Treatment modalities, adverse events, and survival outcomes in older patients with head and neck squamous cell carcinoma

Head & Neck ◽  
2021 ◽  
Author(s):  
Sania Amr ◽  
Dina Ioffe ◽  
Ikumi Suzuki ◽  
Ranee Mehra ◽  
Kevin Cullen ◽  
...  
Medicina ◽  
2021 ◽  
Vol 57 (11) ◽  
pp. 1151
Author(s):  
Shinsuke Suzuki ◽  
Satoshi Toyoma ◽  
Yohei Kawasaki ◽  
Koh Koizumi ◽  
Nobuko Iikawa ◽  
...  

Background and Objectives: In recent years, the effectiveness of chemotherapy after immune checkpoint inhibitor administration has attracted attention in various cancers, including head and neck cancers. However, individual assessments of the administered chemotherapy regimens are insufficient. This study aimed to evaluate the efficacy and safety of chemotherapy after immune checkpoint inhibitor administration in recurrent metastatic head and neck cancer by focusing on a single regimen. Materials and Methods: We retrospectively reviewed clinical and radiological data from the medical records of 18 patients with recurrent or metastatic (R/M) head and neck squamous cell carcinoma (HNSCC) who received systemic chemotherapy with weekly cetuximab and paclitaxel (Cmab + PTX) after progression following immune checkpoint inhibitor (ICI) therapy. The objective response rate (ORR) and disease control rate (DCR) were assessed using Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1. Progression-free survival (PFS) and overall survival (OS) were estimated using the Kaplan–Meier method. Adverse events (AEs) were recorded using National Cancer Institute Common Terminology Criteria for Adverse Events, version 4.0. Results: In all patients, the ORR, DCR, median PFS, and median OS were 44.4%, 72.2%, 3.8 months, and 9.6 months, respectively. Regarding AEs, three patients developed grade 3 neutropenia. Grade 3 anemia, paronychia, asthenia, and peripheral neuropathy were observed in one patient each. There were no treatment-related deaths. Conclusions: Cmab + PTX was shown to maintain high efficacy and acceptable safety for R/M HNSCC that progressed after ICI therapy. Further research is needed to establish optimal treatment sequences and drug combinations for recurrent R/M HNSCC.


2021 ◽  
Author(s):  
Fan Yang ◽  
Liu-qing Zhou ◽  
Yan-jun Wang

Abstract Background: Epidemiologic studies have demonstrated that X-ray repair cross-complementary group 1 (XRCC1) is one of the susceptibility factors in head and neck squamous cell carcinoma(HNSCC) patients. However, its clinical prognostic impact remains controversial. Thus, a meta-analysis was performed to clarify the survival value of XRCC1 in HNSCC patients.Methods: Following the Preferred Reporting Items or Systematic Reviews Meta Analyses (PRISMA) 2020 guidelines, literature searches were systematically performed by PubMed, EMBASE and Web of Science with a manual retreive to evaluate the prognostic consequence of XRCC1 in HNSCC patients. Hazard ratios (HRs) and 95% confidence intervals (CIs) were collected to estimate the correlation between XRCC1 and the survival outcomes of HNSCC patients.Results: Ten studies including 2086 HNSCC patients who satisfied the inclusion and exclusion criteria were included in this meta-analysis. The meta-analysis showed that high XRCC1 expression and Arg399Gln and Arg194Trp were significantly correlated with poorer overall survival (OS), with HRs of 1.97 (95% CI, 1.36–2.84, P<0.001), 1.30 (95% CI, 1.12–1.51, P<0.001), and 1.65 (95% CI, 1.18–2.32 P<0.05), respectively.Conclusion: XRCC1 was associated with poorer survival outcomes in HNSCC patients. Hence, XRCC1 is a potential therapeutic target for HNSCC.


2013 ◽  
Vol 2013 ◽  
pp. 1-13 ◽  
Author(s):  
Aidan G. Major ◽  
Luke P. Pitty ◽  
Camile S. Farah

Head and neck squamous cell carcinoma (HNSCC) is one of the world’s top ten most common cancers. Current survival rates are poor with only 50% of patients expected to survive five years after diagnosis. The poor survival rate of HNSCC is partly attributable to the tendency for diagnosis at the late stage of the disease. One of the reasons for treatment failure is thought to be related to the presence of a subpopulation of cells within the tumour called cancer stem cells (CSCs). CSCs display stem cell-like characteristics that impart resistance to conventional treatment modalities and promote tumour initiation, progression, and metastasis. Specific markers for this population have been investigated in the hope of developing a deeper understanding of their role in the pathogenesis of HNSCC and elucidating novel therapeutic strategies.


Author(s):  
Priscila Marinho De Abreu ◽  
Jessica Kelly Venturin ◽  
Izabella Sol ◽  
Anna Clara Gregório Có ◽  
Jéssica Graça Sant'anna ◽  
...  

Cancers ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3759
Author(s):  
Jih-Chin Lee ◽  
Alexander T.H. Wu ◽  
Jia-Hong Chen ◽  
Wen-Yen Huang ◽  
Bashir Lawal ◽  
...  

Despite advancements in diagnostic and standard treatment modalities, including surgery, radiotherapy, and chemotherapy, overall survival rates of advanced-stage head and neck squamous cell carcinoma (HNSCC) patients have remained stagnant for over three decades. Failure of these treatment modalities, coupled with post-therapy complications, underscores the need for alternative interventions and an in-depth understanding of the complex signaling networks involved in developing treatment resistance. Using bioinformatics tools, we identified an increased expression of c-Met, STAT3, and CD44 corresponding to a poor prognosis and malignant phenotype of HNSCC. Subsequently, we showed that tumorsphere-derived exosomes promoted cisplatin (CDDP) resistance and colony and tumorsphere formation in parental HNSCC cells, accompanied by an increased level of oncogenic/immune evasive markers, namely, c-Met, STAT3, CD44, and PD-L1. We then evaluated the therapeutic potential of a new small molecule, HNC0014. The molecular docking analysis suggested strong interactions between HNC0014 and oncogenic molecules; c-Met, STAT3, CD44, and PD-L1. Subsequently, we demonstrated that HNC0014 treatment suppressed HNSCC tumorigenic and expression of stemness markers; HNC0014 also reduced cancer-associated fibroblast (CAF) transformation by Exosp- and CAF-induced tumorigenic properties. HNC0014 treatment alone suppressed tumor growth in a cisplatin-resistant (SAS tumorspheres) mouse xenograft model and with higher inhibitory efficacy when combined with CDDP. More importantly, HNC0014 treatment significantly delayed tumor growth in a syngeneic mouse HNSCC model, elicited an antitumor immune profile, and reduced the total c-Met, STAT3, and their phosphorylated forms, PD-L1 and CD44, contents in serum exosomes. Collectively, our findings provide supports for HNC0014 as a multi-targeted immunotherapeutic lead compound for further development.


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