The safety and efficacy of anti-PD-1/anti-PD-L1 antibody therapy in the treatment of previously treated, advanced gastric or gastro-oesophageal junction cancer: A meta-analysis of prospective clinical trials.
Programmed death ligand 1 (PD-L1) is expressed in many malignancies and plays a critical role in escape from immune surveillance through inhibition of its receptor programmed death 1.
Additional end points were progression-free survival (PFS), toxicity, biomarkers of response as determined by programmed death-ligand 1 (PD-L1) status, and on-therapy quality-of-life (QOL) metrics using the Functional Assessment of Cancer Therapy Kidney Symptom Index-19 and the Brief Fatigue Inventory.
This phenomenon seems to occur with both anti-cytotoxic T-lymphocyte-associated protein 4 and anti-programmed death-1/programmed death ligand-1, and across different solid malignancies.
The authors examined the performance of PD-L1 immunostaining in liquid-based cytology (LBC) to determine whether it could be a biomarker of malignancy or aggressive disease.
Cancer immunotherapy, particularly a class of antibodies targeting the CTLA4 and PD-1/PD-L1 negative regulators of immune response (collectively called the immune checkpoint), is one of the most promising approaches for cancer treatment and the use of immune checkpoint inhibitors (ICI) has demonstrated remarkable success in several types of cancer.
This has led to the development of drugs that block distinct immune checkpoints, such as Programmed Death 1 (PD-1) and its major ligand PD-L1, that have shown great promise in treating diverse types of cancer.
The immune checkpoint inhibitors (ICPIs) agents anti-T lymphocytes-associated antigen 4 (CTLA-4) and anti-programmed cell death protein-1 (PD-1) and its ligands (PD-L1/PD-L2) have opened a new scenario in the treatment of cancer.
Immune check-point inhibitors such as anti-PD-1/PD-L1 antibodies have proved successful for mismatch repair-deficient endometrial cancers and HPV-targeted therapies are under development for HPV-related malignancies.
We highlight the convergence of mesenchymal traits and PD-L1 expression and examine the functions of this immune inhibitory molecule, which confers cancer cell resistance and aggressiveness.
Programmed cell death protein 1 (PD-1)/programmed death-ligand 1 (PD-L1) is a negative immune checkpoint pathway that inhibit immune responses, and upregulation of this pathway has implications in many malignancies.
In the multivariate analysis, PD-L1 expression in both cancer and stroma cells (HR 2.20; P = 0.002) was an independent predictor of poor overall survival.
Patients respond well to chemotherapy with cure rates of 80-90% and the recent finding of PD-L1 expression, an immune checkpoint, warrants the use of immunotherapy for some patients with recurrent and/or refractory HL.
The evaluation of Programmed cell Death Ligand 1 (PD-L1) expression in the tumor cells with immunohistochemistry is a mandatory diagnostic step in the treatment of lung cancer.
Furthermore, elevation of PD-L1 expression on TC after neoadjuvant chemotherapy was associated with reduced chemotherapy response and inferior progression-free survival in patients with lung cancer.
Besides being a predictive biomarker of response to immunotherapy in lung cancer in general, programmed death-ligand 1 (PD-L1) is not so well correlated with treatment outcomes of lung adenocarcinoma (ADC) harbouring epidermal growth factor receptor (EGFR) mutations, as reported studies are inconclusive and seldom addressed the issues of response to treatment and resistance.
These results demonstrated that tumor-infiltrating TAMs are extrinsic regulators of tumor PD-L1 expression, indicating that combination therapy targeting both tumor PD-L1 and stromal TAMs might be a possible strategy for effective treatment of lung cancer.