Objective: Prognostic effect of KRAS mutation and side of tumor in colorectal cancer is a highly controversial subject. Therefore, we evaluated the association between FDG uptake pattern in F-fluoro-2-deoxy-glucose positron emission tomography/computed tomography (F-FDG PET/CT) imaging and KRAS mutation and tumor localization in patients with a diagnosis of colon cancer and assessed the effects of these three factors on prognosis and survival.
Methods: Eighty-three patients with colorectal cancer were retrospectively included in this study. F-FDG PET/CT study was performed for pretreatment staging. The maximum standardized uptake value (SUV) of the primary tumor and survival data of patients were compared between groups. KRAS mutations were detected with the help of real-time Polymerase Chain Reaction technique through genomic DNA extracted from paraffin-embedded tumor tissue blocks. Tumor lesions with potential KRAS mutations were classified as mutant KRAS and wild type.
Results: Twenty five patients were female while 58 were male. The mean age of the patients was 59.8±11.3 years. Mean follow-up was 35.5±18.9 months. Primary tumor was localized in the left colon in 83.1% of patients and in the right colon in 16.9%. KRAS mutation was detected in 54.2% (n=45) of patients. Mean SUV of patients with primary tumor was estimated to be 21.1±9.1 (range= 6.0-47.5). Mean tumor SUV of patients with a KRAS mutation (24.0±9.0) was found to be significantly higher than those without KRAS mutation (17.7±8.2) (p=0.001). Mean survival was significantly shorter in patients with locoregional nodal metastasis than in patients without locoregional nodal metastasis as well as in patients with distant nodal metastasis than in patients without distant nodal metastasis and in patients with organ metastasis in initial PET/CT than in patients without organ metastasis. Also, mean survival was nearly statistically-significantly shorter in patients with tumors located in left colon (34.2±19.4) than in right colon (43.2±14.6) (p=0.059). However, we found no significant impact of KRAS mutation on survival.
Conclusion: In our study, we found that tumor localization had no significant effect on prognosis in patients with colon cancer. On the other hand, FDG uptake was observed to be higher in the presence of KRAS mutation and it was concluded that coexistence of KRAS mutation with higher SUV is a negative prognostic factor.
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http://dx.doi.org/10.4274/mirt.galenos.2019.33866 | DOI Listing |
JTO Clin Res Rep
December 2024
Department of Pathology and Medical Biology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Introduction: Programmed death-ligand 1 (PD-L1) is the main predictive biomarker used to identify patients with NSCLC who are eligible for treatment with immune checkpoint inhibitors. Despite its utility, the predictive capacity of PD-L1 is limited, necessitating the exploration of supplementary predictive biomarkers. In this report, we describe the prognostic value of / mutation status for overall survival (OS) in patients with NSCLC treated with first-line immunotherapy or combined chemoimmunotherapy.
View Article and Find Full Text PDFTher Adv Med Oncol
December 2024
Division of Medical Oncology and Hematology, Princess Margaret Cancer Centre (PMCC), University Health Network (UHN), 700 University Avenue, 7-812, Toronto, ON M5G 2M9, Canada.
Background: Given advancements in adjuvant treatments for non-small-cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK)-targeted therapies, it is important to consider postoperative targeted therapies for other early-stage oncogene-addicted NSCLC. Exploring baseline outcomes for early-stage NSCLC with these rare mutations is crucial.
Objectives: This study aims to assess relapse-free survival (RFS) and overall survival (OS) in patients with resected early-stage NSCLC with rare targetable driver mutations.
Trends Cancer
December 2024
Charité - Universitätsmedizin Berlin, Institute of Pathology, Berlin, Germany; German Cancer Consortium (DKTK), Partner Site Berlin, German Cancer Research Center (DKFZ), Heidelberg, Germany; Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA; Department of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA. Electronic address:
In 1982, the RAS genes HRAS and KRAS were discovered as the first human cancer genes, with KRAS later identified as one of the most frequently mutated oncogenes. Yet, it took nearly 40 years to develop clinically effective inhibitors for RAS-mutant cancers. The discovery in 2013 by Shokat and colleagues of a druggable pocket in KRAS paved the way to FDA approval of the first covalently binding KRAS inhibitors, sotorasib and adagrasib, in 2021 and 2022, respectively.
View Article and Find Full Text PDFPancreatology
December 2024
Department of Internal Medicine, Eunpyeong St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, South Korea. Electronic address:
Background: Endoscopic ultrasound-guided tissue acquisition (EUS-TA) has become essential for diagnosing pancreatic ductal adenocarcinoma (PDAC) and is increasingly utilized for comprehensive genome profiling (CGP) to advance precision medicine. This systematic review and meta-analysis assess the feasibility and clinical utility of EUS-TA samples for CGP in PDAC.
Methods: We conducted a thorough systematic literature search in PubMed, EMBASE, and the Cochrane Library up to October 2023.
Biomed Pharmacother
December 2024
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.
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