Subscribe: Japanese Journal of Clinical Oncology - Advance Access
Preview: Japanese Journal of Clinical Oncology - Advance Access

Japanese Journal of Clinical Oncology Advance Access

Published: Tue, 14 Nov 2017 00:00:00 GMT

Last Build Date: Tue, 14 Nov 2017 00:44:57 GMT


Asia Consensus Statement on NCCN Clinical Practice Guideline for bladder cancer


The Asia Consensus Statement (ACS) on the NCCN Guideline (NCCN-ACS) for treatment of bladder cancer version 1.2016 is designed to provide documentation of modifications of the ‘parent’ NCCN Guideline: Bladder Cancer (Version 2.2015). When considering ethnic differences or differences in health regulatory environments between Western and Asian countries, a process of adaptation to match the circumstances is helpful for utilizing the guidelines. The NCCN-ACS for bladder cancer consist of 11 ACSs, focused on diagnosis, imaging, surgical treatment, adjuvant intravesical chemotherapy or immunotherapy, periopererative (neodjuvant or adjuvant) chemotherapy and radiation oncology including bladder preservation. This mini-review will briefly summarize the bladder cancer version 1.2016 of the NCCN-ACS.

Head and neck cancer in Hong Kong


Head and neck cancer is a major cause of morbidity and mortality in Hong Kong. HNC is well-known for its heterogeneity in epidemiology, clinical behavior, clinic-pathological features and patient characteristics. Treatment strategies for this heterogeneous disease vary greatly in different parts of the world, depending on availability of resources, local expertise and experience. Extensive research in head and neck cancer, particularly nasopharyngeal carcinoma, has been conducted in Hong Kong in the past few decades. In this article, we will review the available local evidence and summarize common practice in management of head and neck cancer in Hong Kong.

Immune checkpoint inhibitor-related myocarditis


Immune checkpoint inhibitors have demonstrated significant clinical benefit in many cancers. The clinical benefit afforded by these treatments can be accompanied by a unique and distinct spectrum of adverse events. Recently, several fatal cases of immune checkpoint inhibitor-related myocarditis were reported. Although its frequency is comparatively lower than that of other immune-related adverse events, myocarditis can lead to circulatory collapse and lethal ventricular arrhythmia. Immune checkpoints, cytotoxic T-lymphocyte antigen 4 (CTLA-4) and programmed cell death protein 1 (PD-1), play important roles in establishing peripheral tolerance to the heart. Evidence from studies using genetically engineered mouse models suggests that CTLA-4 signaling terminates proliferation and promotes anergy during the primary response to cardiac self-peptide recognition. PD-1 signaling restrains autoreactive T cells that enter the peripheral tissues and recognize cardiac-peptide, maintaining them in an anergic state. Patients affected by immune checkpoint inhibitor-related myocarditis often experience rapid onset of profound hemodynamic compromise progressing to cardiogenic shock. Early diagnosis is mandatory to address specific therapy and correct the timing of circulatory support. However, the diagnosis of myocarditis is challenging due to the heterogeneity of clinical presentations. Owing to its early onset, nonspecific symptomatology and fulminant progression, especially when these drugs are used in combination, oncologists should be vigilant for immune checkpoint inhibitor-related myocarditis. With many questions yet to be answered, from basic immune biology to clinical management, future research should aim to optimize the use of these drugs by identifying predictive biomarkers of either a response to therapy or the risks of myocarditis development.

Evaluation of renal function change during first-line tyrosine kinase inhibitor therapy for metastatic renal cell carcinoma


The change in renal function induced by first-line tyrosine kinase inhibitor therapy for metastatic renal cell carcinoma remains unclear.
One hundred and thirty-four patients were evaluated. Sunitinib (SU) and sorafenib (SO) were administered to 91 (67.9%) and 43 (32.1%) patients, respectively. The change in estimated glomerular filtration rate (ΔeGFR) was calculated as [(eGFR at each time point – pre-treatment eGFR)/pre-treatment eGFR] × 100. ΔeGFR was compared between SU- and SO users using a mixed-effects model for repeated measures data with two or greater. Additionally, predictors for ΔeGFR ≤ −10% at 6 months after therapy initiation were evaluated using multivariate logistic regression analysis.
Throughout the 24 months after therapy initiation, ΔeGFR was negatively greater in SU users, compared with that in SO users (P < 0.0001). In SU users, renal dysfunction was observed regardless of pre-treatment chronic kidney disease (CKD) status, whereas the magnitude of renal dysfunction was milder in SO users. In SO users without pre-treatment CKD, renal function did not significantly deteriorate. Moreover, ΔeGFR ≤ −10% was more frequently observed in SU users after 3 months (P = 0.0121) and 6 months (P = 0.0009). Finally, SU usage was an independent predictor for ΔeGFR ≤ −10% at 6 months (odds ratio 8.87, P = 0.0053), along with pre-treatment hypertension (odds ratio 4.69, P = 00072).
Deterioration of renal function was stronger with SU than SO. During SU therapy, renal function should be monitored and pre-treatment kidney function should be taken into consideration for therapy selection.