Results 61 to 70 of about 9,645 (157)
CRISPR‐Cas systems offer transformative genome editing capabilities for precise manipulation of cellular genes. This enables two main therapeutic avenues: ex vivo modification of patient cells for re‐transplantation or direct in vivo gene targeting via advanced delivery methods.
Bahareh Farasati Far+4 more
wiley +1 more source
Abstract Chromosomal translocations involving chromosome 9q34 and 22q11 generate the BCR-ABL1 fusion gene. The location of the translocation within the BCR gene dictates which exons are excluded or included in the resulting fusion with the ABL1 gene.
Rahia Tahir+10 more
openaire +2 more sources
Leukemia-associated fusion proteins, dek-can and bcr-abl, represent immunogenic HLA-DR-restricted epitopes recognized by fusion peptide-specific CD4+ T lymphocytes [PDF]
Although CD4(+) helper T lymphocytes have been demonstrated to play an important role in antitumor immune response, only a few epitopes of tumor-associated antigens recognized by HLA class II-restricted CD4(+) T lymphocytes have been identified.
Shigeru Fujita+8 more
openaire +2 more sources
Delivery as nanoparticles reduces imatinib mesylate-induced cardiotoxicity and improves anticancer activity [PDF]
Clinical effectiveness of imatinib mesylate in cancer treatment is compromised by its off-target cardiotoxicity. In the present study, we have developed physically stable imatinib mesylate-loaded poly(lactide-co-glycolide) nanoparticles (INPs) that could
Balakumar, Krishnamoorthy+6 more
core +2 more sources
A computational dynamic model of combination treatment for type II inhibitors with asciminib
Abstract Despite continuous strides forward in drug development, resistance to treatment looms large in the battle against cancer as well as communicable diseases. Chronic myeloid leukemia (CML) is treated with targeted therapy and treatment is personalized when resistance arises.
J. Roadnight Sheehan+2 more
wiley +1 more source
The Functional Interplay Between the t(9;22)-Associated Fusion Proteins BCR/ABL and ABL/BCR in Philadelphia Chromosome Positive Acute Lymphatic Leukemia [PDF]
Abstract The successful targeting of BCR/ABL by selective ABL-kinase inhibitors (AKI) such as Imatinib, Nilotinib, or Dasatinib alone is unable to eradicate the leukemic clone in Philadelphia chromosome positive (Ph+ ) leukemia. The t(9;22)(q34;q11) is a balanced translocation.
Anahita Rafiei+4 more
openaire +2 more sources
Imatinib mesylate, a BCR/ABL fusion protein inhibitor, is the first-line treatment against chronic myelogenous leukemia. In spite of its advantageous viewpoints, imatinib still has genuine impediments like undesirable side effects and tumor resistance ...
Alphy Rose James+9 more
doaj +1 more source
Leukemias bearing mixed lineage leukemia (MLL) rearrangement (MLL-R) resulting in expression of oncogenic MLL fusion proteins (MLL-FPs) represent an especially aggressive disease subtype with the worst overall prognoses and chemotherapeutic response. MLL-
Aditya Barve+7 more
doaj +1 more source
Molecular mechanisms in haematological malignancies [PDF]
Haematopoiesis requires the constant production of large numbers of peripheral blood cells. This process is under tight control of transcription factor networks as well as cytokines, growth factors and hormones.
Avellino, Roberto+2 more
core
MTSS1 is a critical epigenetically regulated tumor suppressor in CML [PDF]
Chronic myeloid leukemia (CML) is driven by malignant stem cells that can persist despite therapy. We have identified Metastasis suppressor 1 (Mtss1/MIM) to be downregulated in hematopoietic stem and progenitor cells from leukemic transgenic SCLtTA/Bcr ...
Braunschweig, T.+18 more
core +1 more source