Topic
K562 cells
About: K562 cells is a research topic. Over the lifetime, 5017 publications have been published within this topic receiving 170352 citations. The topic is also known as: K562 & K 562.
Papers published on a yearly basis
Papers
TL;DR: A compound, designed to inhibit the Abl protein tyrosine kinase, was evaluated for its effects on cells containing the Bcr–Abl fusion protein and it was found that this compound may be useful in the treatment of bcr–abl–positive leukemias.
Abstract: The bcr-abl oncogene, present in 95% of patients with chronic myelogenous leukemia (CML), has been implicated as the cause of this disease. A compound, designed to inhibit the Abl protein tyrosine kinase, was evaluated for its effects on cells containing the Bcr-Abl fusion protein. Cellular proliferation and tumor formation by Bcr-Abl-expressing cells were specifically inhibited by this compound. In colony-forming assays of peripheral blood or bone marrow from patients with CML, there was a 92-98% decrease in the number of bcr-abl colonies formed but no inhibition of normal colony formation. This compound may be useful in the treatment of bcr-abl-positive leukemias.
3,848 citations
TL;DR: This CML cell-line represents a unique source of CML cells with meaningful indicators of malignancy for clinical and experimental studies.
3,105 citations
TL;DR: It is demonstrated that P210bcr/abl expression can induce chronic myelogenous leukemia and retrovirus-mediated expression of the protein provides a murine model system for further analysis of the disease.
Abstract: In tumor cells from virtually all patients with chronic myelogenous leukemia, the Philadelphia chromosome, a fusion of chromosomes 9 and 22, directs the synthesis of the P210bcr/abl protein. The protein-tyrosine kinase activity and hybrid structure of P210bcr/abl are similar to the oncogene product of the Abelson murine leukemia virus, P160gag/v-abl, which induces acute lymphomas. To determine whether P210bcr/abl can induce chronic myelogenous leukemia, murine bone marrow was infected with a retrovirus encoding P210bcr/abl and transplanted into irradiated syngeneic recipients. Transplant recipients developed several hematologic malignancies; prominent among them was a myeloproliferative syndrome closely resembling the chronic phase of human chronic myelogenous leukemia. Tumor tissue from diseased mice harbored the provirus encoding P210bcr/abl. These results demonstrate that P210bcr/abl expression can induce chronic myelogenous leukemia. Retrovirus-mediated expression of the protein provides a murine model system for further analysis of the disease.
2,308 citations
TL;DR: Single-enzyme phenotypes were found in erythrocytes, platelets and cultured blood macrophages indicating that these cells have a common stem cell which is the site of the abnormality in CML, and strong evidence that the disease has a clonal origin.
934 citations
TL;DR: Results demonstrate that murine CML recapitulates important features of human CML and should be an excellent model for addressing specific issues relating to the pathogenesis and treatment of this disease.
803 citations
Related Topics (5)
Performance Metrics
| Year | Papers |
|---|---|
| 2025 | 25 |
| 2024 | 69 |
| 2023 | 223 |
| 2022 | 195 |
| 2021 | 115 |
| 2020 | 130 |