Division of Hematology Oncology, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts.
Department of Surgery and Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
J Histochem Cytochem. 2018 Aug;66(8):549-561. doi: 10.1369/0022155418766503. Epub 2018 Mar 27.
Phosphorylation is the most extensively studied posttranslational modification of proteins. There are approximately 500 kinases known in the human genome. The kinase-activated pathways regulate almost every aspect of cell function and a deregulated kinase cascade leads to impaired cellular function. Impaired regulation of several kinase cascades, including the epidermal growth factor receptor (EGFR) pathway, leading to tumor pathogenesis, is well documented. Thus, a phosphospecific test with prognostic or predictive value was expected in oncology. However, no phosphospecific IHC test is used in oncology clinics. Human topoisomerase I (topoI) inhibitors, camptothecin and its analogues (CPT), are used extensively to treat various solid tumors. Depending on tumor type, the response rate is only 13-32%. We have demonstrated that the deregulated kinase cascade is at the core of CPT resistance. DNA-PKcs, a kinase central to the DNA-double-strand break (DSB) response pathway, phosphorylates topoI at serine 10 (topoI-pS10), and cells with higher basal levels of topoI-pS10 degrade topoI rapidly and are resistant to this class of drug. The higher basal level of topoI phosphorylation is due to continual activation of DNA-PKcs, and one potential mechanism of this pathway activation is failure of upstream effector phosphatases such as phosphatase and tensin homolog (PTEN). Based on this understanding, we have developed an IHC-based test (P-topoIDx) that can stratify the responder and non-responder patient population.
磷酸化是蛋白质最广泛研究的翻译后修饰。人类基因组中大约有 500 种激酶。激酶激活的途径调节细胞功能的几乎各个方面,而失调的激酶级联反应导致细胞功能受损。几个激酶级联反应的调节受损,包括表皮生长因子受体(EGFR)途径,导致肿瘤发病机制,这是有充分记录的。因此,人们期望在肿瘤学中有一个具有预后或预测价值的磷酸特异性试验。然而,没有磷酸特异性 IHC 试验用于肿瘤学临床。人类拓扑异构酶 I(topoI)抑制剂,喜树碱及其类似物(CPT),广泛用于治疗各种实体瘤。根据肿瘤类型,反应率仅为 13-32%。我们已经证明,失调的激酶级联反应是 CPT 耐药的核心。DNA-PKcs,一种在 DNA 双链断裂(DSB)反应途径中起核心作用的激酶,磷酸化 topoI 丝氨酸 10(topoI-pS10),并且具有更高基础水平的 topoI-pS10 的细胞迅速降解 topoI 并对这类药物产生耐药性。更高基础水平的 topoI 磷酸化是由于 DNA-PKcs 的持续激活,并且该途径激活的一个潜在机制是上游效应物磷酸酶(如磷酸酶和张力蛋白同源物(PTEN))的失效。基于这一理解,我们开发了一种基于 IHC 的测试(P-topoIDx),可以对反应者和非反应者患者群体进行分层。