Cancers bearing the KRAS G13D mutation are notable for their distinct clinical behavior relative to other oncogenic KRAS mutations. We hypothesized that primary biochemical or biophysical properties of KRAS G13D might contribute to these clinical observations and as part of our study undertook structural studies using x-ray crystallography. In this data article we discuss several x-ray diffraction datasets that yielded structures of oncogenic KRAS mutants including a high resolution (1.13 Å) structure of KRAS G13D. The datasets are typical for high resolution x-ray diffraction data and allow the construction of atomic resolution, three dimensional structural models with high confidence. This data can be correlated with biochemical information such as defects in substrate binding kinetics, GTPase activities and interactions with the RAS effector RAF kinase.
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http://dx.doi.org/10.1016/j.dib.2015.10.001 | DOI Listing |
Sci Rep
January 2025
Genetic Analysis Department, Tsukiji Registered Clinical Laboratory, Riken Genesis Co., Ltd., Tokyo, Japan.
Comprehensive genomic profiling (CGP) is increasingly used as a clinical laboratory test and being applied to cancer treatment; however, standardization and external quality assessments (EQA) have not been fully developed. This study performed cost-effective EQA and proficiency tests (PT) for CGP testing among multiple institutions those belong to the EQA working group of Japan Association for Clinical Laboratory Science (JACLS). This study revealed that preanalytical processes, such as derived nucleic acids (NA) extraction from formalin fixed paraffine embedded (FFPE) samples, are critical.
View Article and Find Full Text PDFBiomed Pharmacother
January 2025
Department of Pharmacy, College of Pharmacy, Institute of Pharmaceutical Science and Technology, Hanyang University, Ansan, Gyeonggi-do 15588, Republic of Korea. Electronic address:
Colorectal malignancies associated with KRAS and TP53 mutations led us to investigate the effects of combination therapy targeting KRAS, MEK1, or PLK1 in colorectal cancer. MEK1 is downstream of RAS in the MAPK pathway, whereas PLK1 is a mitotic kinase of the cell cycle activated by MAPK and regulated by p53. Bioinformatics analysis revealed that patients with colorectal cancer had a high expression of MAP2K1 and PLK1.
View Article and Find Full Text PDFClin Lung Cancer
November 2024
Division of Hematology and Medical Oncology, Department of Medicine, Weill Medical College of Cornell University, New York, NY.
Background: Stage I nonsmall cell lung cancer (NSCLC) is primarily treated with surgical resection and has a favorable prognosis with an expected recurrence rate of 30%. New methods to risk stratify patients with stage I NSCLC are needed to help select those that might benefit from more active surveillance or adjuvant therapy.
Methods: We analyzed clinical data from 1330 patients (1469 tumors) with NSCLC and correlated it with next-generation sequencing (NGS).
Front Oncol
November 2024
Institute of Pathology, Ruhr University, Bochum, Germany.
Introduction: Understanding the mutational landscape of colon cancer (CC) is crucial for targeted therapy development. Microsatellite instability (MSI-H), rat sarcoma (RAS), and B-Raf proto-oncogene, serine/threonine kinase (BRAF) mutations (MT) are pivotal markers. Further investigation into clinicopathological features of RAS and BRAF MT in microsatellite stable (MSS) and MSI-H tumors is warranted.
View Article and Find Full Text PDFMol Cell Biochem
November 2024
Kindai University Faculty of Pharmacy, Kowakae, Higashiosaka, Osaka, 577-8502, Japan.
Oxaliplatin (L-OHP) and 5-fluorouracil (5-FU) are used to treat colon cancer; however, resistance contributes to poor prognosis. Epithelial-mesenchymal transition (EMT) has been induced in tumor tissues after administration of anticancer drugs and may be involved in drug resistance. We investigated the mechanism of EMT induction in colon cancer cells treated with 5-FU and L-OHP.
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