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Estrogen and Androgen Blockade for Advanced Prostate Cancer in the Era of Precision Medicine
Published in Shaker A. Mousa, Raj Bawa, Gerald F. Audette, The Road from Nanomedicine to Precision Medicine, 2020
Tetsuya Fujimura, Kenichi Takayama, Satoru Takahashi, Satoshi Inoue
Determination of the therapeutic strategy for breast cancer depends on the expression patterns of ERα, progesterone receptor, and human epidermal growth factor receptor 2 (HER 2) in needle biopsy samples [90]. Therapeutic strategies for non-small cell lung cancer are based on mutation of epidermal growth factor receptor (EGFR), Kirsten murine sarcoma virus (KRAS), or anaplastic lymphoma kinase (ALK) [91]. However, pretreatment diagnosis using the estimated gene expression is not yet prevalent in patients with PC. Molecular diagnosis using immunohistochemistry; fluorescent in situ hybridization; and DNA, RNA, and/or micro-RNA analyses have been discussed in recent articles [92–100]. Studies in which gene sets of SC-like cells, micro-RNA, or cell-cycle progression markers reflect more aggressive diseases are limited to localized PC. A recent study has revealed that of the analysis of mutations, such as ATM Serine/Threonine Kinase (ATM) and Breast Cancer 1/2 (BRCA1/2), or the expression of specific genes can indicate the risk, metastatic potential, or radio sensitivity of PC [100, 101]; however, investigations regarding metastatic PC through molecular diagnosis are limited.
Small-Molecule Inhibitors Targeting Receptor Tyrosine Kinases in Cancer
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2020
Mohammad Hojjat-Farsangi, Gholamreza Khamisipour
ALK utilizes several signaling pathways, including JAK/STAT, MEKK2/3-MEK5-ERK5, PI3K-AKT, CRKL-C3G, and MAPK (Hallberg and Palmer, 2016). Various alterations in ALK gene have been noted in different cancers, including point mutations, deletions, and gene rearrangements. In different cancers, fusion of kinase domain of ALK with amino-terminal part of different proteins is frequent and among these fusions, echinoderm microtubule-associated protein-like 4 (EML4)-ALK is the most frequent fusion in NSCLC. Depending on the type of fusion, various signaling pathways and molecules might be activated.
Nanotechnology-Based Delivery Systems For Tyrosine Kinases Inhibitors In Non-Small Cell Lung Cancer Treatment
Published in Devarajan Thangadurai, Saher Islam, Jeyabalan Sangeetha, Natália Cruz-Martins, Biogenic Nanomaterials, 2023
Catarina Sousa, Maria Jacob, Amany M. Beshbishy, Gaber E. Batiha, Natália Cruz-Martins, Maria Gabriela O. Fernandes
Similarly, the EML4-ALK (echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase) fusion gene has been stated as another independent LC driver. ALK gene rearrangements are present in approximately 4% of NSCLC adenocarcinomas and are more often observed in non-smokers and younger patients (Soda et al., 2007; Shaw et al., 2009). Targeting this abnormality with Crizotinib and other ALK inhibitors has been clinically successful (Shaw et al., 2013; Hida et al., 2017; Soria et al., 2017).
Biotransformation of a crizotinib intermediate using a mutant alcohol dehydrogenase of Lactobacillus kefir coupled with glucose dehydrogenase
Published in Preparative Biochemistry and Biotechnology, 2019
Chuhong Zong, Xu Zhang, Fei Yang, Yafeng Zhou, Nan Chen, Zuisu Yang, Guofang Ding, Fangmiao Yu, Yunping Tang
Crizotinib is an effective and selective mesenchymal-epithelial transition factor/anaplastic lymphoma kinase (c-Met/ALK) inhibitor, which was manufactured by Pfizer.[1–3] It was approved for treating the ALK-rearranged non-small cell lung cancer (NSCLC) by the US FDA in 2011. The global market of crizotinib was approximately $5.0 billion by 2017. However, (S)-1-(2, 6-dichloro-3-fluorophenyl) ethanol is an important chiral intermediate for the synthesis of crizotinib in the reported synthetic routes.[4,5] Therefore, extensive efforts have been made to produce pure chiral alcohol.[4–7]