Diagnostic performance of Node Reporting and Data System (Node-RADS) for regional lymph node staging of gastric cancer by CT.

OBJECTIVES: Diagnostic performance of imaging for regional lymph node assessment in gastric cancer is still limited, and there is a lack of consensus on radiological evaluation. At the same time, there is an increasing demand for structured reporting using Reporting and Data Systems (RADS) to standardize oncological imaging. We aimed at investigating the diagnostic performance of Node-RADS compared to the use of various individual criteria for assessing regional lymph nodes in gastric cancer using histopathology as reference. METHODS: In this retrospective single-center study, consecutive 91 patients (median age, 66 years, range 33-91 years, 54 men) with CT scans and histologically proven gastric adenocarcinoma were assessed using Node-RADS assigning scores from 1 to 5 for the likelihood of regional lymph node metastases. Additionally, different Node-RADS criteria as well as subcategories of altered border contour (lobulated, spiculated, indistinct) were assessed individually. Sensitivity, specificity, and Youden's index were calculated for Node-RADS scores, and all criteria investigated. Interreader agreement was calculated using Cohen's kappa. RESULTS: Among all criteria, best performance was found for Node-RADS scores ≥ 3 and ≥ 4 with a sensitivity/specificity/Youden's index of 56.8%/90.7%/0.48 and 48.6%/98.1%/0.47, respectively, both with substantial interreader agreement (κ = 0.73 and 0.67, p < 0.01). Among individual criteria, the best performance was found for short-axis diameter of 10 mm with sensitivity/specificity/Youden's index of 56.8%/87.0%/0.44 (κ = 0.65, p < 0.01). CONCLUSION: This study shows that structured reporting of combined size and configuration criteria of regional lymph nodes in gastric cancer slightly improves overall diagnostic performance compared to individual criteria including short-axis diameter alone. The results show an increase in specificity and unchanged sensitivity. CLINICAL RELEVANCE STATEMENT: The results of this study suggest that Node-RADS may be a suitable tool for structured reporting of regional lymph nodes in gastric cancer. KEY POINTS: • Assessment of lymph nodes in gastric cancer is still limited, and there is a lack of consensus on radiological evaluation. • Node-RADS in gastric cancer improves overall diagnostic performance compared to individual criteria including short-axis diameter. • Node-RADS may be a suitable tool for structured reporting of regional lymph nodes in gastric cancer.

Correction to: The majority of ß-catenin mutations in colorectal cancer is homozygous.

An amendment to this paper has been published and can be accessed via the original article.

The majority of ß-catenin mutations in colorectal cancer is homozygous.

BACKGROUND: ß-catenin activation plays a crucial role for tumourigenesis in the large intestine but except for Lynch syndrome (LS) associated cancers stabilizing mutations of ß-catenin gene (CTNNB1) are rare in colorectal cancer (CRC). Previous animal studies provide an explanation for this observation. They showed that CTNNB1 mutations induced transformation in the colon only when CTNNB1 was homozygously mutated or when membranous ß-catenin binding was hampered by E-cadherin haploinsufficiency. We were interested, if these mechanisms are also found in human CTNNB1 mutated CRCs. RESULTS: Among 869 CRCs stabilizing CTNNB1 mutations were found in 27 cases. Homo- or hemizygous CTNNB1 mutations were detected in 74% of CTNNB1 mutated CRCs (13 microsatellite instabile (MSI-H), 7 microsatellite stabile (MSS)) but only in 3% (1/33) of extracolonic CTNNB1 mutated cancers. In contrast to MSS CRC, CTNNB1 mutations at codon 41 or 45 were highly selected in MSI-H CRC. Of the examined three CRC cell lines, ß-catenin and E-cadherin expression was similar in cell lines without or with hetereozygous CTNNB1 mutations (DLD1 and HCT116), while a reduced E-cadherin expression combined with cytoplasmic accumulation of ß-catenin was found in a cell line with homozygous CTNNB1 mutation (LS180). Reduced expression of E-cadherin in human MSI-H CRC tissue was identified in 60% of investigated cancers, but no association with the CTNNB1 mutational status was found. CONCLUSIONS: In conclusion, this study shows that in contrast to extracolonic cancers stabilizing CTNNB1 mutations in CRC are commonly homo- or hemizygous indicating a higher threshold of ß-catenin stabilization to be required for transformation in the colon as compared to extracolonic sites. Moreover, we found different mutational hotspots in CTNNB1 for MSI-H and MSS CRCs suggesting a selection of different effects on ß-catenin stabilization according to the molecular pathway of tumourigenesis. Reduced E-cadherin expression in CRC may further contribute to higher levels of transcriptionally active ß-catenin, but it is not directly linked to the CTNNB1 mutational status.