chemotherapy alone

chemotherapy alone.Govindan et al [146]NivolumabCisplatin and gemcitabine or pemetrexed; paclitaxel and carboplatinAdvanced NSCLCNivolumab 10 mg/kg plus gemcitabine-cisplatin (squamous) or pemetrexed-cisplatin (nonsquamous) or nivolumab 5 or 10 mg/kg plus paclitaxel-carboplatin (all histologies) Q3W for 4 cycles, followed by nivolumab monotherapy every 3 weeksThe combination regimen, especially the paclitaxel-carboplatin plus nivolumab 5 mg/kg, showed encouraging activity (2-year OS rate: 62%). not yet determined. Future studies should focus on these issues and WS3 help to develop the optimal combination regimen for each cancer. mutant CT26 colon cancer [62]. Despite its positive immunomodulatory effect in murine WS3 tumors, whether teniposide acts as an ICD inducer in human cancers remains elusive. Poly (ADP-ribose) polymerase inhibitors (PARPi), including olaparib and niraparib, inhibit DNA repair in homologous-recombination-deficient malignant cells, leading to synthetic lethality [96]. Such retention and accumulation of DNA damage can activate the cGAS-STING pathway and the subsequent type-I IFN response, as mentioned above. In line with this notion, the administration of olaparib to murine (encoding breast cancer type 1 susceptibility protein) -deficient TNBCs increased the CD8+ T cell abundance and activated antitumor immunity [72]. Despite PARPis generally eliciting antitumor efficacy in mutation status. Such increasing CTL abundance and intra-tumoral PD-L1 level potentiate the combined therapy of PARPi and ICBs [99]. As expected, a combination of niraparib plus pembrolizumab therapy showed promising synergistic antitumor activity in patients with TNBC or ovarian cancer [100, 101], despite the best treatment efficacy still being observed in patients with is silenced in most cancer cells, but is expressed in many normal cells, including lymphocytes; therefore, these medications were traditionally supposed to impair, rather than promote, antitumor immunity [106, 107]. Intriguingly, a recent study showed that GSDME-mediated pyroptosis acts as a form of ICD and effectively activated antitumor CD8+ T-cell immunity in murine melanoma [108]. The combination of B-Raf proto-oncogene, serine/threonine kinase (BRAF) and MAPK/ERK kinase (MEK) inhibitors, the frontline care for sunitinib in patients with advanced RCC (median PFS: 13.8 em vs /em . 8.4 months). Grade 3 treatment-related adverse events were comparable between the two groups.Motzer et al [10]CamrelizumabDecitabineRelapsed or refractory classic Hodgkin LymphomaCamrelizumab 200 mg monotherapy Q3W or decitabine 10 mg/d, days 1 to 5 plus camrelizumab 200 mg, day 8 Q3WThe addition of decitabine to camrelizumab significantly improved the tumor response in patients who were clinically na?ve to the PD-1 blockade.Nie et al [140]Gemcitabine and cisplatinRecurrent or metastatic nasopharyngeal carcinomaCamrelizumab 200 mg (day 1), gemcitabine 1 g/m2 (days 1 and 8), and cisplatin 80 mg/m2 (day 1) every 3 weeks followed by camrelizumab 200 mg maintenance once every 3 weeksThe combination of camrelizumab plus gemcitabine and cisplatin has a manageable toxicity profile and promising preliminary antitumor activity in treatment-naive patients.Fang et al [141]DurvalumabPlatinum and etoposideExtensive-stage SCLCEtoposide 80C100 mg/m2 on days 1 to 3 + carboplatin AUC=5/6 or 75C80 mg/m2 + durvalumab 1500 mg, Q3W for 4 cycles + maintenance durvalumab 1500 mg Q4W vs. platinum Akap7 and etoposide for 6 cyclesDurvalumab plus platinum-etoposide significantly improved OS in patients with ES-SCLC em vs /em . chemotherapy alone (median OS: 13.0 em vs /em . 10.3 months). The safety of the two regimens was similar.Paz-Ares et al [142]IpilimumabCarboplatin and etoposideExtensive-stage SCLCCarboplatin AUC=6 + etoposide 120 mg/m2 day 1 and 100 mg day 2 and 3, Q3W up to 6 cycles + ipilimumab 10 mg/kg day 1 of chemotherapy cycles 3-6 and then once every 12-weeks from week 30The combination therapy showed a beneficial effect in extensive-stage SCLC; however, the toxicity was also significant. Sequential immunotherapy after chemotherapy might be a more feasible approach.Arriola WS3 et al [143]Platinum and etoposideExtensive-stage SCLCInduction: etoposide 100 mg/m2 on days 1 to 3 + carboplatin AUC=5 or cisplatin 75 mg/m2 day 1 Q3W for 4 cycles + 4 cycles of ipilimumab or placebo 10 mg/kg Q3W from cycle 3 of chemotherapy; Maintenance: ipilimumab or placebo 10 mg/kg Q12W The combination of ipilimumab and chemotherapy did not prolong the OS of patients with extensive-stage SCLC.Reck et al [144]Paclitaxel and carboplatinextensive-disease SCLCInduction (Q3W for a maximum of WS3 18 weeks): carboplatin AUC=6 + paclitaxel 175 mg/m2 vs. concurrent ipilimumab (4 cycles of ipilimumab 10 mg/kg + paclitaxel + carboplatin followed by 2 cycles of placebo + paclitaxel + carboplatin) vs. phased ipilimumab (4 cycles of placebo + paclitaxel + carboplatin followed by 2 cycles of ipilimumab + paclitaxel + carboplatin); Maintenance: ipilimumab for phased- and concurrent-ipilimumab arms) or placebo (control arm) Q12W Phased ipilimumab, but not concurrent ipilimumab, significantly prolonged immune-related PFS em vs /em . chemotherapy alone. A numerical, but not significant, improvement of OS was also observed.Reck et al [145]Advanced squamous NSCLCInduction: carboplatin.