Tomomi Maeda-Tateishi, Yuki Nagata, Yasuo Imanishi, Tomoe Hirakawa, Seong-Seng Tan, Masanori Emoto, Min Gi
{"title":"Evaluation of tumor clonality with chemical carcinogenesis in a mouse model of visualized X chromosome inactivation.","authors":"Tomomi Maeda-Tateishi, Yuki Nagata, Yasuo Imanishi, Tomoe Hirakawa, Seong-Seng Tan, Masanori Emoto, Min Gi","doi":"10.1293/tox.2025-0075","DOIUrl":"10.1293/tox.2025-0075","url":null,"abstract":"<p><p>Tumor clonality is determined by somatic mutations in genes that regulate cell proliferation, and this can be either monoclonal or multiclonal. Assays based on X-chromosome inactivation that exploit the random inactivation of one of the two X chromosomes in female embryos have been used to evaluate tumor clonality. However, these methods require technically complex procedures and are not easily applicable to various types of tumors. Here, we visualized the clonality of tumors induced by chemical substances <i>in vivo</i> using X-linked <i>LacZ</i> heterozygous transgenic female mice that displayed a blue or white mosaic pattern of tissue on X-gal staining. In a model of colorectal tumors induced by 1, 2-dimethylhydrazine dihydrochloride and dextran sulfate sodium salt, 18 blue, 20 unstained (white), and seven mixed-colored tumors in intestinal tissues from 20 mice were observed after X-gal staining. Similarly, in a model of diethylnitrosamine-induced liver tumors, multiple blue or white nodules were observed. These findings demonstrated that this is a simple and effective method for visualizing tumor clonality <i>in vivo</i>. This approach may be readily applicable to models of chemically induced carcinogenesis and useful for evaluating the clonality of multifocal lesions.</p>","PeriodicalId":17437,"journal":{"name":"Journal of Toxicologic Pathology","volume":"39 1","pages":"31-38"},"PeriodicalIF":0.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12826865/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146053035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Association between spontaneous neurogenic atrophy of the femoral muscle and islet cell tumors in aged F344 rats.","authors":"Mitsutoshi Uchida, Yumi Wako, Takeshi Kanno, Natsumi Shimoyama, Yutaka Nakahara, Takuya Doi, Yuki Tomonari, Junko Sato","doi":"10.1293/tox.2025-0016","DOIUrl":"10.1293/tox.2025-0016","url":null,"abstract":"<p><p>In aged F344/DuCrlCrlj rats, we observed that all animals with group atrophy of the biceps femoris muscle also had islet cell tumors, suggesting that spontaneous islet cell tumors may induce peripheral neuropathy and muscle atrophy. Among 220 aged male F344/DuCrlCrlj rats examined, 12.3% (27/220) had islet cell tumors, and of these, 22.2% (6/27) had neurogenic muscular atrophy. Sciatic nerve degeneration was observed in 3.2% (7/220) of cases, and all animals with neurogenic muscular atrophy had sciatic nerve degeneration. Notably, no neurogenic muscular atrophy was observed in rats without islet cell tumors. In contrast, rats with neurogenic muscular atrophy tended to have larger islet cell tumors. Although spinal nerve root degeneration was prevalent (90.8%, 198/218), two of the six rats with neurogenic muscular atrophy did not exhibit this pathology. Immunohistochemically, insulin was positive in all islet cell tumors, although glucagon- and somatostatin-positive reactions showed no association with neurogenic muscular atrophy. Experimentally induced hyperinsulinemia in rats is a known cause of neurogenic muscular atrophy, and similar associations have been reported in humans and spontaneous cases of pet rats with islet cell tumors. A complete coincidence between the occurrence of neurogenic muscular atrophy and islet cell tumors in our investigation suggests that some islet cell tumors in F344/DuCrlCrlj rats may be functionally active, and that hyperinsulinemia may contribute to the pathogenesis of neurogenic muscular atrophy.</p>","PeriodicalId":17437,"journal":{"name":"Journal of Toxicologic Pathology","volume":"39 1","pages":"15-23"},"PeriodicalIF":0.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12826866/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146053060","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Wes Baumgartner, Ute Bach, James Baily, Christine Ruehl-Fehlert, Stacey Fossey, Satoshi Furukawa, Yuki Kato, Victoria Laast, Emily Meseck, Heike Schmidt-Posthaus, Helmut Segner, Shiva Kumar Shanmukhappa, Jan Spitsbergen, Jeffrey Wolf
{"title":"INHAND: Non-proliferative and proliferative lesions of fish - Chapter 10. Fish male reproductive system.","authors":"Wes Baumgartner, Ute Bach, James Baily, Christine Ruehl-Fehlert, Stacey Fossey, Satoshi Furukawa, Yuki Kato, Victoria Laast, Emily Meseck, Heike Schmidt-Posthaus, Helmut Segner, Shiva Kumar Shanmukhappa, Jan Spitsbergen, Jeffrey Wolf","doi":"10.1293/tox.2025-0200","DOIUrl":"10.1293/tox.2025-0200","url":null,"abstract":"","PeriodicalId":17437,"journal":{"name":"Journal of Toxicologic Pathology","volume":"39 2 Suppl","pages":"210S-225S"},"PeriodicalIF":1.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13340196/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148405061","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"A canine insulinoma with amphicrine differentiation: morphological and immunohistochemical characteristics.","authors":"Hisaki Tokuno, Masashi Fujimoto, Makoto Tsuji, Miyuu Tanaka, Takeshi Izawa, Mitsuru Kuwamura","doi":"10.1293/tox.2025-0062","DOIUrl":"10.1293/tox.2025-0062","url":null,"abstract":"<p><p>A 10-year-old male toy poodle presented with hypoglycemia. An insulinoma was suspected and a surgical excision of two pancreatic masses was performed. White-gray, demarcated, soft masses were identified in the pancreas. Histopathologically, two types of growth patterns were observed in the same neoplasm: nest and glandular. To investigate cellular differentiation, we performed immunohistochemical and transmission electron microscopy analyses. Both types of neoplastic cells were immunopositive for INSM1, Nkx2.2 and insulin. However, the neoplastic cells exhibiting the nest pattern contained exocrine granules, whereas those with the glandular pattern were immunopositive for cytokeratin. Both types of neoplastic cells showed not only neuroendocrine but also exocrine differentiation in the same neoplastic cell. To the best of our knowledge, this is the first report describing the morphology and immunophenotype of the canine insulinoma with amphicrine differentiation: showing both neuroendocrine and exocrine features.</p>","PeriodicalId":17437,"journal":{"name":"Journal of Toxicologic Pathology","volume":"39 1","pages":"39-44"},"PeriodicalIF":0.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12826864/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146053005","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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