Chang-Hsien Lu

Laryngeal cancer accounts for 10% of head and neck cancers, with glottic cancers comprising two-thirds of cases in our country

Background/Aim: Malnutrition and inflammation are common conditions in patients with head and neck cancer (HNC). This study aimed to evaluate the predictive value of albumin combined with neutrophil-lymphocyte ratio (NLR), referring to the albumin-NLR score (ANS), in the prediction of treatment completeness and safety profiles in HNC patients receiving definitive concurrent chemoradiotherapy (CCRT). Patients and Methods: 461 consecutive HNC patients who received CCRT between 2016 and 2017 at three medical centers in Taiwan were prospectively enrolled and divided into three different groups based on their pretreatment ANS (ANS 0, high albumin and low NLR; ANS 1, low albumin or high NLR; and ANS 2, low albumin and high NLR) for treatment completeness and safety profiles comparison. Results: Overall, 46 patients (10.0%) had incomplete CCRT treatment. Patients in the ANS 2 group experienced a higher rate of incomplete CCRT (20.9%) than those in the ANS 1 (7.4%) and ANS 0 (3.5%) groups. ANS had a better discriminatory ability in predicting CCRT completeness in terms of −2 log-likelihood value, chi-square value, and c-index than the prognostic nutritional index. Patients in the ANS 2 group had significantly higher incidences of grade 3 or higher leukopenia, anemia, neutropenia, thrombocytopenia, non-neutropenic infection, and hypokalemia than those in the other two ANS groups. Conclusion: Our study showed that the ANS can accurately predict the treatment completeness of CCRT in patients with HNC and can be widely used as a simple predictor of treatment tolerance and safety profiles in patients with HNC undergoing CCRT.

Patients with myeloproliferative neoplasms (MPNs) are characterized by systemic inflammation. With the indolent nature of the diseases, second cancers (SCs) have emerged as a challenging issue in afflicted patients. Epidemiological studies have confirmed the excessive risk of SCs in MPNs, but little is known about their molecular basis. To explore further, we used whole exome sequencing to explore the genetic changes in the granulocytes of 26 paired MPN patients with or without SC. We noticed that MPN–SC patients harbor genomic variants of distinct genes, among which a unique pattern of co-occurrence or mutual exclusiveness could be identified. We also found that mutated genes in MPN–SC samples were enriched in immune-related pathways and inflammatory networks, an observation further supported by their increased plasma levels of TGF-β and IL-23. Noteworthily, variants of KRT6A, a gene capable of mediating tumor-associate macrophage activity, were more commonly detected in MPN–SC patients. Analysis through OncodriveCLUST disclosed that KRT6A replaces JAK2V617F as the more prominent disease driver in MPN–SC, whereas a major mutation in this gene (KRT6A c.745T>C) in our patients is linked to human carcinoma and predicted to be pathogenic in COSMIC database. Overall, we demonstrate that inflammation could be indispensable in MPN–SC pathogenesis.