Malignant Phyllodes Tumour with Liposarcomatous Differentiation, Invasive Tubular Carcinoma, and Ductal and Lobular Carcinoma In Situ: Case Report and Review of the Literature

A 43-year-old woman presented with a right breast lump that had enlarged over 5 months. She had chemoradiotherapy for non-Hodgkin's lymphoma in 1989. Histology revealed a malignant phyllodes tumour (PT) with liposarcomatous differentiation and ductal carcinoma in situ (DCIS) within the tumour with invasive tubular carcinoma, DCIS, and lobular carcinoma in situ in the surrounding breast. She had surgery and adjuvant radiotherapy. One year follow-up showed no recurrence or metastatic disease. Liposarcomatous differentiation is uncommon in PTs, and coexisting carcinoma is rare with 38 cases in 31 reports in the literature. Carcinoma is reported in malignant (n = 19), benign (n = 16) and in borderline PTs (n = 3) with invasive carcinoma (n = 18) and pure in situ carcinoma (n = 19) recorded in equal frequency. Carcinoma is more commonly found within the confines of benign PTs; whereas it is more often found surrounding the PT or in the contralateral breast in malignant PTs. Previous radiotherapy treatment is reported in only two cases. The aetiology of co-existing carcinoma is unclear but the rarity of previous radiotherapy treatment suggests that it is incidental. This case highlights the diverse pathology that can occur with PTs, which should be considered when evaluating pathology specimens as they may impact on patient management

Comparison of non-alcoholic fatty liver disease (NAFLD) model using diet-induced NAFLD mice with genetically modified mice

Prevalence of non-alcoholic fatty liver disease (NAFLD) is increasing steadily every year affecting all population both Western and Asian countries. The current treatments available for NAFLD are non-conclusive warranting newer effective pharmacological agents. Newly formulated agents require prior testing using animal models. However, in developing countries, these models are often costly. The possibility of using more affordable animal model in local settings should be investigated. In this study, ten Institute of Cancer Research (ICR) and seven B6.Cg-LepOb/J leptin-knockout (JAX) male mice were recruited. Five ICR and all JAX mice were subjected to high-fat diet (60% kcal fat) and remaining ICR mice were given standard diet (SD) for six weeks. Body weight and food intake were measured weekly while abdominal circumference, random blood glucose and liver span were measured at the end of the HFD study. Livers collected were subjected to histology assessment. Compared to ICR group, JAX group presented with significantly higher body weight (58 ± 0.72, p<0.05), larger body weight changes (16.57 ± 0.81, p<0.05), more HFD intake (197.14 ± 0.812, p<0.05) and larger abdominal circumference (11.79 ± 0.34: p<0.05). Liver from JAX group appeared with general steatosis and presentation of high-grade panacinar steatosis, low number of lobular inflammations and minimal fibrosis. Liver of ICR mice showed Zone 3 steatosis with high number of lobular inflammations without fibrosis. The NAFLD characteristics presented in JAX group suggested that B6.Cg-LepOb/J mice developed characteristics of NAFLD resembling human while ICR is suitable NAFLD model resembling human population resilient towards NAFLD

Prenatal Bisphenol a Exposure and Postnatal Trans Fat Diet Alter Small Intestinal Morphology and Its Global DNA Methylation in Male Sprague-Dawley Rats, Leading to Obesity Development

In this study, we aimed to determine whether a postnatal trans fat diet (TFD) could aggravate prenatal bisphenol A (BPA) exposure effects on offspring&rsquo;s small intestine and adulthood obesity, due to the relatively sparse findings on how the interaction between these two variables interrupt the small intestinal cells. Twelve pregnant rats were administered with either unspiked drinking water (control; CTL) or BPA-spiked drinking water throughout pregnancy. Twelve weaned pups from each pregnancy group were then given either a normal diet (ND) or TFD from postnatal week (PNW) 3 until PNW14, divided into control offspring on normal diet (CTL-ND), BPA-exposed offspring on normal diet (BPA-ND), control offspring on trans fat diet (CTL-TFD), and BPA offspring on trans fat diet (BPA-TFD) groups. Body weight (BW), waist circumference, and food and water intake were measured weekly in offspring. At PNW14, small intestines were collected for global DNA methylation and histological analyses. Marked differences in BW were observed starting at PNW9 in BPA-TFD (389.5 &plusmn; 10.0 g; p &lt; 0.05) relative to CTL-ND (339.0 &plusmn; 7.2 g), which persisted until PNW13 (505.0 &plusmn; 15.6 g). In contrast, water and food intake between offspring were significantly different (p &lt; 0.01&ndash;0.05) at earlier ages only (PNW4&ndash;6 and PNW7&ndash;9, respectively). Furthermore, substantial differences in the general parameters of the intestinal structures were exclusive to ileum crypt length alone, whereby both BPA-ND (150.5 &plusmn; 5.1 &mu;m; p &lt; 0.001), and BPA-TFD (130.3 &plusmn; 9.9 &mu;m; p &lt; 0.05) were significantly longer than CTL-ND (96.8 &plusmn; 8.9 &mu;m). Moreover, BPA-ND (2.898 &plusmn; 0.147%; p &lt; 0.05) demonstrated global small intestinal hypermethylation when compared to CTL-ND and CTL-TFD (1.973 &plusmn; 0.232% and 1.913 &plusmn; 0.256%, respectively). Prenatal BPA exposure may significantly affect offspring&rsquo;s physiological parameters and intestinal function. Additionally, our data suggest that there might be compensatory responses to postnatal TFD in the combined BPA prenatal group (BPA-TFD)