ritonavir has been researched along with Lung-Neoplasms* in 12 studies
1 review(s) available for ritonavir and Lung-Neoplasms
1 trial(s) available for ritonavir and Lung-Neoplasms
11 other study(ies) available for ritonavir and Lung-Neoplasms
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Network Pharmacology and Bioinformatics Analysis Identifies Potential Therapeutic Targets of Paxlovid Against LUAD/COVID-19.
Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has caused a pandemic in many countries around the world. The virus is highly contagious and has a high fatality rate. Lung adenocarcinoma (LUAD) patients may have higher susceptibility and mortality to COVID-19. While Paxlovid is the first oral drug approved by the U.S. Food and Drug Administration (FDA) for COVID-19, its specific drug mechanism for lung cancer patients infected with COVID-19 remains to be further studied.. COVID-19 related genes were obtained from NCBI, GeneCards, and KEGG, and then the transcriptome data for LUAD was downloaded from TCGA. The drug targets of Paxlovid were revealed through BATMAN-TCM, DrugBank, SwissTargetPrediction, and TargetNet. The genes related to susceptibility to COVID-19 in LUAD patients were obtained through differential analysis. The interaction of LUAD/COVID-19 related genes was evaluated and displayed by STRING, and a COX risk regression model was established to screen and evaluate the correlation between genes and clinical characteristics. The Venn diagram was drawn to select the candidate targets of Paxlovid against LUAD/COVID-19, and the functional analysis of the target genes was performed using KEGG and GO enrichment analysis. Finally, Cytoscape was used to screen and visualize the Hub Gene, and Autodock was used for molecular docking between the drug and the target.. Bioinformatics analysis was performed by combining COVID-19-related genes with the gene expression and clinical data of LUAD, including analysis of prognosis-related genes, survival rate, and hub genes screened out by the prognosis model. The key targets of Paxlovid against LUAD/COVID-19 were obtained through network pharmacology, the most important targets include IL6, IL12B, LBP. Furthermore, pathway analysis showed that Paxlovid modulates the IL-17 signaling pathway, the cytokine-cytokine receptor interaction, during LUAD/COVID-19 treatment.. Based on bioinformatics and network pharmacology, the prognostic signature of LUAD/COVID-19 patients was screened. And identified the potential therapeutic targets and molecular pathways of Paxlovid Paxlovid in the treatment of LUAD/COVID. As promising features, prognostic signatures and therapeutic targets shed light on improving the personalized management of patients with LUAD. Topics: Adenocarcinoma of Lung; Computational Biology; COVID-19; COVID-19 Drug Treatment; Drug Combinations; Humans; Interleukin-17; Interleukin-6; Lactams; Leucine; Lung Neoplasms; Molecular Docking Simulation; Network Pharmacology; Nitriles; Proline; Receptors, Cytokine; Ritonavir; SARS-CoV-2; United States | 2022 |
COVID-19 outbreak in Italy: Clinical-radiological presentation and outcome in three oncologic patients.
We present three patients affected by pulmonary squamous cell carcinoma, metastatic esophageal cancer and advanced non-Hodgkin lymphoma, who incurred in coronavirus 2019 (COVID-19) infection during the early phase of epidemic wave in Italy. All patients presented with fever. Social contact with subject positive for COVID-19 was declared in only one of the three cases. In all cases, laboratory findings showed lymphopenia and elevated C-reactive protein (CRP). Chest x-ray and computed tomography showed bilateral ground-glass opacities, shadowing, interstitial abnormalities, and "crazy paving" pattern which evolved with superimposition of consolidations in one patient. All patients received antiviral therapy based on ritonavir and lopinavir, associated with hydroxychloroquine. Despite treatment, two patients with advanced cancers died after 39 and 17 days of hospitalization, while the patient with lung cancer was dismissed at home, in good conditions. Topics: Aged; Anti-Bacterial Agents; Antiviral Agents; Betacoronavirus; Carcinoma, Squamous Cell; Coronavirus Infections; COVID-19; Disease Outbreaks; Drug Therapy, Combination; Esophageal Neoplasms; Fatal Outcome; Humans; Hydroxychloroquine; Italy; Lopinavir; Lung Neoplasms; Lymphoma, Non-Hodgkin; Male; Middle Aged; Neoplasms; Pandemics; Pneumonia, Viral; Ritonavir; SARS-CoV-2; Tomography, X-Ray Computed; Treatment Outcome | 2021 |
Investigating the influence of relevant pharmacogenetic variants on the pharmacokinetics and pharmacodynamics of orally administered docetaxel combined with ritonavir.
The anticancer drug docetaxel exhibits large interpatient pharmacokinetic and pharmacodynamic variability. In this study, we aimed to assess the functional significance of 14 polymorphisms in the CYP3A, CYP1B1, ABCB1, ABCC2, and SLCO1B3 genes for the pharmacokinetics and pharmacodynamics of oral docetaxel, co-administered with ritonavir. None of the tested CYP3A, ABCB1, ABCC2, and SLCO1B3 genotypes and diplotypes showed a significant relation with an altered bioavailability or clearance of either docetaxel or ritonavir. Similarly, no clear effect of CYP1B1 genotype on clinical outcomes was observed in a subgroup of non-small cell lung cancer (NSCLC) patients. Our post hoc power analysis indicated that our pharmacogenetic-pharmacokinetic analysis was only powered for relatively high effect sizes, which were to be expected given the high interpatient variability. This makes it unlikely that future studies will explain the high observed interpatient variability in oral docetaxel pharmacokinetics as a result of any of these separate polymorphisms and diplotypes. Topics: Adult; Algorithms; Antineoplastic Agents, Phytogenic; Antineoplastic Combined Chemotherapy Protocols; Biological Availability; Carcinoma, Non-Small-Cell Lung; Docetaxel; Female; Genetic Variation; Genotype; Humans; Lung Neoplasms; Male; Middle Aged; Pharmacogenetics; Polymorphism, Genetic; Polymorphism, Single Nucleotide; Ritonavir | 2021 |
Prolonged SARS-CoV-2 viral shedding in patients with solid tumours and associated factors.
Topics: Adenosine Monophosphate; Aged; Alanine; Antineoplastic Agents; Antiviral Agents; Breast Neoplasms; COVID-19; COVID-19 Drug Treatment; COVID-19 Nucleic Acid Testing; COVID-19 Serological Testing; COVID-19 Serotherapy; Dexamethasone; Drug Combinations; Female; Follow-Up Studies; Glucocorticoids; Humans; Hydroxychloroquine; Immunization, Passive; Immunotherapy; Latent Infection; Lopinavir; Lung Neoplasms; Male; Molecular Targeted Therapy; Neoplasms; Proportional Hazards Models; Risk Factors; Ritonavir; SARS-CoV-2; Spain; Time Factors; Virus Shedding | 2021 |
Treatment and Outcome of a Patient With Lung Cancer Infected With Severe Acute Respiratory Syndrome Coronavirus-2.
Topics: Acrylamides; Aniline Compounds; Antineoplastic Agents; Antiviral Agents; Betacoronavirus; Coronavirus Infections; COVID-19; COVID-19 Drug Treatment; Drug Combinations; Humans; Lopinavir; Lung; Lung Neoplasms; Male; Middle Aged; Pandemics; Pneumonia, Viral; Ritonavir; SARS-CoV-2; Tomography, X-Ray Computed | 2020 |
Favourable outcome of coronavirus disease 2019 in a patient with anaplastic lymphoma kinase-positive non-small-cell lung cancer receiving alectinib.
Topics: Aged; Anaplastic Lymphoma Kinase; Anti-HIV Agents; Betacoronavirus; Carbazoles; Carcinoma, Non-Small-Cell Lung; Coronavirus Infections; COVID-19; COVID-19 Drug Treatment; Drug Combinations; Humans; Hydroxychloroquine; Lopinavir; Lung; Lung Neoplasms; Male; Masks; Noninvasive Ventilation; Pandemics; Piperidines; Pneumonia, Viral; Ritonavir; SARS-CoV-2; Tomography, X-Ray Computed; Treatment Outcome | 2020 |
Nivolumab in HIV-related non-small-cell lung cancer.
Topics: Antineoplastic Agents; Carcinoma, Non-Small-Cell Lung; CD4 Lymphocyte Count; Cisplatin; Darunavir; Deoxycytidine; Docetaxel; Gemcitabine; Heterocyclic Compounds, 3-Ring; HIV Infections; Humans; Lung Neoplasms; Male; Middle Aged; Nivolumab; Oxazines; Piperazines; Pyridones; Ritonavir; Vinorelbine | 2017 |
Protease inhibitors exposure is not related to lung cancer risk in HIV smoker patients: a nested case-control study.
We aimed at assessing in persons living with HIV with a smoking history an association between lung cancer risk and protease inhibitors exposure, especially ritonavir.. A nested case-control study was conducted within the ANRS CO4 FHDH, CO3 Aquitaine and Tenon's Hospital Cohorts.. Cases and controls were eligible if they were ex-smokers or current smokers at the index date, and had a CD4 cell count reported in the year preceding the index date. Cases were incident cases of lung cancer diagnosed between 1 January 2000 and 31 December 2011. All cancer cases were validated and histological types identified when available. Three controls were randomly selected by incidence density sampling using calendar time as the time axis, with individual matching on cohort, age (± 5 years), route of HIV acquisition, sex and hospital. Analyses were performed using conditional logistic regression adjusted for nadir CD4 cell count and smoking status. Ritonavir and protease inhibitors exposures were represented in separate models using categorical variables (never exposed, ever exposed). Several sensitivity analyses were performed.. This study performed in 1447 persons living with HIV with a smoking history (383 lung cancer cases and 1064 control patients) did not evidence any association between lung cancer risk and protease inhibitors exposure including ritonavir.. These results suggest that the risk of lung cancer is not influenced by pharmacologically induced P450 cytochrome protease inhibitors inhibition among smokers or ex-smokers. Topics: Adult; Case-Control Studies; Cohort Studies; Female; HIV Infections; HIV Protease Inhibitors; Humans; Lung Neoplasms; Male; Middle Aged; Risk Assessment; Risk Factors; Ritonavir; Smoking | 2015 |
The human immunodeficiency virus protease inhibitor ritonavir inhibits lung cancer cells, in part, by inhibition of survivin.
Ritonavir is a potential therapeutic agent in lung cancer, but its targets in lung adenocarcinoma are unknown, as are candidate biomarkers for its activity.. RNAi was used to identify genes whose expression affects ritonavir sensitivity. Synergy between ritonavir, gemcitabine, and cisplatin was tested by isobologram analysis.. Ritonavir inhibits growth of K-ras mutant lung adenocarcinoma lines A549, H522, H23, and K-ras wild-type line H838. Ritonavir causes G0/G1 arrest and apoptosis. Associated with G0/G1 arrest, ritonavir down-regulates cyclin-dependent kinases, cyclin D1, and retinoblastoma protein phosphorylation. Associated with induction of apoptosis, ritonavir reduces survivin messenger RNA and protein levels more than twofold. Ritonavir inhibits phosphorylation of c-Src and signal transducer and activator of transcription protein 3, which are important events for survivin gene expression and cell growth, and induces cleavage of PARP1. Although knock down of survivin, c-Src, or signal transducer and activator of transcription protein 3 inhibits cell growth, only survivin knock down enhances ritonavir inhibition of growth and survivin overexpression promotes ritonavir resistance. Ritonavir was tested in combination with gemcitabine or cisplatin, exhibiting synergistic and additive effects, respectively. The combination of ritonavir/gemcitabine/cisplatin is synergistic in the A549 line and additive in the H522 line, at clinically feasible ritonavir concentrations (<10 μM).. Ritonavir is of interest for lung adenocarcinoma therapeutics, and survivin is an important target and potential biomarker for its sensitivity. Ritonavir cooperation with gemcitabine/cisplatin might be explained by involvement of PARP1 in repair of cisplatin-mediated DNA damage and survivin in repair of gemcitabine-mediated double-stranded DNA breaks. Topics: Adenocarcinoma; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Blotting, Western; Cell Cycle; Cell Proliferation; Cisplatin; Cyclin D1; Deoxycytidine; DNA Breaks, Double-Stranded; Drug Therapy, Combination; Gemcitabine; HIV Protease Inhibitors; Humans; Inhibitor of Apoptosis Proteins; Lung Neoplasms; Poly (ADP-Ribose) Polymerase-1; Poly(ADP-ribose) Polymerases; Reverse Transcriptase Polymerase Chain Reaction; Ritonavir; RNA, Messenger; RNA, Small Interfering; Survivin; Tumor Cells, Cultured | 2011 |
Lung cancer as an immune reconstitution disease in an HIV-1 positive man receiving HAART.
A case of small-cell lung cancer with prompt worsening of the clinical course was observed in a patient with significant immune restoration after receiving effective highly active antiretroviral therapy (HAART) for seven months. Rapid and enormous enlargement of metastatic liver was the main symptom. Chest x-ray showed an enlargement of the left hilus. The patient died 22 days after the onset of the fulminant disease. We suggest that the occurrence and aggressive course of the lung cancer resulted from the development of immune reconstitution syndrome. Topics: Adult; Antiretroviral Therapy, Highly Active; Carcinoma, Small Cell; Fatal Outcome; HIV Seropositivity; Humans; Lamivudine; Liver Neoplasms; Lung Neoplasms; Lymphatic Metastasis; Male; Ritonavir; Saquinavir; Zidovudine | 2006 |
A long-term survival case of small cell lung cancer in an HIV-infected patient.
We report a case of small cell lung cancer in a patient with human immunodeficiency virus (HIV) infection. The patient was a 51-year-old man diagnosed 8 years previously as seropositive for HIV, who was admitted to our hospital for re-evaluation of antiretroviral medications due to multidrug resistance. Chest radiograph revealed an abnormal hilar shadow subsequently confirmed to be small cell lung cancer. He received chemotherapy concurrently with highly active antiretroviral therapy (HAART), and lived for 14 months after the diagnosis. The prognosis of lung cancer in HIV-seropositive patients is very poor, and adverse effects of chemotherapy occur more frequently than in other patients. However, the simultaneous antiretroviral agents and combination chemotherapy was successful. Such treatment may be effective despite an otherwise poor prognosis, including HIV infection. Topics: Alkynes; Anti-HIV Agents; Antineoplastic Combined Chemotherapy Protocols; Antiretroviral Therapy, Highly Active; Benzoxazines; Camptothecin; Carbamates; Carboplatin; Carcinoma, Small Cell; Cisplatin; Cyclopropanes; Didanosine; Dideoxynucleosides; Drug Administration Schedule; Furans; HIV Infections; HIV Long-Term Survivors; Humans; Irinotecan; Lung Neoplasms; Male; Middle Aged; Oxazines; Ritonavir; Sulfonamides; Tomography, X-Ray Computed | 2005 |