Search results for “targeted therapy

About 6 results in articles

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6 articles

Immunotherapy Usage Has Not Increased Sub-Lobar Pulmonary Resections Despite Reduced Pneumonectomies

Feb 2026

Objective The landscape of non-small cell lung cancer (NSCLC) has changed due to liberalized utilization of computed tomography, developments in immunotherapy and targeted treatments, and guidelines encouraging sublobar resections. We analyzed the implications of these advances for surgical procedures over a 16-year period. Methods The National Cancer Database was used to identify NSCLC incident cases from 2004 to 2020. Histology, stage, grade, and treatment were analyzed using descriptive statistics and logistic regression. Results 2,028,553NSCLC patients were identified. Each year was associated with an increase in Stage I for NSCLC (OR1.05, 95%CI 1.05-1.05) and histological subtypes (adenocarcinoma: OR1.03, 95%CI 1.03-1.04; squamous: OR1.02, 95%CI 1.02-1.02; neuroendocrine: OR1.11, 95%CI 1.11-1.12), with no change in adenosquamous histology. A similar increase was observed for well- or moderately-differentiated histology (OR1.04, 95%CI 1.04-1.04). The proportion of patients receiving chemotherapy decreased (OR0.98, 95%CI 0.98-0.98), while more patients were treated with immunotherapy or targeted therapy, including an increase of 14% using immunotherapy or targeted therapy as first-line treatment. There was a decrease in the likelihood of receiving pneumonectomy (OR 0.91, 95%CI 0.91-0.91). Despite guidelines advocating sublobar resections, these procedures only increased by 1.1% per year. Conclusions Over the 16-year study period, there was a significant trend towards diagnosis of Stage I NSCLC. The most pronounced change in treatment patterns has been more patients receiving immunotherapy and less chemotherapy. Despite a promising decrease in pneumonectomies, the frequency of sublobar resections remains stagnant, indicating limited uptage in current practice.

RETRACTED: A Microglia Initiated Target Therapy in Neuroinflammation for Alzheimer’s Patients

Apr 2024 DOI 10.14302/issn.2998-4211.jalr-24-4926

This article has been retracted on 20 March 2025. VIEW THE RETRACTION NOTICE (https://doi.org/10.14302/issn.2998-4211.jalr-25-5855) The research is focused on neuroinflammation a normal physiological process which is known to be associated with neurodegenerative diseases could be the potential targeted therapy via the microglia cells, it starts with defining Alzheimer’s; a neurodegenerative disease which causes deposition of Aβ (amyloid beta) protein in the cerebral cortex as well as NFT (neurofibrillary tangles) in the hippocampus and basal ganglia. The paper then describes process of neuroinflammation, microglia’s role, apolipoprotein E4 gene in relation to Alzheimer’s, which leads to different stem cell research and how pruning microglia as well as targeting microglia receptors in the brain is being used in current research trials, we included multiple meta-analysis showing microglia receptors being targeted currently by emerging drugs like propofol, antibodies CSF1R inhibitor etc, which are currently under trial phase, the research ends with concluding potential diagnostic markers like sirt1 considered to be an anti-aging protein which can be used as therapeutic interventions and Lps effect on Sirt 1. A Microglia initiated target therapy in Neuroinflammation for Alzheimer’s Patients.

Evolution of Janus Kinase 2 V617F-negative idiopathic myelofibrosis into Philadelphia+ chronic myeloid leukemia

Mar 2023 DOI 10.14302/issn.2641-5518.jcci-23-4506

Limited data exist on the mechanisms promoting clonal expression of BCR-ABL1 cells in various myeloproliferative disorders. We present a patient whose Janus Kinase (JAK) 2 V617F-negative idiopathic myelofibrosis (IMF) transformed to Philadelphia-positive chronic myeloid leukemia (CML). A 55-year-old man had anemia and splenomegaly. Trephine biopsy showed excess fibrosis without a JAK2 V617F mutation. Diagnosis of high-risk IMF with t(3;12) and del(16q) was made. Five years later a repeated trephine biopsy showed extensive fibrosis and t(9;22) with der(22)t(9;22). BCR-ABL1 fusion gene with typical p210 fusion transcript was found resulting in the diagnosis of CML. A modest treatment response was achieved with tyrosine kinase inhibitor (TKI) therapies, but the disease eventually progressed to a myeloid blast phase. With AML-based chemotherapy plus azacytidine and a second generation TKI the patient survived for years but succumbed 11 years after the initial diagnosis. Clonal evolution may cause atypical disease characteristics or a poor response to targeted therapy in myeloproliferative disorders.

Nephrology Advances Open Access

Action Mechanisms and Therapeutic Targets of Renal Fibrosis

Nov 2018 DOI 10.14302/issn.2574-4488.jna-18-2443

Renal fibrosis was a chronic and progressive process affecting kidneys in chronic kidney disease (CKD), regardless of cause. Although no effective targeted therapy yet existed to retard renal fibrosis, a number of important recent advances have highlighted the cellular and molecular mechanisms underlying the renal fibrosis. The advances including TGF-β/Smad pathway, oxidative stress and inflammation, hypoxia and gut microbiota-derived from uremic solutes were highlighted that could provide therapeutic targets. New therapeutic targets and strategies that are particularly promising for development of new treatments for patients with CKD were also highlighted.

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