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Engineered Composites for 3D Mammary Tissue Systems
Published in Karen J.L. Burg, Didier Dréau, Timothy Burg, Engineering 3D Tissue Test Systems, 2017
Cheryl T. Gomillion, Chih-Chao Yang, Didier Dréau, Karen J. L. Burg
The majority of breast cancers originate in the ducts of the breast (85%), whereas others typically originate in the lobules (Korkola et al. 2003). The progression of breast cell growth from a normal to cancerous state is a spontaneous, multistep process. The progression of breast cancer begins with a hyperproliferation of cells or hyperplasia. The epithelial cells still appear normal in structure; however, they begin to divide uncontrollably and more cells are present within the duct. In the atypia stage, the epithelial cells look “atypical” or slightly abnormal upon microscopic examination. This condition is often diagnosed as benign; however, the patient may still be diagnosed as precancerous, indicating that they may have a high likelihood of developing cancer later (Habal 2006; Polyak 2007). Breast cancer can progress to ductal carcinoma in situ (DCIS). In DCIS, the epithelial cells have an abnormal appearance and are fast growing beginning to form clusters within the lining of the duct. When the in situ carcinomas occur in the lobule, it is designated as lobular carcinoma in situ (LCIS) (Habal 2006; Parmar and Cunha 2004; Polyak 2007). In invasive cancer, the abnormal cells of the duct have begun to infiltrate into the surrounding normal breast tissue. The invasive phenotype that is associated with the tumor cell secretion of enzymes is able to degrade the extracellular matrix (ECM) of the ductal basement membrane. These secretions also play a key role in allowing breast cancer cells to intravasate and extravasate the blood vessels or the lymphatic vessels in distant organs (Polyak 2007; Schedin and Keely 2011). The homing of breast cancer cells primarily occur in the lung, the liver, the bones, and the brain, and as the metastases grow in these organs, it negatively affects the entire physiology of the individual.
Evaluation of the carcinogenicity of carbon tetrachloride
Published in Journal of Toxicology and Environmental Health, Part B, 2023
Samuel M. Cohen, Christopher Bevan, Bhaskar Gollapudi, James E. Klaunig
The exposure–response relationship between hepatic cytotoxicity and tumor formation for CCl4 is best demonstrated by the 13-week and two-year inhalation JBRC rodent studies, with liver histopathological changes examined at 13 weeks and liver histopathologic effects examined at the end of the two-year study (Nagano et al. 2007a, 2007b). The CCl4 concentrations evaluated were 0, 10, 30, 90, 270, or 810 ppm in the 13-week study and 0, 5, 25, or 125 ppm in the two-year study. In rats exposed for 13 weeks, histopathological changes indicative of cellular damage (“fatty change”) and inflammation were detected in all CCl4 treatment groups. At ≥30 ppm CCl4, proliferative (increased mitoses) and regenerative (fibrosis, proliferative ducts, cirrhosis) responses occurred. At ≥270 ppm, eosinophilic and basophilic foci, which are associated with hyperplastic or preneoplastic changes, were noted. Liver tumors in rats were observed at an exposure level associated with hepatotoxicity following subchronic and chronic exposure; tumors were not found at an exposure level below the level that induced cytotoxicity (<10 ppm for 13-week exposure and 5 ppm for 104-week exposure). A similar but less consistent exposure–response relationship for cytotoxicity and tumor formation was noted for mice (Nagano et al. 2007a, 2007b). In mice exposed for 13 weeks, exposure-dependent histopathological findings indicative of cytotoxicity, damage, proliferation, and preneoplastic changes were found. Histopathological findings indicative of fatty change were observed in male mice exposed to ≥10 ppm and in female mice exposed to ≥30 ppm CCl4. In male and female mice exposed to ≥30 ppm, a significantly elevated incidence of liver collapse was detected. Liver collapse was characterized by shrunken parenchymal tissue in the centrilobular zone, presumably resulting from necrotic loss of hepatocytes, and accompanied by proliferation of bile ducts and oval cells. In male and female mice exposed to ≥270 ppm, the incidences of nuclear enlargement of hepatocytes with atypia and altered cell foci were significantly increased. The incidence of liver adenomas and carcinomas in male and female (see discussion above) mice in the 104-week study was elevated compared to concurrent controls at ≥25 ppm, an exposure level that also produced cytotoxicity; it is also similar to an exposure level (30 ppm) that produced a proliferative response in the 13-week study.