ABSTRACT
Cancer immunotherapy, in the form of vaccination, adoptive cellular transfer, or immune checkpoint inhibitors, has emerged as a promising practice within the field of oncology. However, despite the developing field's potential to revolutionize cancer treatment, the presence of immunotherapeutic-resistant tumor cells in many patients present a challenge and limitation to these immunotherapies. These cells not only indicate immunotherapeutic resistance, but also show multi-modal resistance to conventional therapies, abnormal metabolism, stemness, and metastasis. How can immunotherapeutic-resistant tumor cells render multi-malignant phenotypes? We reasoned that the immune-refractory phenotype could be associated with multi-malignant phenotypes and that these phenotypes are linked together by a factor that acts as the master regulator. In this review, we discussed the role of the embryonic transcription factor NANOG as a crucial master regulator we named “common factor†in multi-malignant phenotypes and presented strategies to overcome multi-malignancy in immunotherapeutic-resistant cancer by restraining the NANOG-mediated multi-malignant signaling axis. Strategies that blunt the NANOG axis could improve the clinical management of therapy-refractory cancer.
ABSTRACT
Cancer immunotherapy, in the form of vaccination, adoptive cellular transfer, or immune checkpoint inhibitors, has emerged as a promising practice within the field of oncology. However, despite the developing field's potential to revolutionize cancer treatment, the presence of immunotherapeutic-resistant tumor cells in many patients present a challenge and limitation to these immunotherapies. These cells not only indicate immunotherapeutic resistance, but also show multi-modal resistance to conventional therapies, abnormal metabolism, stemness, and metastasis. How can immunotherapeutic-resistant tumor cells render multi-malignant phenotypes? We reasoned that the immune-refractory phenotype could be associated with multi-malignant phenotypes and that these phenotypes are linked together by a factor that acts as the master regulator. In this review, we discussed the role of the embryonic transcription factor NANOG as a crucial master regulator we named “common factor” in multi-malignant phenotypes and presented strategies to overcome multi-malignancy in immunotherapeutic-resistant cancer by restraining the NANOG-mediated multi-malignant signaling axis. Strategies that blunt the NANOG axis could improve the clinical management of therapy-refractory cancer.
Subject(s)
Humans , Immunotherapy , Metabolism , Neoplasm Metastasis , Phenotype , Transcription Factors , VaccinationABSTRACT
Cancer immunotherapy, in the form of vaccination, adoptive cellular transfer, or immune checkpoint inhibitors, has emerged as a promising practice within the field of oncology. However, despite the developing field's potential to revolutionize cancer treatment, the presence of immunotherapeutic-resistant tumor cells in many patients present a challenge and limitation to these immunotherapies. These cells not only indicate immunotherapeutic resistance, but also show multi-modal resistance to conventional therapies, abnormal metabolism, stemness, and metastasis. How can immunotherapeutic-resistant tumor cells render multi-malignant phenotypes? We reasoned that the immune-refractory phenotype could be associated with multi-malignant phenotypes and that these phenotypes are linked together by a factor that acts as the master regulator. In this review, we discussed the role of the embryonic transcription factor NANOG as a crucial master regulator we named “common factor†in multi-malignant phenotypes and presented strategies to overcome multi-malignancy in immunotherapeutic-resistant cancer by restraining the NANOG-mediated multi-malignant signaling axis. Strategies that blunt the NANOG axis could improve the clinical management of therapy-refractory cancer.
ABSTRACT
Background and Objectives@#Adenotonsillar enlargement is a common cause of pediatric illnesses, including obstructive respiratory disease and recurrent airway infection. The current tonsil grading systems evaluate tonsil size, but the correlation with actual tonsillar size in a clinical setting has not been established.Materials and Method: Between May and July of 2018, we recruited 31 children who underwent adenotonsillectomy with no major craniofacial abnormalities. The actual size of the palatine tonsils, the long (L1) and short (S1) axes of the tonsil beyond the anterior pillar, and the real axes (L2 and S2) after tonsil extraction from the fossa were measured during surgery. Adenoid size was determined by measuring the adenoid-nasopharynx (AN) ratio through lateral view x-ray of the neck. @*Results@#Though S1 was related to the Friedman scale (p<0.001), measured real axes were not (L2: p=0.058, S2: p=0.056). Also, adenoid size and AN ratio did not relate statistically to the Friedman scale (p=0.565). One of the measured real tonsil size parameters (S2) was related to AN ratio (p=0.048). @*Conclusion@#For pediatric patients undergoing tonsillectomy and adenoidectomy, the Friedman grading scale based on physical examination may not reflect the actual size of the tonsils. Therefore, for children with obstructive sleep disorder or recurrent tonsillitis, intraoperative measurement of tonsil size can be helpful.