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Journal articles on the topic 'Kral y Ma'

Author: Grafiati

Published: 4 June 2021

Last updated: 29 July 2025

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1

Maroli, Sree Lakshmi Velandi, Roman E. Reggiardo, Reem Khojah, and Daniel H. Kim. "Abstract LB_B21: Extracellular RNA signatures of mutant KRAS-driven lung cancer." Molecular Cancer Therapeutics 22, no. 12_Supplement (2023): LB_B21. http://dx.doi.org/10.1158/1535-7163.targ-23-lb_b21.

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Abstract RAS genes are the most frequently mutated oncogenes in cancer, yet the effects of oncogenic RAS signaling on the noncoding transcriptome remain unclear. We analyzed the transcriptomes of human airway and bronchial epithelial cells transformed with mutant KRAS to define the landscape of KRAS-regulated noncoding RNAs. We find that oncogenic KRAS signaling upregulates noncoding transcripts throughout the genome, many of which arise from transposable elements (TEs). These TE RNAs exhibit differential expression and are regulated by KRAB zinc-finger (KZNF) genes, which are broadly downregu

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2

Ben-Ammar, Imen, Michel Ducreux, Valérie Boige, et al. "KRAS WT pancreatic adenocarcinomas: Another disease?" Journal of Clinical Oncology 41, no. 4_suppl (2023): 750. http://dx.doi.org/10.1200/jco.2023.41.4_suppl.750.

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750 Background: KRAS mutation is the most common molecular alteration (MA) in pancreatic adenocarcinoma (PDAC), and only 8-10% of patients (pts) harbor KRAS wild-type tumors (WT). This study describes clinical and molecular features of KRAS WT PDAC and compares it to mutant KRAS (m KRAS) PDAC. Methods: A retrospective chart review of clinical/molecular data was performed on all pts with PDAC who had contributive molecular profile at Gustave Roussy. KRAS status was determined on tumor molecular profiling as part of routine care using an in-house panel or Foundation Medicine NGS either on tissue

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3

Al- Islamiyah, Suwaibah, and Diah Sudiarti. "Meningkatkan Hasil Belajar Siswa melalui Model Pembelajaran Inquiry dengan Menggunakan Metode Eksperimen pada Pokok Bahasan Pencemaran Lingkungan Kelas X (Putri) Tahun Pelajaran 2016/2017." JURNAL BIOSHELL 8, no. 2 (2021): 65–69. http://dx.doi.org/10.36835/bio.v8i2.919.

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Penelitian merupakan kegiatan utama dari proses pendidikan. Peneliti melakukan penelitian di kelas X (putri) MA Bustanul Ulum Krai-Yosowilangun-Lumajang dengan responden yang diteliti sebanyak 19 siswa Putri. Peneliti melakukan observasi di kelas X (putri) MA Bustanul Ulum Krai-Yosowilangun dan diperoleh data sekitar 75 % menunjukkan nilai siswa ≤70. Prosedur yang digunakan adalah model siklus berdasarkan hasil penelitian, persentase hasil belajar pada siklus I mencapai 38,131 dan siklus II mencapai hingga 44,605 sedangkan untuk melihat persentase hasil belajar siklus I mencapai 68,421% dan si

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4

Yang, Liu, Yue Cai, Jianwei Zhang, et al. "Colorectal cancer with mucinous component compared to clinicopathological and molecular features as mucinous adenocarcinoma." Journal of Clinical Oncology 35, no. 15_suppl (2017): e15166-e15166. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.e15166.

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e15166 Background: CRC can be divided into 3 groups: regular adenocarcinoma (RA), mucinous adenocarcinoma (MA), and adenocarcinoma with mucinous component (MC, mucin formation <50 % ). MA is distinct from RA, however, little is known about MC. We aimed to compare the clinicopathological and genetic features of 3 groups. Methods: A retrospective chort of consecutive CRC patients with available gene status was enrolled. KRAS,NRAS,BRAF,PIK3CA gene, MSI(IHC method) status were analyzed. Results: A total of 1454 patients were enrolled, including 1179 RA, 106 MA and 169 MC. Similar to MA, MC pati

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5

Nurindah Lailatul Fitriana, Leni, and Muawanah. "IMPLEMENTASI KURIKULUM DARURAT COVID-19 DI MA HIDAYATUL HUSNA BUTUH KRAS KEDIRI." Al-Hasanah : Jurnal Pendidikan Agama Islam 7, no. 2 (2022): 222–44. http://dx.doi.org/10.51729/7274.

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Masa pandemi yang terjadi pada tahun 2020 akibat merebaknya virus Covid-19 telah mengancam di berbagai dunia, terutama di wilayah Indonesia. Menyebabkan perubahan yang besar dalam tatanan kehidupan, kondisi sosial tidak terkecuali pada dunia pendidikan. Program-program yang telah dirancang oleh satuan pendidikan sebagai panduan dalam pelaksanaan kegiatan pembelajar, mau tidak mau harus berubah. Dengan kondisi pandemi covid-19, pemerintah juga mengeluarkan instrukti yaitu melarang masyarakat untuk melakukan aktivitas berkerumun dan kegiatan yang mendatangkan masa. Sehingga hal tersebut berdampa

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6

Rodriguez Freixinos, Victor, Fiorella Ruiz-Pace, Lorena Fariñas-Madrid, et al. "Impact of genomic heterogeneity on PI3K/AKT/mTOR inhibitors (PAMi) efficacy in gynecologic cancer (GYN) patients (pts)." Journal of Clinical Oncology 35, no. 15_suppl (2017): 5569. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.5569.

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5569 Background: Aberrant PI3K/AKT/mTOR activation is common in GYN. Predictive biomarkers to PAMi in GYN have yet to be identified. Methods: Advanced GYN pts with available genomic data, treated with PAMi in phase I/II clinical trials were selected. Mutation (mut) allele fractions (MAFs) were corrected for tumor purity and defined as clonal (cl) (≥ 0.4) or subclonal (scl) ( < 0.4). PAMi efficacy: (i) time to progression (TTP); (ii) clinical benefit rate (CBR: complete/partial response or stable disease > 4 months [m]); and (iii) ratio TTP on PAMi/ TTP on non-standard chemotherapy pre- o

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7

Łonyszyn, Przemysław. "Kraj Basków – sytuacja gospodarcza i polityka rozwoju." Rozwój Regionalny i Polityka Regionalna, no. 20 (August 30, 2012): 21–36. https://doi.org/10.14746/rrpr.2012.20.04.

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Gdy w Polsce lansuje się obraz gospodarki Kraju Basków jako modelowej, okazuje się, że niewiele o niej wiadomo. Niniejszy artykuł ma na celu prezentację i analizę fenomenu baskijskiej ekonomii, która łącząc tradycję i nowoczesność, potrafiła poradzić sobie ze światowym kryzysem, stając się prawdziwą „zieloną wyspą” na terenie Królestwa Hiszpanii z bezrobociem najniższym w kraju. Przedstawiono podstawowe filary (spółdzielczość, parki technologiczne, klastry), na których Baskowie oparli swój rozwój gospodarczy, a także plany międzysektorowego rozwoju.

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8

Kouznetsova, Ekaterina, Lauren McCauley, Elaine Steinke-Neal, et al. "Abstract 2987: A versatile assay suite for the discovery of new KRAS pathway inhibitors." Cancer Research 82, no. 12_Supplement (2022): 2987. http://dx.doi.org/10.1158/1538-7445.am2022-2987.

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Abstract The small GTPase, KRAS, is a known oncogene and a desirable drug target due to prevalence of mutations with poor disease prognosis. The absence of good druggable binding pockets has made modulator compound discovery challenging and unsuccessful. Identification of new inhibitor target sites has led to the resurgence of interest in KRAS drug discovery. To facilitate drug discovery activities targeting KRAS/MAPK pathway, we have produced the full spectrum of pathway proteins including kinases, wild type and mutated KRAS, guanine nucleotide exchange factor and effectors. This poster will

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9

Smolenschi, Cristina, Marine Valery, Alice Boileve, et al. "Is liquid biopsy useful in patients with GI malignancies and exclusive peritoneal disease?" Journal of Clinical Oncology 41, no. 4_suppl (2023): 809. http://dx.doi.org/10.1200/jco.2023.41.4_suppl.809.

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809 Background: Peritoneal carcinomatosis (PC) is a common manifestation in gastro-intestinal (GI) cancers.10-20 % of patients (pts) will present isolated, unresectable peritoneal disease with poor prognosis. In the past years, circulating tumor DNA (ctDNA) has emerged as a novel and less invasive biomarker for molecular diagnosis and disease monitoring. We aimed to evaluate the ability of PC to shed ctDNA into circulation in a cohort of pts with GI cancers and isolated PC treated in our institution. Methods: We reviewed retrospectively the results of liquid biopsies obtained at progression or

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10

Goldstein, Daniel A., Julia Andrea Elvin, Kai Wang, et al. "Comprehensive genomic profiling of cancer of the appendix to reveal new routes to targeted therapies." Journal of Clinical Oncology 33, no. 3_suppl (2015): 608. http://dx.doi.org/10.1200/jco.2015.33.3_suppl.608.

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608 Background: Cancers of the appendix are rare forms of malignancy that include two major mucin producing tumors, mucinous adenocarcinoma (MA) and goblet cell carcinoid (GCC). There is no clear standard of care for management of these malignancies. We queried whether comprehensive genomic profiling (CGP) of MA and GCC would reveal differences in the pattern of genomic alterations (GA) of these two subtypes of appendiceal cancer and serve as a guide for targeted therapies for this disease. Methods: DNA was extracted from 40 microns of FFPE sections from 20 clinically advanced appendiceal carc

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Shiekh, Laiba, Matthew Cheung, Linyuhui Zheng, et al. "Abstract C017: Targeting KRAS selectively induce metabolic reprogramming in pancreatic cancer." Cancer Research 84, no. 17_Supplement_2 (2024): C017. http://dx.doi.org/10.1158/1538-7445.pancreatic24-c017.

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Abstract Pancreatic ductal adenocarcinoma (PDAC) is a lethal disease largely due to the lack of effective treatments that overcome the tumor drug resistance. Oncogenic KRAS mutation contribute to most PDAC and drive multiple metabolic pathways to promote tumor growth. Despite this overarching role of KRAS, inhibition of KRAS/MAPK pathway often lead to resistance by yet unclear mechanism. Here we find that the pharmacological inhibition of KRAS/MAPK pathway induces distinct responses in various pancreatic cancer cells. Specifically, while KRAS/MAPK inhibition suppressed growth in some cells, th

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12

Li, Chendi, Jeremy Chang, Christopher J. Graser, et al. "Abstract B081: Aurora kinase A inhibition overcomes adaptive resistance to KRAS G12C inhibitor by G1-checkpoint induced apoptosis in KRAS non-small cell lung cancer." Molecular Cancer Therapeutics 22, no. 12_Supplement (2023): B081. http://dx.doi.org/10.1158/1535-7163.targ-23-b081.

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Abstract Cancer cells gain drug-tolerant states and evade therapy. In response to KRAS G12C inhibitor (G12Ci), KRAS mutant non-small cell lung cancer (NSCLC) cells maintain a drug-tolerant state by aurora kinase A (AURKA). AURKA can phosphorylate c-Raf to maintain new KRAS signaling, however, how AURKA becomes activated to cause KRAS G12Ci resistance is unclear. We show here that KRAS G12C + AURKA inhibition cause synthetic lethality in KRAS G12C NSCLC cells. LY3499446 (KRAS G12Ci) and LSN3321213 (aurora kinase A inhibitor) induced apoptosis that is independent of inhibited MAPK reactivation.

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13

Der, Channing J. "Abstract IA-05: Targeting KRAS for pancreatic cancer treatment." Cancer Research 84, no. 17_Supplement_2 (2024): IA—05—IA—05. http://dx.doi.org/10.1158/1538-7445.pancreatic24-ia-05.

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Abstract The approval of clinically effective inhibitors for KRAS G12C mutant non-small cell lung cancers in 2021 and 2022 marks a significant milestone in anti-KRAS oncogene drug discovery. This success has fueled intense efforts to develop inhibitors targeting additional KRAS mutations. However, primary and treatment-associated acquired resistance limit the depth and duration of efficacy of KRAS G12C selective and likely other KRAS inhibitors. Thus, a major challenge moving forward will be the elucidation of mechanisms of resistance to then guide development of effective combination anti-KRA

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14

Bhamra, Inder, Helen Mason, Simon Woodcock, et al. "Abstract A101: Novel KRAS inhibitors suppress MAPK pathway signalling and display potent anti-proliferative activity across a broad range of KRAS mutant cell lines." Molecular Cancer Therapeutics 22, no. 12_Supplement (2023): A101. http://dx.doi.org/10.1158/1535-7163.targ-23-a101.

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Abstract KRAS is the most frequently mutated oncogene across different cancer types. Redx Pharma are developing novel, orally bioavailable, small molecule inhibitors of KRAS. These compounds display activity against a broad spectrum of the most frequently occurring KRAS mutations whilst maintaining selectivity over NRAS and HRAS protein isoforms. Isoform selective multi-KRAS inhibitors were identified using biochemical SOS1-independent nucleotide exchange assays (NEA) and validated by surface plasmon resonance (SPR) spectroscopy. Compounds of interest were the further triaged using relevant ca

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15

Shen, Jiao, Blake E. Smith, Winiffer Conce Alberto, et al. "Abstract C020: Identification of KRAS-specific TCRs from human peripheral blood." Cancer Research 84, no. 17_Supplement_2 (2024): C020. http://dx.doi.org/10.1158/1538-7445.pancreatic24-c020.

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Abstract Mutant KRAS is the predominant driver oncogene in pancreatic cancer accounting for approximately 90% of KRAS mutations. However, these mutant KRAS peptides exhibit weak binding affinity to most human leukocyte antigens (HLAs), impeding their recognition by the immune system and the subsequent generation of a corresponding T cell response. Identification of KRAS-mutant specific T cells would be useful to track tumor-specific T cell responses in patients and could also be used for adoptive transfer of TCR-transduced cells. Current efforts to identify KRAS-specific T cells have been limi

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16

Ergashev, Asqar Jong'oboyevich, Madina Ravshan qizi Tojiboyeva, and Mohichehra Rustam qizi Erkaboyeva. "AYOLLARDA KO'KRAK BEZI SARATONI KASALLIGI." Educational Research in Universal Sciences 3, no. 12 (2024): 292–99. https://doi.org/10.5281/zenodo.14499458.

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<em>Ushbu maqolada<strong> </strong></em><em>ko‘krak    bezi  saratoni  - ayollar   orasida   eng   keng    tarqalgan   onkologik    kasalliklardan    biri bo‘lib u</em><em>    ko‘krak   bezining     hujayralari    o‘sib,   nazoratsiz   ravishda    ko‘payishi    natijasida    rivojlananishi xaqida ma’</em><em>lumotlar berilga</

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17

Maddess, Matthew L., David L. Sloman, Xiaoshen Ma, et al. "Abstract B074: Discovery of MK-1084, a low dose selective clinical stage KRAS G12C inhibitor." Molecular Cancer Therapeutics 22, no. 12_Supplement (2023): B074. http://dx.doi.org/10.1158/1535-7163.targ-23-b074.

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Abstract KRAS mutations are the predominant oncogenic drivers in multiple indications including non-small cell lung carcinoma (NSCLC), colorectal carcinoma (CRC) and pancreatic ductal adenocarcinoma (PDAC). KRAS has long been considered a challenging target due to the perceived lack of druggable binding pockets and high flexibility of the protein. However, recent progress in discovering and developing covalent inhibitors against the GDP-loaded form of G12C mutant KRAS has provided a strategy for targeting mutant-specific KRAS as the cysteine residue in the switch II pocket offers a handle for

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Von Hoff, Daniel D., Ramesh K. Ramanathan, Douglas B. Evans, et al. "Actionable targets in pancreatic cancer detected by immunohistochemistry (IHC), microarray (MA) fluorescent in situ hybridization (FISH), and mutational analysis." Journal of Clinical Oncology 30, no. 15_suppl (2012): 4013. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.4013.

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4013 Background: A great need exists for new therapeutic approaches for patients with pancreatic cancer. Methods: The study cohort included 1029 patients analyzedfor a.) up to 29 different immunohistochemical biomarkers – (e.g., COX-2, MGMT, PGP, RRM1, TOPOI, TOPOII, SPARC etc.)b.); in up to 450 patients’ specimens a whole genome expression analysis was performed using HumanHT-12 v4 beadChips ( Illumina Inc.,San Diego, CA) c.) in up to 695 patients FISH for c-Myc, EGFR, HER2 and TOPO2A gene copy amplifications; and d.) in up to 783 patients sequencing for KRAS, EGFR, PI3CA and BRAF, was perfor

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Wan, Yong, Haiqing Ma, and Jianghong Wu. "Abstract 6049: Cell-based PROTAC screening for cancer drug discovery." Cancer Research 84, no. 6_Supplement (2024): 6049. http://dx.doi.org/10.1158/1538-7445.am2024-6049.

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Abstract Proteolysis-Targeting Chimeras (PROTACs) have emerged as a promising strategy for selectively degrading specific target proteins, thereby offering a novel approach to precision cancer therapy. Among the most notable oncogenes, KRAS with the G12C mutation is responsible for 45%-50% of KRAS mutations in non-small cell lung carcinomas. Additionally, BRD4, a well-studied member of the Bromo- and Extra-Terminal (BET) protein family, is implicated in various hematological and solid tumors. The implementation of cell-based screening for PROTACs targeting either KRAS(G12C) or BRD4 represents

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Willard, Melinda D., Emily Nash Nash Smyth, Ramon Velasquez Tiu, et al. "Genomic characterization of lung tumors and metastatic (Met) sites in advanced (Adv) NSCLC." Journal of Clinical Oncology 37, no. 15_suppl (2019): 2014. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.2014.

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2014 Background: Molecular alterations (MA) found in brain (Br) mets of NSCLC pts can differ from primary and/or other met sites, which may explain why therapies targeting primary tumors are less effective at preventing and treating intracranial disease. We analyzed the frequency of known driver genes in adv NSCLC pts and the association with overall survival (OS). Methods: This retrospective observational study identified pts from the Flatiron- Foundation Medicine NSCLC Clinico-Genomic Database who were diagnosed with adv NSCLC from 1 Jan 2011 to 31 Oct 2017 and had tumor tissue analyzed at a

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Rizqi Maulidah, Azizah Nurdin, Rahadi Arie Hartoko, Fhirastika Annisa Helvian, and Zulfahmi Alwi. "Hubungan Tingkat Stres dengan Kejadian Dismenore Primer pada Siswi SMA/MA di Makassar." Alami Journal (Alauddin Islamic Medical) Journal 9, no. 1 (2025): 21–28. https://doi.org/10.24252/alami.v9i1.50203.

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Dismenore adalah kondisi yang dirasakan wanita pada saat menstruasi yang menimbulkan nyeri perut yang mengganggu aktivitas. Berdasarkan teori, stres bisa meningkatkan risiko kram menstruasi. Seseorang mengalami stres ketika dihadapkan pada kejadian atau kondisi yang dapat membahayakan atau mengganggu kemampuannya untuk mengendalikannya. Prevalensi kejadian dismenore menurut WHO, dismenore dialami oleh 50% remaja di setiap negara. Penelitian ini bertujuan untuk meneliti hubungan tingkat stres dengan kejadian dismenore primer pada siswi SMA di Makassar. Metode yang digunakan adalah cross-section

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22

Avilés, Yanixa Quiñones, Jaffarguriqbal Singh, Wenxue Li, Yong Kong, Yansheng Liu, and Mandar Deepak Muzumdar. "Abstract B063: Differential pathway engagement and the biological consequences of KRAS variants in cancer." Cancer Research 82, no. 22_Supplement (2022): B063. http://dx.doi.org/10.1158/1538-7445.panca22-b063.

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Abstract KRAS is a proto-oncogene found mutated in &gt;90% of pancreatic ductal adenocarcinomas (PDAC) and encodes for a GTPase that mediates signaling transduction through the mitogen-activated protein kinase (MAPK) and PI3K/AKT pathways. Mutations in amino acids G12, G13, and Q61 prevent its inactivation by regulatory GTPase-activating proteins (GAPs), resulting in its constitutive activation. Previous work indicates that KRAS mutants possess unique biochemical differences that could result in divergent allele-specific signaling networks, underscoring unique vulnerabilities and response

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Acosta Eyzaguirre, D. A., H. Verdaguer, E. Buxò, et al. "1549P Molecular alterations (MA) with potential therapeutic implications in KRAS wild-type (WT) pancreatic cancer patients." Annals of Oncology 31 (September 2020): S948. http://dx.doi.org/10.1016/j.annonc.2020.08.2032.

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24

Ge, Xiangyu, Christian F. Ruiz, Wenxue Li, Yanixa Quiñones-Avilés, and Mandar Deepak Muzumdar. "Abstract B056: Wild-type RAS/MAPK signaling complexes mediate adaptive resistance to KRAS inhibition in PDAC." Cancer Research 82, no. 22_Supplement (2022): B056. http://dx.doi.org/10.1158/1538-7445.panca22-b056.

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Abstract Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal malignancy and predicted to be the second most common cause of death in the US within the next decade. A striking hallmark of PDAC is the presence of activating KRAS mutations in &gt;90% of all cases. Studies in animal models and cell lines have suggested that oncogenic KRAS is important for both the initiation and progression of PDAC, making KRAS an attractive target for therapy. Recent FDA approvals of KRAS mutant-specific inhibitors has advanced the clinical treatment of patients with cancers harboring mutant KRAS, yet

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25

Zhan, Di, Lingling Huang, Lei Zhang, et al. "Abstract 5501: An integrated end-to-end platform facilitating the evaluation of next generation KRAS inhibitors." Cancer Research 85, no. 8_Supplement_1 (2025): 5501. https://doi.org/10.1158/1538-7445.am2025-5501.

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Abstract Kirsten rat sarcoma viral oncogene homologue (KRAS) is the most frequently mutated oncogene, and has attracted substantial attention in the preclinical arena. Over the last 40 years, KRAS has been deemed a challenging therapeutic target and has even been described as “undruggable” due to the intrinsic characteristics of KRAS proteins. This has resulted in an urgent and unmet clinical need to target KRAS mutations in KRAS-driven cancer. Recent advances have uncovered a new allosteric site of KRAS (G12C) that facilitates the development of novel covalent allosteric inhibitors targeting

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Lakhavath, Balakrishna, Manoj Pothuganti, Githavani Kummari, Hemasankar Pathange, Rajan Sekar, and Srikant Viswanadha. "Abstract A099: Best in class, potent, SOS1 inhibitors demonstrate single agent activity in preclinical models of KRAS driven tumors." Molecular Cancer Therapeutics 22, no. 12_Supplement (2023): A099. http://dx.doi.org/10.1158/1535-7163.targ-23-a099.

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Abstract KRAS is an oncogene implicated in a wide variety of tumors (~21% of solid tumors harbor KRAS mutations). Interaction of KRAS with its predominant Guanine Exchange Factor (GEF), SOS1, is crucial for activation of KRAS and further KRAS mediated oncogenic signaling. Thus, pharmacological inhibition of SOS1 is expected to be effective in treating RAS driven cancers. Biochemical potency of compounds was confirmed in a SOS1 mediated FRET based guanine exchange factor (GEF) assay. Multiple potent SOS1 inhibitors were identified with potencies in the low double digit nanomolar range. Selectiv

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27

Kwieciński, Adam. "Przegląd orzecznictwa Europejskiego Trybunału Praw Człowieka w sprawach polskich z zakresu prawa karnego wykonawczego." Przegląd Prawa i Administracji 120 (June 30, 2020): 125–33. http://dx.doi.org/10.19195/0137-1134.120.57.

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Niniejsze opracowanie poświęcone jest prezentacji wyroków Europejskiego Trybunału Praw Człowieka w sprawach polskich z przestrzeni prawa karnego wykonawczego. Sprawy tego rodzaju należą bowiem do najczęściej kierowanych do organów strasburskich. Stan taki ma miejsce w zasadzie od początku, odkąd nasz kraj poddał się jurysdykcji Trybunału. Orzeczenia Trybuna-łu w tym zakresie służą nie tylko rozstrzygnięciu konkretnej sprawy, lecz wyznaczają standard po-stępowania z osobami, wobec których wykonywane są orzeczenia w sprawach karnych, najczęściej skutkujących pozbawieniem wolności.

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Xusanov, K.X., and M.Sh. Аxrorov. "PANDEMIYALAR DAVRIDA TIBBIY TASVIRLARNI TAHLIL QILISH UCHUN SUN'IY INTELLEKTGA ASOSLANGAN USULLARNING MUKAMMAL SHARHI." Multidisciplinary Journal of Science and Technology 4, no. 12 (2024): 536–48. https://doi.org/10.5281/zenodo.14536321.

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Covid-19 pandemiyasi tezkor diagnostika zaruratini ochib berdi. Sun'iy intellekt (ai) tibbiy tasvirlarni tahlil qilishda, xususan, ko‘krak qafasi rentgenografiyasi, kt va o‘pka ultratovushida muhim vositaga aylandi. Ushbu maqolada mashinaviy o‘qitish, chuqur o‘qitish, transfer o‘qitish va gibrid yondashuvlar sohasidagi so‘nggi yutuqlar ko‘rib chiqilib, asosiy hissalar, ma’lumotlar to‘plamlari, muammolar va kelajakdagi yo‘nalishlar ta’kidlanadi.

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29

Vallejo, Lourdes Prieto, Chandrasekar Iyer, Noelle Goggin, et al. "Abstract B116: Preclinical characterization of orally bioavailable, highly potent pan-KRAS inhibitors with selectivity over HRAS and NRAS." Molecular Cancer Therapeutics 22, no. 12_Supplement (2023): B116. http://dx.doi.org/10.1158/1535-7163.targ-23-b116.

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Abstract KRAS is altered in ~16% of all cancers and is an oncogenic driver in non-small cell lung, pancreatic, colorectal, and other cancers. Next generation KRAS inhibitors designed to target multiple oncogenic KRAS mutations, while simultaneously sparing wild-type (WT) HRAS and NRAS inhibition, are expected to offer expanded activity and favorable safety. We have discovered a series of highly potent and selective pan-KRAS inhibitors with activity against KRAS G12C, G12D, and G12V mutants, that also display high selectivity over WT HRAS and NRAS, thus providing an expanded therapeutic index.

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Kouznetsova, Ekaterina, Lauren S. McCauley, Rebecca Eells, et al. "Abstract 2624: Assay toolkit for the discovery of new RAS pathway inhibitors." Cancer Research 83, no. 7_Supplement (2023): 2624. http://dx.doi.org/10.1158/1538-7445.am2023-2624.

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Abstract The small GTPase KRAS is a known oncogene that is very frequently mutated in a variety of cancers. Over the past several years, there has been a resurgence of interest in KRAS drug discovery following the identification of new inhibitor target sites and several molecules entering clinical trials. We have produced proteins and set up assays for a large collection of Ras variants, guanine nucleotide exchange factors and effectors to facilitate drug discovery activities targeting KRAS/MAPK pathway. RBC’s extensive kinase assay portfolio enables identification of kinase inhibitors downstr

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Odilova, Yorqinoy Kozimjon qizi, та Anvar Tursunboyevich Axmedov. "AYOLLARDA KOʻKRAK BEZI SARATONI KASALLIKLARI". Universal International Scientific Journal 2, № 4 (2025): 157–66. https://doi.org/10.5281/zenodo.15274909.

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Ko‘krak bezi saratoni ayollar orasida global miqyosda eng keng tarqalgan onkologik kasalliklardan biri bo‘lib, O‘zbekistonda ham sog‘liqni saqlash tizimida muhim muammo sanaladi. Ushbu maqola ko‘krak bezi saratonining epidemiologiyasi, etiologik omillari, diagnostika usullari va davolashning zamonaviy yondashuvlarini ilmiy asosda tahlil qiladi. Ma’lumotlarga ko‘ra, O‘zbekistonda 2020-yilda 4454 yangi holat qayd etilgan bo‘lib, kasallikning erta aniqlanishi va davolash samaradorligi skrining dasturlari va genetik testlarning joriy etilishi b

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Lisczyk, Karolina. "Szanujący się dziennikarz, kraj, film... O wybranych użyciach imiesłowu szanujący się we współczesnej polszczyźnie." Prace Językoznawcze 24, no. 3 (2022): 45–60. http://dx.doi.org/10.31648/pj.7909.

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Cel artykułu stanowi próba odpowiedzi na pytanie o to, co użytkownicy polszczyzny mająna myśli, używając imiesłowu szanujący się. Badaniom poddano 3358 zawierającychgo zdań zaczerpniętych z korpusu monitorującego MoncoPL. Materiał podzielonona jedenaście grup, wyodrębnionych ze względu na łączliwość badanego imiesłowuz rzeczownikami o określonym znaczeniu. Na podstawie analiz stwierdzono, że szanującysię jest wykładnikiem stereotypizacji i w pewnych użyciach ma kontekstowe znaczenietakie samo, jak przymiotniki typowy i dobry.

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Lin, Qingxiang (Nick), Alvin Morales, Haley Barnes, and Ryan Bruce Corcoran. "Abstract C012: Overcoming Cell Subtype-Specific Adaptive Resistance to KRAS G12D Inhibition in KRAS G12D-Mutant Pancreatic Cancer." Cancer Research 84, no. 17_Supplement_2 (2024): C012. http://dx.doi.org/10.1158/1538-7445.pancreatic24-c012.

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Abstract Background: Pancreatic ductal adenocarcinoma (PDAC) has a 5-year survival rate of only 12%, with limited treatment options. Oncogenic KRAS mutations drive PDAC tumor progression, which occur in the majority of PDAC tumors. KRAS G12D is the most common KRAS mutation, found in 36% of PDAC cases, which is associated with the worst clinical outcomes. Mutant-selective KRAS G12D inhibitors (KRASi G12D), such as MRTX1133, have recently demonstrated initial responses in KRAS G12D-mutant preclinical models. However, mechanisms of adaptive resistance to KRAS G12D inhibition are largely under-in

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Bonilla, Monica E. "Abstract C067: Understanding the tumor extrinsic role of oncogenic Kras in pancreatic cancer." Cancer Research 82, no. 22_Supplement (2022): C067. http://dx.doi.org/10.1158/1538-7445.panca22-c067.

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Abstract Pancreatic ductal adenocarcinoma (PDA) is a lethal disease with a 5-year survival rate of 10.8%. Most patients present with locally advanced or metastatic disease which is refractory to therapy. Even when surgical resection is possible, relapse is frequent. Thus, there is a need to understand relapse and treatment resistance in pancreatic cancer to develop more effective treatments. Oncogenic KRAS is a driving mutation in PDA. Work in mouse models demonstrated that oncogenic KRAS drives the initiation of pancreatic cancer. Further, our group and others showed that oncogenic KRAS is re

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Iyer, Chandrasekar, Binghui Li, Trent R. Stewart, et al. "Abstract B115: Preclinical characterization of LY3962673, an orally bioavailable, highly potent, and selective KRAS G12D inhibitor." Molecular Cancer Therapeutics 22, no. 12_Supplement (2023): B115. http://dx.doi.org/10.1158/1535-7163.targ-23-b115.

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Abstract KRAS G12D mutations are activating oncogenic events that occur in approximately 35%, 13%, and 4% of pancreatic, colorectal, and non-small cell lung cancers, respectively and less commonly in other cancers. Here, we describe LY3962673, a highly potent inhibitor of KRAS G12D that is selective against wild-type (WT) KRAS and orally bioavailable. Compound potency and selectivity were measured using surface plasmon resonance (SPR) and cell-based assays monitoring the inhibition of pERK (Thr202/Tyr204) and cell growth. In SPR assays, LY3962673 had Kd values of 0.058 and 4.7 nM for GDP-bound

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Ottaiano, Alessandro, Nicola Normanno, Sergio Facchini, et al. "Study of Ras Mutations’ Prognostic Value in Metastatic Colorectal Cancer: STORIA Analysis." Cancers 12, no. 7 (2020): 1919. http://dx.doi.org/10.3390/cancers12071919.

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Background: Colorectal cancer (CRC) is the second most common cause of cancer-specific death in both sexes in Western countries. KRAS mutations occur in about 50% of metastatic CRCs (mCRCs). The prognostic value of specific KRAS mutations still remains unexplored and unclear. Methods: Two hundred and forty KRAS wild-type and 206 KRAS/NRAS mutant consecutive unresectable mCRC patients with PS Eastern Cooperative Oncology Group (ECOG) 0 or 1, aged < 80 years, and with a life expectancy >3 months entered into this study. DNA was extracted from paraffin-embedded formalin-fixed tumour tissues

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Allgoewer, Chantal, Markus Breunig, Meike Hohwieler, Medhanie Mulaw, and Alexander Kleger. "Abstract C010: Single-cell profiling unleashes KRAS-driven redrafting of the tumor microenvironment before cancer onset." Cancer Research 84, no. 17_Supplement_2 (2024): C010. http://dx.doi.org/10.1158/1538-7445.pancreatic24-c010.

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Abstract Pancreatic cancer is a highly lethal and aggressive disease, commonly characterized by a unique tumor microenvironment, where mutant KRAS signaling plays a pivotal role in its pathophysiology. To deepen our understanding of KRAS-dependent signaling in earliest tumor development, oncogenic KRAS (KRASG12D) expression was induced in human stem cell-derived pancreatic ductal-like organoids (PDLOs), followed by time-resolved single-cell RNA and bulk ATAC sequencing. This unique precancerous state model facilitated a comprehensive characterization of early oncogenic events at cellular resol

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Wu, Jianghong, Shawn McGinley, Yuan Wang, Peter Gallagher, and Haiching Ma. "Abstract 379: Application of NanoBRET target engagement cellular assay for measurement of inhibitor binding to wild type and mutant RAS in live cells." Cancer Research 82, no. 12_Supplement (2022): 379. http://dx.doi.org/10.1158/1538-7445.am2022-379.

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Abstract NanoBRET࣪ target engagement (TE) is the first biophysical technique that broadly enables the quantitative determination of protein inhibitor occupancy in live cells, without disruption of cellular membrane integrity. This quantitative capability is achieved in live cells via BRET with an optimized set of cell-permeable tracers, allow the measurement of compound binding to a selected cellular target protein. RAS is a well-known oncogene that is frequently mutated in most lung, pancreatic and colorectal cancers and is associated with poor disease prognosis. Mutated RAS is locked in the

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Wenger, Andrew, Tal Baron, Adrian Vega-Perez, et al. "Abstract A032: KRAS mutations have distinct effects on the tumor immune microenvironment in pancreatic cancer." Cancer Immunology Research 12, no. 10_Supplement (2024): A032. http://dx.doi.org/10.1158/2326-6074.tumimm24-a032.

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Abstract Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy with abysmal survival rates. The highly immunosuppressive microenvironment of PDAC poses a major barrier to effective therapy. KRAS mutations are near-ubiquitous in PDAC, and studies indicate clinical outcomes vary depending on the specific KRAS genotype. Given that tumor genotype can shape the immune cell composition of tumors, we examined the immune cell composition of pancreatic tumors with specific KRAS mutations, focusing on KRASG12D mutations (representing 40% of PDAC cases which have the worst prognosis)

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Pulido, Ines, Qiyue Luan, Chenghao Yin, et al. "Abstract B093: Treating KRAS(G12D) inhibitor resistance using a KRAS- and HSP90 chaperone-targeted hetero-bispecific small molecule agent." Molecular Cancer Therapeutics 22, no. 12_Supplement (2023): B093. http://dx.doi.org/10.1158/1535-7163.targ-23-b093.

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Abstract KRAS is the most frequently mutated oncoprotein in human cancers. Although long considered “undruggable”, recent breakthroughs in medicinal chemistry have led to FDA-approval of the KRAS(G12C) mutation-specific inhibitors sotorasib and adagrasib for the treatment of KRAS(G12C)-positive non-small cell lung cancer. However, illustrating the need to develop additional novel agents targeting mutated KRAS, the 5-year relative survival rate for pancreatic cancer, which is commonly associated with a variety of different KRAS mutations, is only 12% (all SEER stages) due to poor early detectio

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Li, Chendi, Christopher J. Graser, Qian Qin, et al. "Abstract B080: Non-genetic determinants driving sub-clonal resistance to KRAS G12C combination therapies in KRAS mutant non-small cell lung cancer." Molecular Cancer Therapeutics 22, no. 12_Supplement (2023): B080. http://dx.doi.org/10.1158/1535-7163.targ-23-b080.

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Abstract The FDA approval of the KRAS G12C inhibitor (G12Ci) sotorasib and the advancement of similar drugs into the clinic marks a major milestone in treating KRAS G12C non-small cell lung cancer (NSCLC). However, not all patients respond (sotorasib – ORR = 37.1%, adagrasib - 43%, JDQ443 – 35%), motivating preclinical and clinical investigation into mechanisms of intrinsic and acquired resistance. For instance, clinical studies have reported on-target KRAS mutations and preclinical studies have demonstrated mitogen-activated protein kinase (MAPK) feedback reactivation including EGFR, SHP2, an

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Qurbanov, Baxtiyor Baxodirovich, and Oybek Nayimjon o'g'li Abdivaliyev. "SUN'IY NEYRON TARMOQLARIDAN FOYDALANGAN HOLDA KO'KRAK QAFASI RENTGENOGRAMMASI ASOSIDA PNEVMONIYA KASALLIGINI ANIQLASH." Results of National Scientific Research International Journal 4, no. 3 (2025): 55–70. https://doi.org/10.5281/zenodo.15075231.

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<em>Ushbu maqolada sun’iy neyron tarmoqlaridan foydalangan holda ko‘krak qafasi rentgenogrammasi asosida pnevmoniya kasalligini aniqlash muhokama qilinadi. Katta ma’lumotlar asosida sun’iy neyron tarmoqlaridan foydalanib, sun’iy intellektga asoslangan algoritmik modelini o‘qitish jarayoni tasvirlangan va ushbu modellar yordamida pnevmoniya kasalligi tashxisini aniqligini oshirishi mumkin, bu COVID-19 epidemiyasiga qarshi kurashda foydali bo’lishi mumkin. Ko‘krak qafasi rentgenogrammasi asosida pnevmoniya kasalligini aniqlash judayam qiyin va mas&

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Takeda, Mitsunobu, Zecheng Yang, Madeline S. Theardy, et al. "Abstract IA-08: Syndecan 1 is a therapeutic target for KRAS-driven pancreatic cancer." Cancer Research 84, no. 17_Supplement_2 (2024): IA—08—IA—08. http://dx.doi.org/10.1158/1538-7445.pancreatic24-ia-08.

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Abstract KRAS inhibitors targeting G12C mutation have been approved by FDA for the treatment of non-small cell lung cancers and have shown promising clinical responses in pancreatic ductal adenocarcinoma (PDAC). RAS inhibitors targeting additional KRAS mutations or multiple RAS isoforms are under clinical development. Although targeting KRAS exhibits anti-tumor effect in PDAC, majority of tumors inevitably develop resistant disease, as is the case for most targeted therapies. In this new era of targeting KRAS driven cancer, understanding mechanisms driving this resistance to RAS targeted thera

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Schischlik, Fiorella, Antonio Tedeschi, Dorothea Rudolph, et al. "Abstract A092: Determinants of sensitivity to BI KRASmulti inhibitor using high-throughput in-vitro drug screens." Molecular Cancer Therapeutics 22, no. 12_Supplement (2023): A092. http://dx.doi.org/10.1158/1535-7163.targ-23-a092.

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Abstract BI 3706674 is a novel small molecule inhibitor targeting KRAS in its inactive (GDP-bound) state and is currently undergoing IND enabling studies. Here, we assess the sensitivity of BI 3706674 in a large panel of cancer cell lines with the aim to identify biomarkers predictive of patient response. We employ two complementary, high-throughput cell viability screening setups: the pooled PRISM (Profiling Relative Inhibition Simultaneously in Mixtures) platform (868 cancer cell lines representing 80 tumor types) and a well-based custom screen performed in collaboration with Horizon Discove

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Wilkin, Jerzy. "Projekt naukowy „Ciągłość i zmiana. Sto lat rozwoju polskiej wsi” realizowany przez Instytut Rozwoju Wsi i Rolnictwa PAN – informacja i zaproszenie." Wieś i Rolnictwo, no. 1 (178) (March 20, 2018): 159–60. https://doi.org/10.53098/wir012018/09.

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Inspiracją do podjęcia się przygotowania wszechstronnej syntezy naukowej ewolucji wsi i rolnictwa w Polsce, jej mechanizmów, prawidłowości i efektów, analizowanych w długiej perspektywie czasowej, jest przypadająca w 2018 r. stuletnia rocznica odzyskania przez nasz kraj niepodległości po okresie zaborów. Wspomniane stulecie jest dla badaczy społecznych fascynującym okresem zmian we wszystkich dziedzinach życia, w tym fundamentalnych przemian systemowych. Wieś i rolnictwo odegrały w tych przemianach bardzo ważną rolę. Tytułowy projekt naukowy ma charakter interdyscyplinarny, integrujący dorobek

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Wu, Jianghong, Yuan Wang, Shawn McGinley, et al. "Abstract 2764: Application of NanoBRET target engagement cellular assay for development of inhibitors against protein kinases, RAS, and epigenetic proteins in cancer therapy." Cancer Research 83, no. 7_Supplement (2023): 2764. http://dx.doi.org/10.1158/1538-7445.am2023-2764.

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Abstract NanoBRET target engagement (TE) is the first biophysical technique that broadly enables the quantitative determination of protein inhibitor occupancy in live cells, without disruption of cellular membrane integrity. This quantitative capability is achieved in live cells via BRET with an optimized set of cell-permeable tracers, allowing the measurement of compound binding to a selected cellular target protein. Our NanoBret assay is scaled to 384-well plate format and Z’ analysis demonstrated the assay to be High Throughput Screening compatible. Protein kinases, RAS, and epigenetic prot

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Lieb, Simone, Sabine Jurado, Sergej Nowoshilow, Krzysztof M. Zak, and Marco H. Hofmann. "Abstract B083: Secondary KRAS mutations lead to acquired resistance to KRASG12D inhibitor in colorectal cancer." Molecular Cancer Therapeutics 22, no. 12_Supplement (2023): B083. http://dx.doi.org/10.1158/1535-7163.targ-23-b083.

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Abstract KRAS is the most frequently mutated oncogene, with high prevalence in tumor types with a significant unmet clinical need, such as colorectal cancer (CRC). Activating mutations in the KRAS gene leading to amino acid exchange at position 12 from Glycine to Asparagine, G12D, occur in approximately 12.5% of CRC. The approval of mutant specific KRASG12C inhibitors MRTX849 and AMG510 by the FDA raised the question if KRAS targeted therapy approaches could provide benefit to cancer patients with other mutant alleles. Several KRASG12D inhibitors have recently been described and MRTX1133, a se

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Hobbs, Guy Aaron, Rachel Burge, Amanda Linke, Kamala Sundararaj, and John P. O'Bryan. "Abstract B057: KRAS mutant-specific protein interactions reveal mechanisms in pancreatic cancer tumorigenesis and metabolic regulation." Cancer Research 82, no. 22_Supplement (2022): B057. http://dx.doi.org/10.1158/1538-7445.panca22-b057.

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Abstract Pancreatic ductal adenocarcinoma (PDAC) is the third most deadly human cancer in the US with a five-year survival rate of 11%. KRAS is mutated in over 95% of PDAC patients and is a key driver of tumorigenesis. Despite the promise of targeted inhibition of the RAF-MEK-ERK MAPK signaling pathway, arguably the most critical KRAS-mediated signaling pathway, clinical trials targeting MEK/ERK signaling as a single-agent therapy have been unsuccessful, indicating the role of additional KRAS-specific signaling pathways. The most frequent KRAS mutations in PDAC are KRAS G12D (40%), KRAS G12V (

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Wenger, Andrew, Tal Baron, Erika Hissong, et al. "Abstract PR012: KRAS mutation-specific effects on the tumor immune microenvironment drive tumor progression in pancreatic cancer." Cancer Research 84, no. 22_Supplement (2024): PR012. http://dx.doi.org/10.1158/1538-7445.tumbody-pr012.

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Abstract Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy with abysmal survival rates. The highly immunosuppressive microenvironment of PDAC poses a major barrier to effective therapy. KRAS mutations are near-ubiquitous in PDAC, and studies indicate clinical outcomes vary depending on the specific KRAS genotype. Given that tumor genotype can shape the immune cell composition of tumors, we examined the immune cell composition of pancreatic tumors with specific KRAS mutations, focusing on KRASG12D mutations (representing 40% of PDAC cases which have the worst prognosis)

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Smith, Brian, Alok K. Sharma, Roger Ma, et al. "Abstract A033: KRAS codon 12 oncogenic mutations modulate protein conformation within the Switch II/Helix3 pocket." Molecular Cancer Research 21, no. 5_Supplement (2023): A033. http://dx.doi.org/10.1158/1557-3125.ras23-a033.

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Abstract Up to 30% of cancers harbor activating mutations in one of three RAS genes, HRAS, NRAS, or KRAS, that drive uncontrolled cellular proliferation, alter cellular metabolism, movement, differentiation, and promote cell survival and tumor immune evasion. The frequency of mutation varies across alleles and specific substitutions, with KRAS mutations occurring in roughly 81% of patients, and KRAS G12D, KRAS G12V, and KRAS G12C substitutions constituting 33%, 23%, and 12% of these cases, respectively. Cancer types exhibit characteristic preferences for RAS substitutions, the reason for which

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