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Aim: Improvement in oncological survival for rectal cancer increases attention to anorectal dysfunction. Diagnostic questionnaires can evaluate quality of life but are subjective and dependent on patients’ compliance. Anorectal manometry can objectively assess the continence mechanism and identify functional sphincter weakness and rectal compliance. Neoadjuvant chemoradiotherapy is presumed to affect anorectal function. We aim to assess anorectal function in rectal cancer patients who undergo total mesorectal excision, with or without neoadjuvant chemoradiation, using anorectal manometry measurements.Method: MEDLINE, Embase, and Cochrane databases were searched for studies comparing perioperative anorectal manometry between neoadjuvant chemoradiation and upfront surgery for rectal cancers. Primary outcomes were resting pressure, squeeze pressure, sensory threshold volume and maximal tolerable volume.Results: Eight studies were included in the systematic review, of which seven were included for metanalysis. 155 patients (45.3%) had neoadjuvant chemoradiation before definitive surgery, and 187 (54.6%) underwent upfront surgery. Most patients were male (238 vs. 118). The standardized mean difference of mean resting pressure, mean and maximum squeeze pressure, maximum resting pressure, sensory threshold volume, and maximal tolerable volume favored the upfront surgery group but without statistical significance.Conclusion: Currently available evidence on anorectal manometry protocols failed to show any statistically significant differences in functional outcomes between neoadjuvant chemoradiation and upfront surgery. Further large-scale prospective studies with standardized neoadjuvant chemoradiation and anorectal manometry protocols are needed to validate these findings.

The incidences of spontaneous tumors of the murine hybrids (C57BL/6J x C3Hf)Fl (B6C3F1) and (C57BL/6J x BALB/c)Fl (B6CF1) were compared in untreated mice kept until 110 weeks of age. Male B6C3F1 and B6CF1 mice had respectively 16 % and 20 % incidence of lymphomas, 26 % and 4 % of liver tumors and 12 % and 22 % of lung tumors. Among B6C3F1 and B6CF1 females, a 36 % and 12 % incidence of lymphomas, a 6 % and zero incidence of liver tumors, and a 4 % and 16 % of lung tumors were observed. A few other tumors were seen in both hybrids. Groups of male and female mice of the 2 hybrids received 5 i.p. injections of 1000 mg/kg urethan once every other day starting at 10 days of age, and were kept under observation until 65–80 weeks of age. Treated B6C3F1 mice had an earlier mortality than B6CF1 mice due to tumor development. The statistical analysis, allowing for survival, showed a significantly higher lymphoma incidence in male and female B6C3F1 than B6CF1 mice, which had instead a higher incidence of lung tumors. Hepatocellular tumors were seen in both sexes of the 2 hybrids, with a higher frequency in B6C3F1 mice. Male mice of both hybrids had a higher incidence of liver tumors than females.

The expression of moloney murine leukemia virus (Mo-MuLV), intracisternal A particle (IAP), virus-like 30S sequence (VL30), early transposon (ET) endogenous retroviral sequences was analysed in the liver of untreated C3Hf, C57BL/6J and AKR mice, and in the lungs of untreated A/J, BALB/c, C3Hf and C57BL/6J mice. C3Hf mice are genetically susceptible to hepatocarcinogenesis, whereas the other strains are resistant. A/J and BALB/c mice are genetically susceptible to lung carcinogenesis, whereas the other strains are resistant. Both in liver and lung tissues we found differences between murine strains in the pattern of basal retrovirus expression. The effect of inhibition of protein synthesis on the levels of retroviral mRNAs was studied in the same tissues and strains 3 h following in vivo cycloheximide treatment. Cycloheximide treatment increased the liver and lung levels of virus Mo-MuLV, IAP, ET related transcripts in a strain dependent way, whereas VL30 mRNA levels increased in both tissues of all strains examined. These results suggested the existence of labile proteins that regulate the abundance of specific retroviral mRNAs in murine liver and lung in a strain specific fashion. No clear relationships between pattern of retrovirus expression and genetical susceptibility to hepatocarcinogenesis was found. The strains genetically resistant to lung carcinogenesis (C3Hf, C57BL/6J) showed higher lung basal levels and higher cycloheximide inducibility of mRNAs homologous to Mo-MuLV than the susceptible strains (A/J, BALB/c).

An infantile carcinogenesis assay was carried out with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) injections administered intraperitoneally at 0, 1, 30 and 60 μg/kg b.w. doses to (C57BL/6J × C3Hf)F1 (B6C3) and to (C57BL/6J × BALB/c)F1 (B6C) mice, starting from the 10th day of life, once weekly repeated 5 times. Animals were then observed until 78 weeks of age. The induction of thymic lymphomas was related to treatment at 60 μg/kg dose level in both sexes of both hybrids, and at 30 μg/kg dose level in both sexes of B6C mice and in male but not female B6C3 mice. The incidence of hepatocellular adenomas was increased by TCDD treatment at 60 μg/kg dose level in B6C3 of both sexes but not in B6C mice. Hepatocellular carcinomas were seen at increased incidence at 30 and 60 μg/kg doses in B6C3 males but not in B6C3 females or in B6C mice of both sexes. The incidence of other tumor types was not related to treatment in both hybrids. A long-term carcinogenesis bioassay with TCDD was carried out in B6C3 mice treated by gavage at 0, 2.5 and 5.0 μg/kg b.w. doses from 6 weeks of age, once weekly for 52 weeks. The animals were observed until 110 weeks of age. An increased incidence of hepatocellular adenomas and carcinomas was related to treatment, at both doses and in both sexes. The incidence of other tumor types was uniformly low in treated and control groups, without any association with treatment, in both sexes.

3-(5-nitro-2-furyl)-imidazo(1,2-α)pyridine was tested for carcinogenicity by long-term administration in the diet to CTM mice at 0.1, 0.2 and 0.4 % dose levels and to Wistar rats at 0.2 and 0.4 % dose levels, and by short-term intraperitoneal injections to suckling BALB/c mice. The compound was a strong carcinogen. In CTM mice it induced carcinomas of the esophagus and forestomach at all dose levels and thymic lymphosarcomas at the two highest doses. In male and female rats, esophagus and forestomach papillomas were observed at all dose levels, whereas esophagus and forestomach carcinomas and kidney tumors were observed only at the high dose. In female rats, an increased incidence of mammary tumors was seen at the high dose. The treatment of BALB/c suckling mice by intraperitoneal injections did not induce a clear carcinogenic response.

The tumor incidence was studied in 4 groups of BALB/c mice kept under observation in the same experimental conditions as untreated controls in the course of bioassays of chemical carcinogenesis. Two parameters that reflect the variations of environmental factors were studied: body growth and survival rate. Their possible influence on tumor incidence was also considered. Fluctuations were observed in the incidence of different tumor types among the groups, but the level of significance was reached only when comparing the incidence of hepatomas, adrenal cortex tumors and subcutaneous fibrosarcomas among males and the incidence of angiomas and angiosarcomas among females. No association was found between the variations of tumor incidence and body growth and survival rate, which remained constant among the groups.