A clinical and pathological analysis was done on 87 autopsy cases of carcinoma of the bladder. Of the 87 cases 68 were men and 19 were women, with a mean age of 64 years. The average survival time was 39 months from the onset of symptoms to death. The patients with multiple tumors had a longer average survival time than the patients with single tumors (51 compared to 40 months), and the average survival times were definitely more favorable for men than for women (43 compared to 23 months). Histological examination revealed transitional cell carcinoma in 77 patients, squamous cell carcinoma in 4, vesical adenocarcinoma in 3 and urachal adenocarcinoma in 3. Squamous cell carcinoma and vesical adenocarcinoma seemed to be more malignant neoplasms. Metastasis was noted in 58 of 87 cases (66.7 per cent) and occurred most frequently in lymph nodes (37.9 per cent), liver (29.9 per cent), lungs (29.9 per cent) and bones (24.1 per cent). Of the 87 cases of bladder carcinoma 11 had primary carcinoma in organs other than the bladder.

Jack Russell terriers (JRTs) with gastrointestinal (GI) neoplastic polyps have been recently reported to harbor an identical germline variant in the adenomatous polyposis coli (APC) gene, c.[462_463delinsTT], in the heterozygous state, which indicates that this disease is an autosomal dominant hereditary disorder. Many individual cases of this disease have been observed in clinical practice; however, familial transmission has not been demonstrated due to the difficulty in tracing the family members of household dogs, especially after the disease’s onset in adulthood. Recently, we encountered two cases of GI polyposis in maternal half sisters. These two cases facilitated the identification of additional relatives spanning three generations, including parents, full and half siblings of the dam (aunt and uncle), littermate and non-littermate siblings, and a nephew. Genetic analysis revealed that 11 of the 14 examined JRTs in this family carried the heterozygous germline APC variant, and eight dogs with the variant already had a current and/or past medical history of GI neoplastic polyps. Some cases in the family showed significantly more severe disease phenotypes than those initially reported, suggesting that the severity of this disease can vary considerably among individuals. Moreover, familial aggregation of severe cases suggested that the genetic modifier involved in increasing severity may have been transmitted in this family in addition to the germline APC variant. Furthermore, in addition to this family, we reported two other families of JRTs affected by hereditary GI polyposis that consisted of five full and half siblings and a mother–daughter pair, respectively. These findings unequivocally establish the transgenerational transmission of hereditary GI polyposis associated with the germline APC variant in JRT lineages.