PubMed HealthSearch

PubMed · 8141718

Repeat thrombolysis.

Abstract

Since 20% of patients with myocardial infarction (MI) have had a previous infarction, and reinfarction within one year after infarction occurs in 9% of cases, it is important to clarify the role of repeat thrombolysis. After streptokinase (SK) administration, IgG antibodies rise to a peak at two weeks and slowly fall over the next 12 months, but 50% of patients still have antibody levels sufficient to neutralise a standard dose of SK up to four years after initial SK administration. On this evidence, SK or anistreplase should not be readministered, except perhaps in the first two to three days after initial treatment. The efficacy of tissue plasminogen activator (t-PA) and urokinase is not affected by prior treatment with SK.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

D Cross. 1993. Repeat thrombolysis.. https://doi.org/10.1111/j.1445-5994.1993.tb04755.x

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

ERBB3 overexpression due to miR-205 inactivation confers sensitivity to FGF, metabolic activation, and liability to ERBB3 targeting in glioblastoma.

In glioblastoma (GBM), the most frequent and lethal brain tumor, therapies suppressing recurrently altered signaling pathways failed to extend survival. However, in patient subsets, specific genetic lesions can confer sensitivity to targeted agents. By exploiting an integrated model based on patient-derived stem-like cells, faithfully recapitulating the original GBMs in vitro and in vivo, here, we identify a human GBM subset (∼9% of all GBMs) characterized by ERBB3 overexpression and nuclear accumulation. ERBB3 overexpression is driven by inheritable promoter methylation or post-transcriptional silencing of the oncosuppressor miR-205 and sustains the malignant phenotype. Overexpressed ERBB3 behaves as a specific signaling platform for fibroblast growth factor receptor (FGFR), driving PI3K/AKT/mTOR pathway hyperactivation, and overall metabolic upregulation. As a result, ERBB3 inhibition by specific antibodies is lethal for GBM stem-like cells and xenotransplants. These findings highlight a subset of patients eligible for ERBB3-targeted therapy.

Antibodies