphocytes are still unknown. Herein, the count of B lymphocytes in HO-1 gene knockout (HO-1) mice was significantly lower than that of the HO-1 gene wild-type (HO-1) mice.

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Entinostat combined with Fludarabine synergistically enhances the induction of apoptosis in TP53 mutated CLL cells via the HDAC1/HO-1 pathway.

Life Sci

September 2019

Department of Hematology, Affiliated Hospital of Guizhou Medical University, Guiyang 550004, China; Key Laboratory of Hematological Disease Diagnostic and Treat Centre of Guizhou Province, Guiyang 550004, China; Department of Hematology, Guizhou Provincial Laboratory of Hematopoietic Stem Cell Transplantation Center, Guiyang 550004, China. Electronic address:

TP53 mutation is an indicator of poor prognostic in chronic lymphocytic leukemia (CLL). Worse still, CLL patients with TP53 mutation are associated with poor efficacy to current chemotherapeutic, such as Fludarabine. Here, we confirmed that high expression of HDAC1 in CLL patients with TP53 mutation, which is closely related to poor prognosis and drug-resistance.

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Article Synopsis
  • Heme oxygenase-1 (HO-1) helps cancer cells grow and makes them harder to kill with the drug vincristine in a type of cancer called DLBCL.
  • Patients with higher levels of HO-1 protein have worse outcomes compared to those with lower levels.
  • Reducing HO-1 can make cancer cells more sensitive to treatment and improve survival in experiments using mice.
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The correlation between Heme oxygenase-1 (HO-1) and dominant-negative Ikaros isoform 6 (IK6) is unclear. Firstly, we detected that IK6 existed in 20 of 42 (47.6%) adult BCR-ABL1-positive B-lineage acute lymphoblastic leukemia (BCR-ABL1-positive B-ALL) by using reverse transcribed polymerase chain reaction (PCR) and nucleotide sequencing.

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Heme oxygenase-1 suppresses the apoptosis of acute myeloid leukemia cells via the JNK/c-JUN signaling pathway.

Leuk Res

May 2015

Guiyang Medical College, Guiyang 550004, China; Department of Hematology, the Affiliated Hospital of Guiyang Medical College, Guiyang 550004, China; Guizhou Provincial Laboratory of Hematopoietic Stem Cell Transplantation Center, Guiyang 550004, China. Electronic address:

There are few studies on the correlation between heme oxygenase-1 (HO-1) and acute myeloid leukemia (AML). We found that HO-1 was aberrantly overexpressed in the majority of AML patients, especially in patients with acute monocytic leukemia (M5) and leukocytosis, and inhibited the apoptosis of HL-60 and U937 cells. Moreover, silencing HO-1 prolonged the survival of xenograft mouse models.

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