For patients with locally advanced rectal cancer (LARC) with pathological complete response (pCR), the clinical significance of the distribution extent of acellular mucin pools (AMP) distribution remains unclear, so this study was conducted to address key unanswered questions. We performed a retrospective analysis of 317 patients with LARC with pCR after preoperative chemoradiotherapy and total mesorectal resection from January 2011 to June 2020. Based on AMP existence and the deepest tissue layer of distribution, patients were assigned new stages. The patient information was recorded, and the main outcome measures included 5-year disease-free survival (DFS) and 5-year overall survival (OS). A total of 83/317 (26.2%) patients exhibited AMP, and disease recurrence occurred in 46/317 (14.5%) patients. Over the 5-year median follow-up period, the patients with AMP showed 5-year DFS rates (75.9% vs. 88.9%, P=0.004) and 5-year OS rates (85.5% vs. 95.7%, P=0.002) statistically lower than those of patients without AMP. Disease recurrence was seen in 15/54 (27.8%) patients with AMP within the subserosa and/or the serosa, or adipose tissue. Univariate and multivariate analysis showed that the existence of AMP within the subserosa and/or the serosa, or adipose tissue was an independent risk factor for DFS [hazard ratio (HR): 2.344; 95% confidence interval (CI): 1.256–4.376; P=0.007] and OS [HR: 3.374; 95% CI: 1.438–7.917; P=0.005]. The new stages based on the deepest extent of AMP were related to worse DFS (P=0.004) and OS (P=0.003) rates among patients with pCR. In conclusion, the presence of AMP might reduce the prognosis of LARC patients with pCR after chemoradiotherapy, especially in patients with AMP in deeper tissue layers. Therefore, the influence of the deepest AMP extent might be worth considering in staging. Moreover, the revised staging of patients with pCR according to the deepest extent of AMP, which is unrelated to the clinical T stage, might facilitate postoperative management.

ABSTRACT. To find the underlying cause of noncompaction of the ventricular myocardium (NVM), three Chinese families with probands who presented this problem were studied. After the family members were evaluated by echocardiography, the gene G4.5 (taffazin) was scanned by sequencing. Although X-linked inheritance could not be ruled out, NVM were thought to have a vague rule of inheritance in our data from 8 patients and 28 family members. We also did not identify any mutations in G4.5 in all samples. Our data suggest that other genes are responsible for the familial form of this disease.

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