RNA degradation precedes DNA cleavage in autoreactive CD4 T cells suppressed by calicheamicin γ1

Thomas, Sunil; Preda-Pais, Anca; Casares, Sofía; Brumeanu, Teodor‐D.

doi:10.1016/j.intimp.2004.01.002

Cited by 3 publications

(1 citation statement)

References 9 publications

(11 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Gemtuzumab ozogamicin (GO), a CD33 antibody–calicheamicin conjugate, is taken up by cells after binding to CD33, and exerts its effects by cleaving double-stranded DNA in lysosomes, causing cytotoxicity and apoptosis [ 117 ]. It is believed that free calicheamicin is 1000 times more effective than doxorubicin as an antitumor agent, and many clinical trials have evaluated its efficacy for untreated and relapsed/refractory AML [ 118 , 119 ].…”

Section: Antibody–drug Conjugates For Amlmentioning

confidence: 99%

New Therapeutic Strategies for Adult Acute Myeloid Leukemia

Ishii

Yano

2022

Cancers

View full text Add to dashboard Cite

Acute myeloid leukemia (AML) is a genetically heterogeneous hematological malignancy. Chromosomal and genetic analyses are important for the diagnosis and prognosis of AML. Some patients experience relapse or have refractory disease, despite conventional cytotoxic chemotherapies and allogeneic transplantation, and a variety of new agents and treatment strategies have emerged. After over 20 years during which no new drugs became available for the treatment of AML, the CD33-targeting antibody–drug conjugate gemtuzumab ozogamicin was developed. This is currently used in combination with standard chemotherapy or as a single agent. CPX-351, a liposomal formulation containing daunorubicin and cytarabine, has become one of the standard treatments for secondary AML in the elderly. FMS-like tyrosine kinase 3 (FLT3) inhibitors and isocitrate dehydrogenase 1/2 (IDH 1/2) inhibitors are mainly used for AML patients with actionable mutations. In addition to hypomethylating agents and venetoclax, a B-cell lymphoma-2 inhibitor is used in frail patients with newly diagnosed AML. Recently, tumor protein p53 inhibitors, cyclin-dependent kinase inhibitors, and NEDD8 E1-activating enzyme inhibitors have been gaining attention, and a suitable strategy for the use of these drugs is required. Antibody drugs targeting cell-surface markers and immunotherapies, such as antibody–drug conjugates and chimeric antigen receptor T-cell therapy, have also been developed for AML.

show abstract

Section: Antibody–drug Conjugates For Amlmentioning

confidence: 99%