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Journal articles on the topic 'Metabolism, Cell Cycle, Cancer, Kras'

Author: Grafiati

Published: 9 March 2023

Last updated: 31 July 2025

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1

Chiu, Ching-Feng, Ming-I. Hsu, Hsiu-Yen Yeh, et al. "Eicosapentaenoic Acid Inhibits KRAS Mutant Pancreatic Cancer Cell Growth by Suppressing Hepassocin Expression and STAT3 Phosphorylation." Biomolecules 11, no. 3 (2021): 370. http://dx.doi.org/10.3390/biom11030370.

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Background: The oncogenic Kirsten rat sarcoma viral oncogene homolog (KRAS) mutation was reported to be the signature genetic event in most cases of pancreatic ductal adenocarcinoma (PDAC). Hepassocin (HPS/FGL1) is involved in regulating lipid metabolism and the progression of several cancer types; however, the underlying mechanism of HPS/FGL1 in the KRAS mutant PDAC cells undergoing eicosapentaenoic acid (EPA) treatment remains unclear. Methods: We measured HPS/FGL1 protein expressions in a human pancreatic ductal epithelial (HPNE) normal pancreas cell line, a KRAS-wild-type PDAC cell line (B

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2

Hatipoglu, Ahmet, Deepak Menon, Talia Levy, Maria A. Frias, and David A. Foster. "Inhibiting glutamine utilization creates a synthetic lethality for suppression of ATP citrate lyase in KRas-driven cancer cells." PLOS ONE 17, no. 10 (2022): e0276579. http://dx.doi.org/10.1371/journal.pone.0276579.

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Metabolic reprogramming is now considered a hallmark of cancer cells. KRas-driven cancer cells use glutaminolysis to generate the tricarboxylic acid cycle intermediate α-ketoglutarate via a transamination reaction between glutamate and oxaloacetate. We reported previously that exogenously supplied unsaturated fatty acids could be used to synthesize phosphatidic acid–a lipid second messenger that activates both mammalian target of rapamycin (mTOR) complex 1 (mTORC1) and mTOR complex 2 (mTORC2). A key target of mTORC2 is Akt–a kinase that promotes survival and regulates cell metabolism. We repor

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Chen, Yaoyu, Jinhong Chen, Yali Guo, et al. "Abstract B173: The anti-tumor activity of CDK2 inhibition alone or in combination with other anti-cancer agents in human cancers." Molecular Cancer Therapeutics 22, no. 12_Supplement (2023): B173. http://dx.doi.org/10.1158/1535-7163.targ-23-b173.

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Abstract Cyclin-dependent kinase 2 (CDK2) plays a crucial role in the regulation of the cell cycle and is involved in a variety of biological processes. It is responsible for phosphorylating proteins involved in G1 and S phase cell cycle progression, DNA damage response, intracellular transport, protein degradation, signal transduction, and DNA and RNA metabolism. CDK2 activity is particularly significant in cells exhibiting CCNE1 amplification or overexpression. Additionally, CDK2 activity has been linked to potential resistance against chemotherapy or targeted therapy. Several studies have i

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Shechter, Sharon, Sapir Ya’ar Bar, Hamdan Khattib, Matthew J. Gage, and Dorit Avni. "Riok1, A Novel Potential Target in MSI-High p53 Mutant Colorectal Cancer Cells." Molecules 28, no. 11 (2023): 4452. http://dx.doi.org/10.3390/molecules28114452.

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The vulnerabilities of cancer cells constitute a promising strategy for drug therapeutics. This paper integrates proteomics, bioinformatics, and cell genotype together with in vitro cell proliferation assays to identify key biological processes and potential novel kinases that could account, at least in part, for the clinical differences observed in colorectal cancer (CRC) patients. This study started by focusing on CRC cell lines stratified by their microsatellite (MS) state and p53 genotype. It shows that cell-cycle checkpoint, metabolism of proteins and RNA, signal transduction, and WNT sig

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Conroy, Lindsey R., Susan Dougherty, Traci Kruer, et al. "Loss of Rb1 Enhances Glycolytic Metabolism in Kras-Driven Lung Tumors In Vivo." Cancers 12, no. 1 (2020): 237. http://dx.doi.org/10.3390/cancers12010237.

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Dysregulated metabolism is a hallmark of cancer cells and is driven in part by specific genetic alterations in various oncogenes or tumor suppressors. The retinoblastoma protein (pRb) is a tumor suppressor that canonically regulates cell cycle progression; however, recent studies have highlighted a functional role for pRb in controlling cellular metabolism. Here, we report that loss of the gene encoding pRb (Rb1) in a transgenic mutant Kras-driven model of lung cancer results in metabolic reprogramming. Our tracer studies using bolus dosing of [U-13C]-glucose revealed an increase in glucose ca

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Der, Channing J. "Abstract IA06: Targeting the ERK-MYC signaling network for the treatment of KRAS-mutant cancers." Molecular Cancer Research 21, no. 5_Supplement (2023): IA06. http://dx.doi.org/10.1158/1557-3125.ras23-ia06.

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Abstract KRAS is mutationally activated in 95% of pancreatic ductal adenocarcinomas (PDAC) and essential for maintenance of PDAC tumorigenic growth. The recent clinical evaluation of inhibitors of one KRAS mutant (KRASG12C) supports the therapeutic value of direct targeting of KRAS for PDAC treatment. However, this mutant comprises less than 2% of KRAS mutations in PDAC. Therefore, we have evaluated direct inhibitors of the predominant KRAS mutations (G12D, G12V and G12R) in PDAC. Additionally, both innate and treatment-associated resistance mechanisms will limit the effectiveness of direct KR

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7

Singh, Pankaj Kumar. "Abstract SY13-01: Targeting the metabolic basis of resistance to Kras signaling inhibition in pancreatic cancer." Cancer Research 85, no. 8_Supplement_2 (2025): SY13–01—SY13–01. https://doi.org/10.1158/1538-7445.am2025-sy13-01.

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Abstract Pancreatic ductal adenocarcinoma patients show poor prognosis due in part to poor response to standard-of-care therapies. Hence, there is an urgent need to identify novel therapeutic strategies. Oncogenic Kras mutations are a key driver of PDAC tumorigenesis. Novel Kras-targeted therapies have demonstrated improved efficacies in preclinical models and are currently under trial in the clinic. However, resistance has been observed against these therapies. Metabolic alterations play a key role in regulating therapy responsiveness. Notably, Krasis a key regulator of metabolic reprogrammin

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Wang, Wenping, Samuel Wang, Ioana Dobrescu, et al. "Abstract 3803: CRISPR screening identifies methionine synthase as a potential therapeutic target in KRAS-driven NSCLC." Cancer Research 85, no. 8_Supplement_1 (2025): 3803. https://doi.org/10.1158/1538-7445.am2025-3803.

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Abstract One-carbon metabolism, which integrates the folate and methionine cycles, is crucial for cancer growth. Methionine synthase (MTR), a key enzyme in this pathway, converts 5-methyltetrahydrofolate (5-CH3-THF) to active tetrahydrofolate (THF), a cofactor required for nucleotide synthesis. Concurrently, MTR catalyzes the conversion of homocysteine to methionine, effectively linking the folate and methionine cycles. Given its central role, MTR has gained attention as a potential therapeutic target in cancer research, though its function in KRAS-driven lung cancer remains poorly understood.

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9

Vande Voorde, Johan, Rory T. Steven, Arafath K. Najumudeen, et al. "Metabolic profiling stratifies colorectal cancer and reveals adenosylhomocysteinase as a therapeutic target." Nature Metabolism 5, no. 8 (2023): 1303–18. http://dx.doi.org/10.1038/s42255-023-00857-0.

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AbstractThe genomic landscape of colorectal cancer (CRC) is shaped by inactivating mutations in tumour suppressors such as APC, and oncogenic mutations such as mutant KRAS. Here we used genetically engineered mouse models, and multimodal mass spectrometry-based metabolomics to study the impact of common genetic drivers of CRC on the metabolic landscape of the intestine. We show that untargeted metabolic profiling can be applied to stratify intestinal tissues according to underlying genetic alterations, and use mass spectrometry imaging to identify tumour, stromal and normal adjacent tissues. B

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10

Rana, Manjul, Rita G. Kansal, Jie Fang, Benjamin T. Allen, Jun Yang, and Evan S. Glazer. "Abstract B044: Bromodomain and Extra-Terminal Protein inhibition decreases pancreatic cancer proliferation via MYC-independent pathways." Cancer Research 82, no. 22_Supplement (2022): B044. http://dx.doi.org/10.1158/1538-7445.panca22-b044.

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Abstract Introduction: The bromodomain and extra-terminal (BET) protein family contains proteins which have evolutionarily conserved bromodomains (BRDs) that specifically recognize acetylated lysine residues on the histone tails of chromatin and regulate gene transcription. Deregulation of these BRD-containing proteins has been seen in carcinogenesis as they are also known to play role in the regulation of the cell-cycle and MYC oncogenes. BMS-986158 is an oral BET inhibitor which has been used in the clinical trials for both hematologic and advanced solid tumor cancers. We hypothesized that B

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Arthi, Boro, Krishnaswamy Sujatha, Sridhar Gopal, et al. "Study of Expression of MST3 in Myeloid Leukaemia." Medical Sciences 13, no. 2 (2025): 33. https://doi.org/10.3390/medsci13020033.

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Myeloid leukaemia (ML) is a cancer that occurs by the accumulation of abnormally multiplied myeloid cells in bone marrow, peripheral blood, and other related tissue. MST3 is a gene of the GCK family that has a role in apoptosis, along with other cellular functions like cellular differentiation, cell cycle, metabolism, and others. Objectives: The objectives of this study were to count RBCs and WBCs, study MST3 expression in ML and control samples, and perform an in silico correlation study on the KRAS and NRAS genes. Methods: The counting of RBCs and WBCs was carried out using a hemacytometer,

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Singh, Sajal Raj, Rakesh Bhaskar, Shampa Ghosh, et al. "Exploring the Genetic Orchestra of Cancer: The Interplay Between Oncogenes and Tumor-Suppressor Genes." Cancers 17, no. 7 (2025): 1082. https://doi.org/10.3390/cancers17071082.

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Cancer is complex because of the critical imbalance in genetic regulation as characterized by both the overexpression of oncogenes (OGs), mainly through mutations, amplifications, and translocations, and the inactivation of tumor-suppressor genes (TSGs), which entail the preservation of genomic integrity by inducing apoptosis to counter the malignant growth. Reviewing the intricate molecular interplay between OGs and TSGs draws attention to their cell cycle, apoptosis, and cancer metabolism regulation. In the present review, we discuss seminal discoveries, such as Knudson’s two-hit hypothesis,

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Arfin, Saniya, Dhruv Kumar, Andrea Lomagno, Pietro Luigi Mauri, and Dario Di Silvestre. "Differentially Expressed Genes, miRNAs and Network Models: A Strategy to Shed Light on Molecular Interactions Driving HNSCC Tumorigenesis." Cancers 15, no. 17 (2023): 4420. http://dx.doi.org/10.3390/cancers15174420.

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Head and neck squamous cell carcinoma (HNSCC) is among the most common cancer worldwide, accounting for hundreds thousands deaths annually. Unfortunately, most patients are diagnosed in an advanced stage and only a percentage respond favorably to therapies. To help fill this gap, we hereby propose a retrospective in silico study to shed light on gene–miRNA interactions driving the development of HNSCC. Moreover, to identify topological biomarkers as a source for designing new drugs. To achieve this, gene and miRNA profiles from patients and controls are holistically reevaluated using protein–p

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Qian, Yu, David Molkentine, Chendong Yang, et al. "Abstract 271: MYC mediates enhanced lactate reutilization and resistance to anti-angiogenesis therapy in preclinical models of LKB1-deficient NSCLC." Cancer Research 83, no. 7_Supplement (2023): 271. http://dx.doi.org/10.1158/1538-7445.am2023-271.

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Abstract Deletion or loss of function mutations of the STK11/LKB1 tumor suppressor are associated with primary resistance to immunotherapy in KRAS-mutant lung adenocarcinoma (LUAD) and drive metabolic reprogramming of tumor cells. We observed that LKB1-deficient tumors were resistant to anti-angiogenic therapy in the hypoxic and nutrient-depleted or acidic tumor microenvironment (TME). We determined that MYC which is elevated in LKB1-deficient cells, regulated the expression of the lactate transporter, MCT4. Moreover, knockdown of MYC decreases glycolysis and cell proliferation. Therefore, we

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An, Julia, Calvin Chen, Ying-Yu Chen, Jina Park, Stephen Baylin, and Michael Topper. "Abstract LB421: Targeting STAT3 in combination with epigenetic therapy induces tumor suppressive IL-24 in non-small cell lung cancer." Cancer Research 85, no. 8_Supplement_2 (2025): LB421. https://doi.org/10.1158/1538-7445.am2025-lb421.

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Abstract Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related deaths worldwide, with 5-year survival rates of less than 30%. Therefore, there is a critical need for novel combinatorial strategies to enhance the efficacy of current approaches. A current approach for the treatment of advanced NSCLC was developed in our lab and others utilizing DNA methyltransferase inhibition (DNMTi) paired with histone deacetylase inhibition (HDACi) to sensitize patients to immunotherapy. However, most patients do not benefit durably from epigenetic therapy alone or in combination with othe

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Chau, Ian, Lobna Elkhadragy, Ron C. Gaba, Lawrence B. Schook, and Kyle Schachtschneider. "The Oncopig hepatocellular carcinoma model: An innovative large animal platform for evaluating treatment effects." Journal of Clinical Oncology 43, no. 4_suppl (2025): 619. https://doi.org/10.1200/jco.2025.43.4_suppl.619.

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619 Background: Hepatocellular carcinoma (HCC) is an aggressive disease associated with poor prognosis and limited treatment options. Systemic therapies for advanced HCC include sorafenib, lenvatinib, and atezolizumab plus bevacizumab. However, given the limited efficacy of systemic treatment options, novel treatment approaches including combination of systemic and locoregional therapies (LRTs) is required to improve patient outcomes. These approaches require advanced large animal models to prove effectiveness. Pigs represent an ideal platform that provide both regulatory acceptable and clinic

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Renatino-Canevarolo, Rafael, Mark B. Meads, Maria Silva, et al. "Dynamic Epigenetic Landscapes Define Multiple Myeloma Progression and Drug Resistance." Blood 136, Supplement 1 (2020): 32–33. http://dx.doi.org/10.1182/blood-2020-142872.

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Multiple myeloma (MM) is an incurable cancer of bone marrow-resident plasma cells, which evolves from a premalignant state, MGUS, to a form of active disease characterized by an initial response to therapy, followed by cycles of therapeutic successes and failures, culminating in a fatal multi-drug resistant cancer. The molecular mechanisms leading to disease progression and refractory disease in MM remain poorly understood. To address this question, we have generated a new database, consisting of 1,123 MM biopsies from patients treated at the H. Lee Moffitt Cancer Center. These samples ranged

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Liu, Xiaoling, Yichen Jia, Changyuan Shi, et al. "CYP4B1 is a prognostic biomarker and potential therapeutic target in lung adenocarcinoma." PLOS ONE 16, no. 2 (2021): e0247020. http://dx.doi.org/10.1371/journal.pone.0247020.

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CYP4B1 belongs to the mammalian CYP4 enzyme family and is predominantly expressed in the lungs of humans. It is responsible for the oxidative metabolism of a wide range of endogenous compounds and xenobiotics. In this study, using data from The Cancer Genome Atlas (TCGA) project and the Gene Expression Omnibus (GEO) database, a secondary analysis was performed to explore the expression profile of CYP4B1, as well as its prognostic value in patients with lung adenocarcinoma (LUAD). Based on the obtained results, a significantly decreased CYP4B1 expression was discovered in patients with LUAD whe

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Dellinger, Thanh Hue, Xiwei Wu, Hyejin Cho, et al. "Whole transcriptome changes correlate to exceptional ovarian cancer responders: A sub-analysis of a HIPEC Phase I trial." Journal of Clinical Oncology 38, no. 15_suppl (2020): 6060. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.6060.

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6060 Background: Advanced stage ovarian cancer patients benefit from hyperthermic intraperitoneal chemotherapy (HIPEC), prolonging overall survival by nearly 12 months. However, molecular changes triggered by HIPEC are not well characterized, and no molecular signatures of response are known. We analyzed early gene expression changes after HIPEC treatment in ovarian tumors. Methods: This is an interval subgroup analysis of a single institution Phase I trial using HIPEC with cisplatin 75 mg/m2 at time of optimal cytoreduction. Snap-frozen biopsies from tumor and normal peritoneum from 20 patien

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Jayaswal, Navin, and Allison N. Tegge. "Abstract 222: Unraveling tumor progression in breast cancer: The impact of differential DNA methylation." Cancer Research 85, no. 8_Supplement_1 (2025): 222. https://doi.org/10.1158/1538-7445.am2025-222.

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Abstract Breast cancer affects over 300, 000 Americans annually, with 42, 780 deaths projected in 2024. DNA methylation, an epigenetic modification, has been associated with breast cancer progression (e.g., BRCA1 gene promoter hypermethylation). We hypothesize that we can identify differentially methylated CpG sites linked to cancer progression, thereby revealing the biological functions and pathways involved in tumor progression.We used DNA methylation data characterizing over 487, 000 CpG sites from 1, 032 female breast cancer patients in the Cancer Genome Atlas. CpG methylation was quantifi

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Moreno, Carlos S., Cynthia L. Winham, Emma R. Klein, et al. "Abstract 6081: Integrative genomic analysis of primary prostate tumors and corresponding lymph node metastases." Cancer Research 83, no. 7_Supplement (2023): 6081. http://dx.doi.org/10.1158/1538-7445.am2023-6081.

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Abstract Background: Prostate cancer (PCa) is a highly heterogeneous disease, and mortality is mainly due to metastases. However, the molecular underpinnings that lead to the initial steps of metastasis have not been well characterized. We have performed integrative whole exome sequencing and transcriptome analysis of primary prostate tumor foci and corresponding lymph node metastases (LNM). Design: Primary tumor foci (PTF) and LNM from 40 patients with high-risk PCa were analyzed by RNAseq. Two or more PTF and all available LNM greater than 0.4cm were subjected to sequencing. Of these 40 pati

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Ross, P. M. "Cellular and adenovirus dl312 DNA metabolism in cycling or mitotic human cultures exposed to supralethal gamma radiation." Journal of Cell Biology 109, no. 5 (1989): 1993–2002. http://dx.doi.org/10.1083/jcb.109.5.1993.

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Cellular repair of DNA damage due to lethal gamma irradiation was studied to reveal differences between strains and cell cycle stages that are otherwise difficult to detect. Cycling and metaphase-blocked cultures of normal fibroblasts and carcinoma cells were compared for repair of gamma sites (gamma radiation-induced nicks, breaks, and alkalilabile sites in DNA) at supralethal exposures ranging from 7 to 150 krad 137Cs radiation and at postirradiation incubations of 20-180 min. Fibroblasts from normal human skin or lung repaired gamma sites efficiently when cycling but did not repair them whe

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Moreno, Carlos S., Cynthia L. Winham, Emma R. Klein, et al. "Abstract A046: Integrated genomic analysis of primary prostate tumor foci and corresponding lymph node metastases identifies pathways associated with metastatic disease." Cancer Research 83, no. 11_Supplement (2023): A046. http://dx.doi.org/10.1158/1538-7445.prca2023-a046.

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Abstract Background: Prostate cancer (PCa) is a highly heterogeneous disease, and mortality is mainly due to metastases. However, the molecular underpinnings that lead to the initial steps of metastasis have not been well characterized. We have performed integrative whole exome sequencing and transcriptome analysis of primary prostate tumor foci and corresponding lymph node metastases (LNM). Design: Primary tumor foci (PTF) and LNM from 40 patients with high-risk PCa were analyzed by RNAseq. Two or more PTF and all available LNM greater than 0.4cm were subjected to sequencing. Of these 40 pati

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Boda, Akash, Casey Ager, Kimal Rajapakshe, et al. "758 High-potency synthetic STING agonists rewire the myeloid stroma in the tumour microenvironment to amplify immune checkpoint blockade efficacy in refractory pancreatic ductal adenocarcinoma." Journal for ImmunoTherapy of Cancer 9, Suppl 2 (2021): A793. http://dx.doi.org/10.1136/jitc-2021-sitc2021.758.

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BackgroundPancreatic ductal adenocarcinoma (PDAC) is one of the most lethal malignancies and is clinically unresponsive to immune checkpoint blockade (ICB) immunotherapy.1 2 High densities of immunosuppressive myeloid cells,3 a paucity of antigen-presenting cells4–6 and T cell exclusion from tumour microenvironment7 all contribute to the refractory nature of PDAC to immune-based therapies. We and others have shown that innate immune activation of myeloid stroma via engagement of the STING (Stimulator of Interferon Genes) pathway can mediate proinflammatory remodeling and trigger a flood of T c

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Bicer, Fuat, Ahmet Anil Ozluk, Midhun Malla, et al. "The impact of metformin on clinical outcomes of metastatic colorectal cancer with known molecular profile treated with cytotoxic chemotherapy or immune checkpoint inhibitor." Journal of Clinical Oncology 42, no. 16_suppl (2024): e15580-e15580. http://dx.doi.org/10.1200/jco.2024.42.16_suppl.e15580.

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e15580 Background: Colorectal cancer (CRC) is the third most common cancer in the US, with a dismal 5-year OS of 13% in mCRC. Concomitant metformin with chemotherapy or immune checkpoint inhibitors (ICIs) revealed improved outcomes in various cancers. Metformin's anti-cancer effects stem its effects on cancer metabolism, cell cycle modulation, cancer stem cells, gut microbiota, immunomodulatory properties. The aim of this retrospective study was to study the impact of concomitant metformin use with the type of systemic therapy (chemotherapy or ICIs) in CRC. Methods: CRC tumors were analyzed by

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Li, Long Shan, Kenneth Huffman, Huiyu Li, et al. "Abstract 2690: In vivo CRISPR screen identifies SOAT1 as a chemotherapy chemosensitizing target for non-small cell lung cancer (NSCLC)." Cancer Research 83, no. 7_Supplement (2023): 2690. http://dx.doi.org/10.1158/1538-7445.am2023-2690.

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Abstract Purpose: To identify druggable gene targets that would sensitize NSCLCs to available chemotherapy agents. Experimental Procedures: We developed a CRISPR-Cas9 lentivirus library of 12,474 sgRNAs targeting 660 FDA proved ‘druggable’ putative proteins (18 guides/gene) and investigated their potential to chemosensitize (“drop out” in the presence of taxane) the NSCLC lung adenocarcinoma (LUAD) line NCI-H2009 (TP53 and KRAS mutant) in parallel studies in vitro (tissue culture) & in vivo (xenografts). Key elements of our experiments were: the use low doses of paclitaxel (IC10 values for

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Kalofonos, H. P., A. Antonacopoulou, P. Matsouka, and E. Giannopoulou. "Effect of panitumumab on autophagy in colon cancer." Journal of Clinical Oncology 27, no. 15_suppl (2009): e22151-e22151. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e22151.

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e22151 Background: Panitumumab, a human monoclonal antibody raised against EGFR, has been approved by the Food and Drug Administration (FDA) and the European Medicines Agency (EMEA) for the treatment of patients with EGFR-expressing mCRC and wild type kras. The ratio of reduced/oxidised form of glutathione (GSH/GSSG) is an indicator of the redox status in cells. The aim of the current study was to investigate the effect of panitumumab on the redox status of colon cancer cell lines Caco-2, DLD-1 and HT-29 regarding proliferation, apoptosis, necrosis, cell cycle arrest and autophagy. Methods: Ce

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Redding, Alexandra, Guillaume Fonteneau, and Elda Grabocka. "Abstract A029: Unfolding the role of cell state on stress granule heterogeneity and function in KRAS-driven pancreatic cancer." Molecular Cancer Research 21, no. 5_Supplement (2023): A029. http://dx.doi.org/10.1158/1557-3125.ras23-a029.

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Abstract Phenotypic and functional heterogeneity is a common feature of cancer cells that poses as a major therapeutic challenge. Previous work has implicated the phase-separation organelles, stress granules (SGs), as important mediators of tumorigenesis that function as a mutant KRAS-driven stress-adaptive mechanism to enhance cellular fitness. We have found that mutant KRAS pancreatic cancer cells show a high degree of intercellular heterogeneity in SG formation, ranging from no SGs to markedly high levels. Given the function of SGs in cancer cell fitness and the role of cancer cell heteroge

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Parkinson, Hayley, James Breen, Nhi Hin, et al. "A Functional Genomic Screen to Identify Novel Genes Involved in Multiple Myeloma Tumour Development." Blood 142, Supplement 1 (2023): 1947. http://dx.doi.org/10.1182/blood-2023-174601.

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Multiple myeloma (MM) is an incurable malignancy characterised by uncontrolled proliferation of plasma cells (PCs) in the bone marrow (BM). MM is a genetically heterogeneous disease with each patient's PCs harbouring unique genetic mutations, however the development of MM tumours is not only dependent on the underlying genetics but also on the selective pressures applied by the BM microenvironment. Hence, we hypothesise that identifying the dependencies which promote MM cell outgrowth in the BM microenvironment will allow for the identification of new drug targets. This project aims to use an

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Oliveira, Susana Mendonça, Patrícia Dias Carvalho, André Serra-Roma, et al. "Fibroblasts Promote Resistance to KRAS Silencing in Colorectal Cancer Cells." Cancers 16, no. 14 (2024): 2595. http://dx.doi.org/10.3390/cancers16142595.

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Colorectal cancer (CRC) responses to KRAS-targeted inhibition have been limited due to low response rates, the mechanisms of which remain unknown. Herein, we explored the cancer-associated fibroblasts (CAFs) secretome as a mediator of resistance to KRAS silencing. CRC cell lines HCT15, HCT116, and SW480 were cultured either in recommended media or in conditioned media from a normal colon fibroblast cell line (CCD-18Co) activated with rhTGF-β1 to induce a CAF-like phenotype. The expression of membrane stem cell markers was analyzed by flow cytometry. Stem cell potential was evaluated by a spher

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Leal-Esteban, Lucia C., and Lluis Fajas. "Cell cycle regulators in cancer cell metabolism." Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1866, no. 5 (2020): 165715. http://dx.doi.org/10.1016/j.bbadis.2020.165715.

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Abounar, Summer A., Nefertiti A. El-Nikhely, Kati Turkowski, Rajkumar Savai, and Hesham Saeed. "CRISPR/Cas-Mediated Knockdown of PD-L1 and KRAS in Lung Cancer Cells." International Journal of Molecular Sciences 25, no. 16 (2024): 9086. http://dx.doi.org/10.3390/ijms25169086.

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Cancer cells can escape death and surveillance by the host immune system in various ways. Programmed cell death ligand 1 (PD-L1) is a transmembrane protein that is expressed by most cell types, including cancer cells, and can provide an inhibitory signal to its receptor PD-1, which is expressed on the surface of activated T cells, impairing the immune response. PD-L1/PD-1-mediated immune evasion is observed in several KRAS-mutated cancers. In the current study, we used the CRISPR/Cas9 system to knock down PD-L1 and KRAS in adenocarcinoma lung cells (A549 and H1975). Knockdown of PD-L1 was vali

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Nolan, Aoife, Cinzia Raso, Walter Kolch, Alex von Kriegsheim, Kieran Wynne, and David Matallanas. "Proteomic Mapping of the Interactome of KRAS Mutants Identifies New Features of RAS Signalling Networks and the Mechanism of Action of Sotorasib." Cancers 15, no. 16 (2023): 4141. http://dx.doi.org/10.3390/cancers15164141.

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RAS proteins are key regulators of cell signalling and control different cell functions including cell proliferation, differentiation, and cell death. Point mutations in the genes of this family are common, particularly in KRAS. These mutations were thought to cause the constitutive activation of KRAS, but recent findings showed that some mutants can cycle between active and inactive states. This observation, together with the development of covalent KRASG12C inhibitors, has led to the arrival of KRAS inhibitors in the clinic. However, most patients develop resistance to these targeted therapi

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Song, Jisu, Heejung Seo, Mi-Ryung Kim, Sang-Jae Lee, Sooncheol Ahn, and Minjung Song. "Active Compound of Pharbitis Semen (Pharbitis nil Seeds) Suppressed KRAS-Driven Colorectal Cancer and Restored Muscle Cell Function during Cancer Progression." Molecules 25, no. 12 (2020): 2864. http://dx.doi.org/10.3390/molecules25122864.

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Kirsten rat sarcoma viral oncogene homolog (KRAS)-driven colorectal cancer (CRC) is notorious to target with drugs and has shown ineffective treatment response. The seeds of Pharbitis nil, also known as morning glory, have been used as traditional medicine in East Asia. We focused on whether Pharbitis nil seeds have a suppressive effect on mutated KRAS-driven CRC as well as reserving muscle cell functions during CRC progression. Seeds of Pharbitis nil (Pharbitis semen) were separated by chromatography and the active compound of Pharbitis semen (PN) was purified by HPLC. The compound PN efficie

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Lin, Tsung-Jen, Kuo-Chu Lai, An-Sheng Lee, Chien-Hsin Chang, Chiung-Lin Liu, and Ching-Hu Chung. "Novel Antrodia cinnamomea Extract Reduced Cancer Stem-Like Phenotype Changes and Resensitized KRAS-Mutant Colorectal Cancer via a MicroRNA-27a Pathway." Cancers 11, no. 11 (2019): 1657. http://dx.doi.org/10.3390/cancers11111657.

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Colorectal cancer (CRC) is one of the most common causes of death in Taiwan. Previous studies showed that Antrodia cinnamomea (AC) can treat poisoning, diarrhea, and various types of cancer. Therefore, we purified a novel ubiquinone derivative, AC009, and investigated its antitumor effects. Cell viability assays revealed that AC009 reduced the viability of several human CRC cell lines. AC009 treatment resulted in cell-cycle arrest/apoptosis, and these effects may occur via caspase and Bcl-2 signaling pathways. We demonstrated that AC009 could significantly inhibit in vivo tumor growth in xenog

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Principe, Daniel, Mary Pasquinelli, Ryan Nguyen, Lawrence Feldman, Alexandre Aissa, and Frank D. Weinberg. "Abstract 7366: Loss of STK11 suppresses lipid metabolism to attenuate KRAS-induced immunogenicity in patients with non-small cell lung cancer." Cancer Research 84, no. 6_Supplement (2024): 7366. http://dx.doi.org/10.1158/1538-7445.am2024-7366.

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Abstract Background: Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related death in the United States. Though NSCLC is genetically heterogeneous, as many as 30% of NSCLC patients harbor gain-of-function mutations in the KRAS oncogene. Recent studies have demonstrated that KRAS mutations lead to extensive remodeling of the tumor immune microenvironment. However, though the effect of co-mutations in genes such as TP53 and STK11 are known to have prognostic relevance in KRAS-mutated patients, their mechanistic effect on tumor immunogenicity is largely unknown. Methods: In the

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Kim, Chorong, Da Sol Lee, Minwoo Han, Seonmin Lee, Kyu-pyo Kim, and Changhoon Yoo. "Abstract 4325: CX-4945 (Silmitasertib) induces cell death through impairment of lysosomal utilization in KRAS mutant cholangiocarcinoma cell lines." Cancer Research 84, no. 6_Supplement (2024): 4325. http://dx.doi.org/10.1158/1538-7445.am2024-4325.

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Abstract Purpose: Macropinocytosis is a non-selective endocytosis that uptakes extracellular substances such as nutrients and macromolecules into the cells. In KRAS-driven cancer such as pancreatic ductal adenocarcinoma, the macropinocytosis and following lysosomal utilization are enhanced to overcome metabolic stress. In this study, we investigated the role of CK2 in micropinocytosis and the following metabolic process in the KRAS mutant CCA cell line. Materials and Methods: The BSA uptake indicating micropinocytosis was performed by flow cytometry using the HuCCT1, cholangiocarcinoma cell li

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Weinberg, Frank D., Jen Godden, Denise Shieh, et al. "Abstract 2766: Metabolic and tumor immune cell landscapes are significantly different amongst KRAS mutational variants in non-small cell lung cancer." Cancer Research 85, no. 8_Supplement_1 (2025): 2766. https://doi.org/10.1158/1538-7445.am2025-2766.

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Abstract Approximately 30% of patients (pts) with non-small cell lung cancer (NSCLC) have alterations in the KRAS oncogene. In NSCLC KRAS mutational variants are diverse and therapeutically relevant. However, it is unclear how each variant is associated with the tumor biology, including lipid metabolism and the immune microenvironment. Since perturbed tumor immune infiltration and lipid metabolism are linked to NSCLC outcomes, we evaluated and characterized KRAS variants and association with lipid metabolism and immune infiltration. Using the Tempus Database, 5, 925 de-identified records from

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Chen, Meixi, Jiajing Pan, and Guanyang Wang. "Identification and Functional Analysis of Hub Genes in Cell Cycle Pathway Linked to the Development of Lung Cancer with Non-Small Cells." Highlights in Science, Engineering and Technology 74 (December 29, 2023): 1501–12. http://dx.doi.org/10.54097/pz3fvz54.

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Non-small cell lung cancer (NSCLC) is the most prevalent cause of cancer-related fatalities. We combined different gene expression datasets to screen out eight hub genes (CDC6, PLK1, BUB1B, CHEK1, TTK, CDC20, CCNB2, and PTTG1) associated with the Cell cycle pathway, which also showed significant poor prognosis and late upregulation of LUAD in NSCLC. KRAS and EGFR are the star molecules in lung cancer. KRAS causes overexpression of hub genes through up-regulation of the cell cycle pathway, and the up-regulation of hub genes in NSCLC can be confirmed at amounts of mRNA and proteins. Hub genes ha

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Liu, Shuang, Junfen Shi, Chang Lu, et al. "Abstract 1928: Targeting FAK to improve the therapy of KRAS G12C mutant cancers." Cancer Research 84, no. 6_Supplement (2024): 1928. http://dx.doi.org/10.1158/1538-7445.am2024-1928.

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Abstract Despite the pivotal role of KRAS G12C in tumor initiation and progression, currently available KRAS G12C inhibitors have relatively modest activity compared to other approved therapies targeting other classic oncogenic drivers. Fortunately, efforts to improve the anti-tumor response to KRAS G12C targeted therapy have benefited from the use of combination approaches. Here, we found that treatment with KRAS G12C inhibitors induces sustained activation of focal adhesion kinase (FAK) in KRAS G12C mutant cell lines from various cancer types, including non-small cell lung cancer, colorectal

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Oya, Yuko, Katsuhiro Masago, Hirokazu Matsushita, and Hiroaki Kuroda. "Association of the KRAS genotype and clinicopathologic findings of resected non–small cell lung cancer." Journal of Clinical Oncology 40, no. 16_suppl (2022): 8545. http://dx.doi.org/10.1200/jco.2022.40.16_suppl.8545.

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8545 Background: This study assessed the clinicopathological background of early-stage KRAS-mutated non-small-cell lung cancer and analyzed the biological process of KRAS-mutated tumor using an RNA sequencing procedure. Methods: We used a cohort of consecutive series of 179 surgically resected early-stage non-small-cell lung cancers harboring KRASmutations and analyzed the clinicopathological features, including the KRAS genotypes, affecting the recurrence-free survival and prognosis. Consequently, we performed RNA sequencing to determine the gene expression profiles of nineteen KRAS-mutated n

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Oya, Yuko, Katsuhiro Masago, Hirokazu Matsushita, and Hiroaki Kuroda. "Association of the KRAS genotype and clinicopathologic findings of resected non–small cell lung cancer." Journal of Clinical Oncology 40, no. 16_suppl (2022): 8545. http://dx.doi.org/10.1200/jco.2022.40.16_suppl.8545.

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8545 Background: This study assessed the clinicopathological background of early-stage KRAS-mutated non-small-cell lung cancer and analyzed the biological process of KRAS-mutated tumor using an RNA sequencing procedure. Methods: We used a cohort of consecutive series of 179 surgically resected early-stage non-small-cell lung cancers harboring KRASmutations and analyzed the clinicopathological features, including the KRAS genotypes, affecting the recurrence-free survival and prognosis. Consequently, we performed RNA sequencing to determine the gene expression profiles of nineteen KRAS-mutated n

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Mullany, Lisa K., Zhilin Liu, Erin R. King, Kwong-Kwok Wong, and JoAnne S. Richards. "Wild-Type Tumor Repressor Protein 53 (TRP53) Promotes Ovarian Cancer Cell Survival." Endocrinology 153, no. 4 (2012): 1638–48. http://dx.doi.org/10.1210/en.2011-2131.

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Loss of Pten in the KrasG12D;Amhr2-Cre mutant mice leads to the transformation of ovarian surface epithelial (OSE) cells and rapid development of low-grade, invasive serous adenocarcinomas. Tumors occur with 100% penetrance and express elevated levels of wild-type tumor repressor protein 53 (TRP53). To test the functions of TRP53 in the Pten;Kras (Trp53+) mice, we disrupted the Trp53 gene yielding Pten;Kras(Trp53−) mice. By comparing morphology and gene expression profiles in the Trp53+ and Trp53− OSE cells from these mice, we document that wild-type TRP53 acts as a major promoter of OSE cell

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Chippalkatti, Rohan, and Daniel Abankwa. "Promotion of cancer cell stemness by Ras." Biochemical Society Transactions 49, no. 1 (2021): 467–76. http://dx.doi.org/10.1042/bst20200964.

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Cancer stem cells (CSC) may be the most relevant and elusive cancer cell population, as they have the exquisite ability to seed new tumors. It is plausible, that highly mutated cancer genes, such as KRAS, are functionally associated with processes contributing to the emergence of stemness traits. In this review, we will summarize the evidence for a stemness driving activity of oncogenic Ras. This activity appears to differ by Ras isoform, with the highly mutated KRAS having a particularly profound impact. Next to established stemness pathways such as Wnt and Hedgehog (Hh), the precise, cell cy

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Sato, Hiromichi, Kazuki Sasaki, Tomoaki Hara, et al. "Pancreatic Cancer Research beyond DNA Mutations." Biomolecules 12, no. 10 (2022): 1503. http://dx.doi.org/10.3390/biom12101503.

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Pancreatic ductal adenocarcinoma (PDAC) is caused by genetic mutations in four genes: KRAS proto-oncogene and GTPase (KRAS), tumor protein P53 (TP53), cyclin-dependent kinase inhibitor 2A (CDKN2A), and mothers against decapentaplegic homolog 4 (SMAD4), also called the big 4. The changes in tumors are very complex, making their characterization in the early stages challenging. Therefore, the development of innovative therapeutic approaches is desirable. The key to overcoming PDAC is diagnosing it in the early stages. Therefore, recent studies have investigated the multifaced characteristics of

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Maity, Swastika, Krishnaprasad Baby, Bharath Harohalli Byregowda, et al. "Exploring acenocoumarol and silodosin as allosteric EGFR inhibitors for the treatment of non-small cell lung cancer." F1000Research 13 (November 21, 2024): 1398. http://dx.doi.org/10.12688/f1000research.157465.1.

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Background Non-small-cell lung cancer (NSCLC) is a highly morbid disease. Chemotherapy for NSCLC lacks specificity and efficacy mainly because of drug resistance. The current study aimed to explore computational tools to target allosteric epidermal growth factor receptor (EGFR) sites and screen for the top molecules in vitro and in vivo xenograft models. Methods Molecular docking, virtual screening, and molecular dynamic studies revealed that acenocoumarol and silodosin are the top two allosteric EGFR inhibitors. They were further tested for cytotoxicity, apoptosis, cell cycle, and gene expres

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Patel, Devanshi, Michelle Pham, Parthiv Medidi, and Holli Ann Loomans-Kropp. "Abstract 6328: Metformin induces cell cycle arrest and inhibits proliferation in KRAS-mutated colorectal cancer." Cancer Research 85, no. 8_Supplement_1 (2025): 6328. https://doi.org/10.1158/1538-7445.am2025-6328.

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Abstract Purpose: Our objective was to evaluate the potential of metformin for colorectal cancer (CRC) prevention. Methods: HT-29 (KRAS wild-type) and SW837 (KRAS G12D mutated) CRC cells were used for in vitro analyses. Cells were treated with 10mM (HT-29) or 2mM (SW837) metformin for up to 96 hours. Proliferation was assessed by raw cell counts, CellTiter 96 Aqueous Proliferation Assay, and 0.5% crystal violet staining. Propidium iodide staining was used to evaluate cell cycle and analyzed on a BD FACS Aria III. Experimental results were analyzed using Student’s t-test or Mann-Whitney U and e

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Hallin, Jill, Laura Hover, Julio Fernandez-Benet, et al. "Abstract B012: Effects of adagrasib on oncogenic signaling, immune cell regulation and biomarkers of response in preliminary clinical analyses." Molecular Cancer Research 21, no. 5_Supplement (2023): B012. http://dx.doi.org/10.1158/1557-3125.ras23-b012.

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Abstract The recent approval of KRAS G12C inhibitors has provided novel treatment options for lung, colorectal and other cancer patients harboring this mutation and has changed the landscape of research for these cancers. Current priorities in the field include characterizing the mechanism of action of KRAS G12C inhibitors and the mechanisms underlying resistance to KRAS inhibition. Utilizing access to pre and post-treatment patient samples from KRYSTAL-1, preliminary gene expression analyses from baseline and post-adagrasib (Cycle 1, Day 8) treated patient samples demonstrated multiple oncoge

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Kim, Boyun, and Jewon Jung. "Metabolomic Approach to Identify Potential Biomarkers in KRAS-Mutant Pancreatic Cancer Cells." Biomedicines 12, no. 4 (2024): 865. http://dx.doi.org/10.3390/biomedicines12040865.

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Pancreatic cancer is characterized by its high mortality rate and limited treatment options, often driven by oncogenic RAS mutations. In this study, we investigated the metabolomic profiles of pancreatic cancer cells based on their KRAS genetic status. Utilizing both KRAS-wildtype BxPC3 and KRAS-mutant PANC1 cell lines, we identified 195 metabolites differentially altered by KRAS status through untargeted metabolomics. Principal component analysis and hierarchical condition trees revealed distinct separation between KRAS-wildtype and KRAS-mutant cells. Metabolite set enrichment analysis highli

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Saiz-Lopez, Patricia, Raquel Alcaraz-Ortega, Ana Maria Lopez, et al. "Cell-free KRAS in pancreatic cancer as a rapid prognostic marker." Journal of Clinical Oncology 38, no. 15_suppl (2020): e15534-e15534. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e15534.

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e15534 Background: KRAS mutations are present over 90% of patients with pancreatic cancer (PC). Liquid biopsies provide the opportunity to genotype alterations in a less invasive way and offer a possibility to monitor the molecular characteristics of a cancer through the course of treatment. We aim to establish an association between the mutational levels of KRAS detected in plasma with patient stage and evolution. Methods: Plasma samples were collected from patients with newly diagnosed PC, before any treatment and during one year. Diagnosis of any previous cancer was an exclusion criterion.

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