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https://www.readbyqxmd.com/read/29458068/ovarian-microcystic-stromal-tumor-with-undetermined-potential-case-study-with-molecular-analysis-and-literature-review
#1
Ying Zhang, Lin Tao, Can Yin, Weiwei Wang, Hong Zou, Yan Ren, Weihua Liang, Jinfang Jiang, Wenjie Zhang, Wei Jia, Feng Li
Ovarian microcystic stromal tumor is a relatively rare tumor type. This tumor is characterized by a unique microcyst structure and essentially all tumors show benign biological behavior. Here, we report a case with a primary ovarian microcystic stromal tumor that experienced recurrence. Pathological findings showed that the original tumor, relapsed tumor in the ovary, and the recurrent tumor in the iliac fossa presented similar histological features. The tumor mainly consisted of microcysts, solid cellular regions, and a fibrous stroma...
February 16, 2018: Human Pathology
https://www.readbyqxmd.com/read/29455666/kras-oncogene-in-non-small-cell-lung-cancer-clinical-perspectives-on-the-treatment-of-an-old-target
#2
REVIEW
Marta Román, Iosune Baraibar, Inés López, Ernest Nadal, Christian Rolfo, Silvestre Vicent, Ignacio Gil-Bazo
Lung neoplasms are the leading cause of death by cancer worldwide. Non-small cell lung cancer (NSCLC) constitutes more than 80% of all lung malignancies and the majority of patients present advanced disease at onset. However, in the last decade, multiple oncogenic driver alterations have been discovered and each of them represents a potential therapeutic target. Although KRAS mutations are the most frequently oncogene aberrations in lung adenocarcinoma patients, effective therapies targeting KRAS have yet to be developed...
February 19, 2018: Molecular Cancer
https://www.readbyqxmd.com/read/29455644/mir-19b-enhances-proliferation-and-apoptosis-resistance-via-the-egfr-signaling-pathway-by-targeting-pp2a-and-bim-in-non-small-cell-lung-cancer
#3
Ulrich Baumgartner, Fabienne Berger, Ali Hashemi Gheinani, Sabrina Sofia Burgener, Katia Monastyrskaya, Erik Vassella
BACKGROUND: Epidermal growth factor receptor (EGFR) mutations enable constitutive active downstream signaling of PI3K/AKT, KRAS/ERK and JAK/STAT pathways, and promote tumor progression by inducing uncontrolled proliferation, evasion of apoptosis and migration of non-small cell lung cancer (NSCLC). In addition, such EGFR mutations increase the susceptibility of patients with NSCLC to tyrosine kinase inhibitor (TKI) therapy, but treated patients will invariably relapse with resistant disease...
February 19, 2018: Molecular Cancer
https://www.readbyqxmd.com/read/29454854/erk1-2-inhibitors-new-weapons-to-inhibit-the-ras-regulated-raf-mek1-2-erk1-2-pathway
#4
REVIEW
Andrew M Kidger, James Sipthorp, Simon J Cook
The RAS-regulated RAF-MEK1/2-ERK1/2 signalling pathway is de-regulated in a variety of cancers due to mutations in receptor tyrosine kinases (RTKs), negative regulators of RAS (such as NF1) and core pathway components themselves (RAS, BRAF, CRAF, MEK1 or MEK2). This has driven the development of a variety of pharmaceutical agents to inhibit RAF-MEK1/2-ERK1/2 signalling in cancer and both RAF and MEK inhibitors are now approved and used in the clinic. There is now much interest in targeting at the level of ERK1/2 for a variety of reasons...
February 15, 2018: Pharmacology & Therapeutics
https://www.readbyqxmd.com/read/29454587/comparison-of-ct-radiogenomic-and-clinical-characteristics-between-egfr-and-kras-mutations-in-lung-adenocarcinomas
#5
J Lv, H Zhang, J Ma, Y Ma, G Gao, Z Song, Y Yang
AIM: To compare computed tomography (CT) radiogenomic and clinical characteristics between patients with epidermal growth factor receptor (EGFR) and Kirsten rat sarcoma viral oncogene (KRAS) mutations in lung adenocarcinomas. MATERIALS AND METHODS: This study was a retrospective analysis of patients with histopathologically confirmed lung adenocarcinoma, who had complete clinical and imaging data, and were tested for EGFR and KRAS mutations. Of the 313 included patients, 116 had effective EGFR mutations (EGFR group), 31 had KRAS mutations (KRAS group), and 166 had no EGFR or KRAS mutations (control group)...
February 14, 2018: Clinical Radiology
https://www.readbyqxmd.com/read/29454261/frequency-of-somatic-tp53-mutations-in-combination-with-known-pathogenic-mutations-in-colon-adenocarcinoma-non-small-cell-lung-carcinoma-and-gliomas-as-identified-by-next-generation-sequencing
#6
Zahra Shajani-Yi, Francine B de Abreu, Jason D Peterson, Gregory J Tsongalis
The tumor suppressor gene TP53 is the most frequently mutated gene in human cancer. It encodes p53, a DNA-binding transcription factor that regulates multiple genes involved in DNA repair, metabolism, cell cycle arrest, apoptosis, and senescence. TP53 is associated with human cancer by mutations that lead to a loss of wild-type p53 function as well as mutations that confer alternate oncogenic functions that enable them to promote invasion, metastasis, proliferation, and cell survival. Identifying the discrete TP53 mutations in tumor cells may help direct therapies that are more effective...
February 13, 2018: Neoplasia: An International Journal for Oncology Research
https://www.readbyqxmd.com/read/29453361/heterogeneity-and-mutation-in-kras-and-associated-oncogenes-evaluating-the-potential-for-the-evolution-of-resistance-to-targeting-of-kras-g12c
#7
Vincent L Cannataro, Stephen G Gaffney, Carly Stender, Zi-Ming Zhao, Mark Philips, Andrew E Greenstein, Jeffrey P Townsend
Activating mutations in RAS genes are associated with approximately 20% of all human cancers. New targeted therapies show preclinical promise in inhibiting the KRAS G12C variant. However, concerns exist regarding the effectiveness of such therapies in vivo given the possibilities of existing intratumor heterogeneity or de novo mutation leading to treatment resistance. We performed deep sequencing of 27 KRAS G12-positive lung tumors to determine the prevalence of other oncogenic mutations within KRAS or within commonly mutated downstream genes that could confer resistance at the time of treatment...
February 16, 2018: Oncogene
https://www.readbyqxmd.com/read/29452455/complex-hur-function-in-pancreatic-cancer-cells
#8
REVIEW
Jonathan R Brody, Dan A Dixon
Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers with dismal patient outcomes. The underlying core genetic drivers of disease have been identified in human tumor specimens and described in genetically engineered mouse models. These genetic drivers of PDAC include KRAS signaling, TP53 mutations, and genetic loss of the SMAD4 tumor suppressor protein. Beyond the known mutational landscape of PDAC genomes, alternative disrupted targets that extend beyond conventional genetic mutations have been elusive and understudied in the context of PDAC cell therapeutic resistance and survival...
February 16, 2018: Wiley Interdisciplinary Reviews. RNA
https://www.readbyqxmd.com/read/29452147/combination-of-kras-activation-and-pten-deletion-contributes-to-murine-hepatopancreatic-ductal-malignancy
#9
Yun-Kai Lin, Zheng Fang, Tian-Yi Jiang, Zheng-Hua Wan, Yu-Fei Pan, Yun-Han Ma, Yuan-Yuan Shi, Ye-Xiong Tan, Li-Wei Dong, Yong-Jie Zhang, Hong-Yang Wang
Kras mutations are among the most common genetic abnormalities in human neoplasms, including cholangiocarcinomas, pancreatic cancer and colon cancer. PTEN has previously been associated with cholangiocarcinoma development in murine models. Here, we have established novel mouse models of neoplasms by liver-specific and biliary-pancreatic Kras activation and PTEN deletion. By liver-specific disruption of PTEN and activation of Kras in mice caused rapid development of intrahepatic biliary epithelial proliferative lesions (Intrahepatic cholangiocarcinoma, ICC), which progress through dysplasia to invasive carcinoma...
February 13, 2018: Cancer Letters
https://www.readbyqxmd.com/read/29450716/could-ivim-and-adc-help-in-predicting-the-kras-status-in-patients-with-rectal-cancer
#10
Yanyan Xu, Qiaoyu Xu, Hongliang Sun, Tongxi Liu, Kaining Shi, Wu Wang
PURPOSE: To evaluate the diagnostic potential of DW-MRI relative parameters for differentiation of rectal cancers with different Kirsten rat sarcoma viral oncogene homologue (KRAS) mutation status. METHODS: Fifty-one patients with rectal cancer underwent diffusion-weighted MR imaging with eight b values. ADCs (including Max-ADC, Min-ADC and Mean-ADC) and IVIM parameters (D, pure diffusion; f, perfusion fraction; D*, pseudodiffusion coefficient) were respectively calculated by mono- and bi-exponential analysis...
February 15, 2018: European Radiology
https://www.readbyqxmd.com/read/29450468/activity-and-safety-of-cetuximab-plus-modified-folfoxiri-followed-by-maintenance-with-cetuximab-or-bevacizumab-for-ras-and-braf-wild-type-metastatic-colorectal-cancer-a-randomized-phase-2-clinical-trial
#11
Chiara Cremolini, Carlotta Antoniotti, Sara Lonardi, Giuseppe Aprile, Francesca Bergamo, Gianluca Masi, Roberta Grande, Giuseppe Tonini, Claudia Mescoli, Giovanni Gerardo Cardellino, Luigi Coltelli, Lisa Salvatore, Domenico Cristiano Corsi, Cristiana Lupi, Donatello Gemma, Monica Ronzoni, Emanuela Dell'Aquila, Federica Marmorino, Francesca Di Fabio, Maria Laura Mancini, Lorenzo Marcucci, Gabriella Fontanini, Vittorina Zagonel, Luca Boni, Alfredo Falcone
Importance: The combination of a triple-drug chemotherapy regimen with an anti-epidermal growth factor receptor (EGFR) agent as a first-line treatment of metastatic colorectal cancer (mCRC) showed promising activity along with safety concerns in single-arm phase 2 trials. The role of maintenance following chemotherapy and anti-EGFR and the optimal regimen to be adopted are not established. Objectives: To evaluate the activity and safety of cetuximab plus modified FOLFOXIRI (mFOLFOXIRI) and explore the role of maintenance with cetuximab or bevacizumab in RAS and BRAF wild-type mCRC...
February 15, 2018: JAMA Oncology
https://www.readbyqxmd.com/read/29449544/peak1-acting-as-a-tumor-promoter-in-colorectal-cancer-is-regulated-by-the-egfr-kras-signaling-axis-and-mir-181d
#12
Lanlan Huang, Chuangyu Wen, Xiangling Yang, Qiong Lou, Xiaoyan Wang, Jia Che, Junxiong Chen, Zihuan Yang, Xiaojian Wu, Meijin Huang, Ping Lan, Lei Wang, Aikichi Iwamoto, Jianping Wang, Huanliang Liu
PEAK1 is upregulated in multiple human malignancies and has been associated with tumor invasion and metastasis, but little is known about the role of PEAK1 in colorectal cancer (CRC) progression. We investigated the expression pattern, function and regulatory mechanisms of PEAK1 in CRC. Here, we found that PEAK1 is overexpressed in CRC tissues and that high PEAK1 expression predicts poor survival in colon cancer but not rectal cancer. Functionally, silencing PEAK1 inhibits cell proliferation, migration, and invasion in vitro and inhibits the growth of tumor xenografts in nude mice...
February 15, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29449271/targeted-therapies-for-targeted-populations-anti-egfr-treatment-for-egfr-amplified-gastroesophageal-adenocarcinoma
#13
Steven B Maron, Lindsay Alpert, Heewon A Kwak, Samantha Lomnicki, Leah Chase, David Xu, Emily O'Day, Rebecca J Nagy, Richard B Lanman, Fabiola Cecchi, Todd Hembrough, Alexa Schrock, John Hart, Shu-Yuan Xiao, Namrata Setia, Daniel V T Catenacci
Previous anti-EGFR trials in unselected gastroesophageal adenocarcinoma (GEA) patients were resoundingly negative. We identified EGFR amplification in 5% (19/363) of patients at the University of Chicago, including 6% (8/140) who were prospectively screened with intention-to-treat using anti-EGFR therapy. Seven pts received >1 dose of treatment: three first line FOLFOX plus ABT-806, one second line FOLFIRI plus cetuximab, and three third/fourth line cetuximab alone. Treatment achieved objective response in 58% (4/7) and disease control in 100% (7/7) with a median progression-free survival of 10 months...
February 15, 2018: Cancer Discovery
https://www.readbyqxmd.com/read/29449169/interaction-of-the-wnt-%C3%AE-catenin-and-ras-erk-pathways-involving-co-stabilization-of-both-%C3%AE-catenin-and-ras-plays-important-roles-in-the-colorectal-tumorigenesis
#14
REVIEW
Sang-Kyu Lee, Jeong-Ha Hwang, Kang-Yell Choi
Cancer development is usually driven by multiple genetic and molecular alterations rather than by a single defect. In the human colorectal cancer (CRC), series of mutations of genes are involved in the different stages of tumorigenesis. For example, adenomatous polyposis coli (APC) and KRAS mutations have been known to play roles in the initiation and progression of the tumorigenesis, respectively. However, many studies indicate that mutations of these two genes, which play roles in the Wnt/β-catenin and RAS-extra-cellular signal regulated kinase (ERK) pathways, respectively, cooperatively interact in the tumorigenesis in several different cancer types including CRC...
January 10, 2018: Advances in Biological Regulation
https://www.readbyqxmd.com/read/29449000/an-immunohistochemical-and-molecular-analysis-of-papillary-proliferation-of-the-endometrium
#15
Colin J R Stewart, Susan Bigby, Tino Giardina, Fabienne Grieu-Iacopetta, Benhur Amanuel
Papillary proliferations of the endometrium (PPEs) are uncommon lesions that are often associated with endometrial polyps. PPEs occasionally precede or co-exist with atypical endometrial hyperplasia or adenocarcinoma, but their pathogenesis and relationship to endometrial neoplasia is uncertain. In the present study 11 PPEs, including eight benign papillary proliferations (BPPs) and three complex papillary hyperplasias (CPHs) were examined immunohistochemically for expression of PAX2, BAF250a, p16, β-catenin and DNA mismatch repair (MMR) proteins...
February 12, 2018: Pathology
https://www.readbyqxmd.com/read/29447458/e-cadherin-loss-accelerates-tumor-progression-and-metastasis-in-a-mouse-model-of-lung-adenocarcinoma
#16
Kerstin W Sinkevicius, Kelly J Bellaria, Juliana Barrios, Patrizia Pessina, Manav Gupta, Christine Fillmore Brainson, Roderick T Bronson, Carla F Kim
Metastatic disease is the primary cause of death of lung cancer patients, but the mouse models of lung adenocarcinoma do not accurately recapitulate the tumor microenvironment or metastatic disease observed in patients. In this study, we conditionally deleted E-cadherin in an autochthonous lung adenocarcinoma mouse model driven by activated oncogenic Kras and p53 loss. Loss of E-cadherin significantly accelerated lung adenocarcinoma progression and decreased survival of the mice. Kras;p53;E-cadherin mice had a 41% lung tumor burden, invasive grade 4 tumors, and a desmoplastic stroma just 8 weeks after tumor initiation...
February 15, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29446257/utilization-of-direct-smears-of-thyroid-fine-needle-aspirates-for-ancillary-molecular-testing-a-comparison-of-two-proprietary-testing-platforms
#17
Kristen L Partyka, Melissa L Randolph, Karen A Lawrence, Harvey Cramer, Howard H Wu
BACKGROUND: Ancillary molecular testing has been recommended for thyroid fine-needle aspirates (FNA) with indeterminate cytologic diagnoses. Rosetta Genomics and Interpace Diagnostics have developed assays that can utilize direct smears as the testing substrate. METHODS: A retrospective study of indeterminate thyroid FNAs with known histologic follow-up was performed. One Diff-Quik-stained smear and one Papanicolaou-stained smear with similar cellularity (at least 60-100 lesional cells) from each case were sent to Rosetta and Interpace, respectively, for analysis...
February 15, 2018: Diagnostic Cytopathology
https://www.readbyqxmd.com/read/29445180/myeloid-derived-interleukin-1%C3%AE-drives-oncogenic-kras-nf-%C3%AE%C2%BA%C3%AE-addiction-in-malignant-pleural-effusion
#18
Antonia Marazioti, Ioannis Lilis, Malamati Vreka, Hara Apostolopoulou, Argyro Kalogeropoulou, Ioanna Giopanou, Georgia A Giotopoulou, Anthi C Krontira, Marianthi Iliopoulou, Nikolaos I Kanellakis, Theodora Agalioti, Anastasios D Giannou, Celestial Jones-Paris, Yoichiro Iwakura, Dimitrios Kardamakis, Timothy S Blackwell, Stavros Taraviras, Magda Spella, Georgios T Stathopoulos
Malignant pleural effusion (MPE) is a frequent metastatic manifestation of human cancers. While we previously identified KRAS mutations as molecular culprits of MPE formation, the underlying mechanism remained unknown. Here, we determine that non-canonical IKKα-RelB pathway activation of KRAS-mutant tumor cells mediates MPE development and this is fueled by host-provided interleukin IL-1β. Indeed, IKKα is required for the MPE-competence of KRAS-mutant tumor cells by activating non-canonical NF-κB signaling...
February 14, 2018: Nature Communications
https://www.readbyqxmd.com/read/29444439/differential-effector-engagement-by-oncogenic-kras
#19
Tina L Yuan, Arnaud Amzallag, Rachel Bagni, Ming Yi, Shervin Afghani, William Burgan, Nicole Fer, Leslie A Strathern, Katie Powell, Brian Smith, Andrew M Waters, David Drubin, Ty Thomson, Rosy Liao, Patricia Greninger, Giovanna T Stein, Ellen Murchie, Eliane Cortez, Regina K Egan, Lauren Procter, Matthew Bess, Kwong Tai Cheng, Chih-Shia Lee, Liam Changwoo Lee, Christof Fellmann, Robert Stephens, Ji Luo, Scott W Lowe, Cyril H Benes, Frank McCormick
KRAS can bind numerous effector proteins, which activate different downstream signaling events. The best known are RAF, phosphatidylinositide (PI)-3' kinase, and RalGDS families, but many additional direct and indirect effectors have been reported. We have assessed how these effectors contribute to several major phenotypes in a quantitative way, using an arrayed combinatorial siRNA screen in which we knocked down 41 KRAS effectors nodes in 92 cell lines. We show that every cell line has a unique combination of effector dependencies, but in spite of this heterogeneity, we were able to identify two major subtypes of KRAS mutant cancers of the lung, pancreas, and large intestine, which reflect different KRAS effector engagement and opportunities for therapeutic intervention...
February 13, 2018: Cell Reports
https://www.readbyqxmd.com/read/29443392/spatial-aspects-of-oncogenic-signaling-determine-response-to-combination-therapy-in-slice-explants-from-kras-driven-lung-tumors
#20
Katja Närhi, Ashwini S Nagaraj, Elina Parri, Riku Turkki, Petra W van Duijn, Annabrita Hemmes, Jenni Lahtela, Virva Uotinen, Mikko I Mäyränpää, Kaisa Salmenkivi, Jari Räsänen, Nina Linder, Jan Trapman, Antti Rannikko, Olli Kallioniemi, Taija Af Hällström, Johan Lundin, Wolfgang Sommergruber, Simon Anders, Emmy W Verschuren
A key question in precision medicine is how functional heterogeneity in solid tumors informs therapeutic sensitivity. We demonstrate that spatial characteristics of oncogenic signaling and therapy response can be modeled in precision-cut slices from Kras-driven non-small cell lung cancer (NSCLC) of varying histopathologies. Unexpectedly, profiling of in situ tumors demonstrates that signaling stratifies mostly according to histopathology, showing enhanced AKT and SRC activity in adenosquamous carcinoma (ASC), and MAPK activity in adenocarcinoma (AC)...
February 14, 2018: Journal of Pathology
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