Volume 04 · Issue 01 · 2018

癌细胞可以通过激活免疫检查点，如细胞毒性T淋巴细胞相关抗原4（CTLA4）和程序性死亡-1（PD-1）受体及其配体PD-L1来避免被免疫系统识别和破坏。免疫检查点抑制剂（ICIs）已被证明在越来越多的适应症中有效且反应持续时间长，例如黑色素瘤和非小细胞肺癌（NSCLC）。¹最近，抗PD-1单克隆抗体派姆单抗在微卫星不稳定性高（MSI-H）或DNA错配修复缺陷（dMMR）肿瘤中显示出显著的抗肿瘤活性。²派姆单抗也已被批准用于PD-L1阳性胃癌。³另一种抗PD-1单克隆抗体Nivolumab已被美国批准用于治疗胃癌和肝细胞癌。分别是食品药品监督管理局（FDA）和日本厚生劳动省。^4,5与此同时，越来越多的临床试验正在进行中，以评估ICIs的疗效，目标是扩大ICIs在晚期癌症中的应用。

The objective, accurate, and standardized evaluation of tumor response to treatment is an indispensable procedure in clinical oncology. Compared to manual measurement, computer-assisted linear measurement can significantly improve the accuracy and reproducibility of tumor burden quantification. For irregular-shaped and infiltrating or diffuse tumors, which are difficult to quantify by linear measurement, computer-assisted volumetric measurement may provide a more objective and sensitive quantification to evaluate tumor response to treatment than linear measurement does. In the evaluation of tumor response to novel oncologic treatments such as targeted therapy, changes in overall tumor size do not necessarily reflect tumor response to therapy due to the presence of internal necrosis or hemorrhages. This leads to a new generation of imaging biomarkers to evaluate tumor response by using texture analysis methods, also called radiomics. Computer-assisted texture analysis technology offers a more comprehensive and in-depth imaging biomarker to evaluate tumor response. The application of computer-assisted quantitative imaging analysis techniques not only reduces the inaccuracy and improves the reliability in tumor burden quantification, but facilitates the development of more comprehensive and intelligent approaches to evaluate treatment response, and hence promotes precision imaging in the evaluation of tumor response in clinical oncology. This article summarizes the state-of-the-art technical developments and clinical applications of quantitative imaging analysis in evaluation of tumor response in clinical oncology.

Accumulating evidence confirmed that many dysregulated signaling pathways and aberrant genetic alterations contribute to the oncogenesis and heterogeneity of lymphoid malignancies. Therapeutically targeting dysregulating signaling pathways and their hidden oncogenic biomarkers are becoming available, but did not show desired therapeutic effect in current clinical practice. It is meaningful to further understand the underlying mechanisms of the dysregulated signaling pathways and to address the potential utility of pathway-related biomarkers. To precisely identify the dysregulation of signaling pathways and the "driver" oncogenic biomarkers, as well as to develop reliable and reproducible risk-stratification based on biomarkers will be challenging. Nevertheless, pathway-based targeted therapy will raise the hope to improve the outcomes of the patients with lymphoid malignancies, especially with aggressive types, and the efficient utility of pathway-related biomarkers in diagnosis, prognosis, prediction of lymphoid malignancies may also be able to power precision medicine.

The uremic syndrome is a metabolic disorder characterized by the impairment of renal handling of several solutes, the resulting accumulation of toxic products and the activation of some adaptive but detrimental mechanisms which all together contribute to the progression of renal damage. In moderate to advanced renal failure, the dietary manipulation of nutrients improves metabolic abnormalities and may contribute to delay the time of dialysis initiation. This commentary focuses on the physiopathological rationale and the clinical application of the very low-protein diet supplemented with ketoanalogs for the management of chronic kidney disease.

As a surgical procedure which could significantly lower the recurrence rate of cancers, total mesorectal excision (TME) has been the gold standard for middle and lower rectal cancer treatment. However, previous studies have shown that the procedure did not achieve the ideal theoretical local recurrence rates of rectal cancers. Some researchers pointed out it was very likely that not all so-called TME treatments completely removed the mesorectum, implying that some of these TME surgical treatments failed to meet oncological quality standards. Therefore, a suitable assessment tool for the surgical quality of TME is necessary. The notion of "macroscopic assessment of mesorectal excision (MAME)" was put forward by some researchers as a better assessment tool for the surgical quality of TME and has been confirmed by a series of studies. Besides providing rapid and accurate surgical quality feedbacks for surgeons, MAME also effectively assesses the prognosis of patients with rectal cancer. However, as a new assessment tool used for TME surgical quality, MAME has an only limited influence on the current guidelines and is yet to be widely applied in most countries. The aims of this review are to provide a detailed introduction to MAME for clinical practice and to summarize the current prognostic significance of MAME.

Gastroesophageal adenocarcinomas (GEACs) remain a global health problem. These are most often diagnosed at advanced stage and the estimated 5-year relative survival rate is about 5%. Although cure is not possible for patients with advanced GEAC, systemic therapy (chemotherapy or biochemotherapy) can palliate symptoms, improve survival and provide a better quality of life. One of the most promising options for some patients with advanced stage GEAC is immunotherapy, which can result in durable responses. Numerous phase III trials evaluating targeted therapies in different lines are ongoing and it is hoped that better bio-markers will emerge to identify patients who can benefit from targeted agents and immunotherapy in the future. Surgery remains as the corner stone for localized GEAC and adjunctive therapies can increase the survival rates by about 10%. The high toxicity and low completion rates of adjuvant therapy led to the strategies of preoperative treatment. With the results of ongoing pre-operative therapy trials we will be able to determine the optimal adjunctive approach for resectable GEAC.

Single-nucleotide polymorphisms (SNPs) in the ataxia telangiectasia-mutated gene ATM have been linked with pneumonitis after radiotherapy for lung cancer but have not been evaluated in terms of pulmonary function impairment. Here we investigated potential associations between SNPs in ATM and changes in diffusing capacity of the lung for carbon monoxide (DLCO) in patients with non-small-cell lung cancer (NSCLC) after radiotherapy.

From November 1998 through June 2009, 448 consecutive patients with inoperable primary NSCLC underwent definitive (≥60 Gy) radiotherapy, with or without chemotherapy. After excluding patients with a history of thoracic surgery, radiation, or lung cancer; without DNA samples available for analysis; or without pulmonary function testing within the 12 months before and the 12 months after radiotherapy, 100 patients were identified who are the subjects of this study. We genotyped two SNPs of ATM previously found to be associated with radiation-induced pneumonitis (rs189037 and rs228590) and evaluated potential correlations between these SNPs and impairment (decreases) in DLCO by using logistic regression analysis.

Univariate and multivariate analyses showed that the AA genotype of ATM rs189037 was associated with decreased DLCO after definitive radiotherapy than the GG/AG genotypes [univariate coefficient, -0.122; 95% confidence interval (CI), -0.236 to -0.008; P = 0.037; and multivariate coefficient, -0.102; 95% CI, -0.198 to -0.005; P = 0.038]. No such correlations were found for rs228590 (univariate coefficient, -0.096; 95% CI, -0.208 to 0.017; P = 0.096).

The AA genotype of ATM rs189037 was associated with higher risk of lung injury than were the GG/AG genotypes in patients with NSCLC treated with radiotherapy. This finding should be validated prospectively with other patient populations.

编辑人员和作者希望对已发表的论文进行更正。¹