Background: To establish a model of pancreatic cancer induced by 7,12-dimethylbenzantracene (DMBA) in Sprague-Dawley (SD) rats, and detect the expression of DNA-repair proteins (MGMT, ERCC₁, hMSH₂, and hMLH₁) and their significance in pancreatic cancer and non-cancerous pancreatic tissues of SD rats.
Methods: DMBA was directly implanted into the parenchyma of rat pancreas (group A and group B), and group B rats were then treated with trichostatin A (TSA). The rats in both groups were executed within 3 to 5 months, and their pancreatic tissues were observed by macrography and under microscopy. Meanwhile, the rats in the control group (group C) were executed at 5 months. Immunohistochemistry was used to assay the expression of MGMT, ERCC₁, hMSH₂, and hMLH₁.
Results: The incidence of pancreatic cancer in group A within 3 to 5 months was 48.7% (18/37), including 1 case of fibrosarcoma. The incidence of pancreatic cancer in group B was 33.3% (12/36), including 1 case of fibrosarcoma. The mean of maximal diameters of tumors in group A was higher than that in group B (P <0.05). No pathological changes were found in pancreas of group C and other main organs (except pancreas) of group A and group B. No statistical differences were found among the positive rates of MGMT, ERCC₁, hMSH₂, and hMLH₁ in ductal adenocarcinoma and non-cancerous pancreatic tissues of group A (P >0.05). The positive rates of MGMT, ERCC₁, hMSH₂, and hMLH₁ were significantly lower in ductal adenocarcinoma than those in non-cancerous tissues of group B (P ≤0.05). All pancreas of group C had positive expression of MGMT, ERCC₁, hMSH₂, and hMLH₁ and two cases of fibrosarcoma showed a negative expression.
Conclusions: DMBA, directly implanted into the parenchyma of pancreas, creates an ideal pancreatic cancer model within a short time. TSA might restrain DNA damage related to the genesis and growth of pancreatic cancer in rats. The DNA-repair proteins, including MGMT, ERCC₁, hMSH₂, and hMLH₁, might play an important role in the genesis of pancreatic cancer induced by DMBA in rats.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3931407 | PMC |
http://dx.doi.org/10.1186/1477-7819-12-32 | DOI Listing |
Ann Med
December 2025
Department of Surgery, Faculty of Medicine, Unit of Hepato-Pancreato-Biliary Surgery and Abdominal Organ Transplantation, Doce de Octubre University Hospital, Instituto de Investigación (imas12), Complutense University, Madrid, Spain.
Background: Delayed gastric emptying (DGE) is a frequent complication of pancreatoduodenectomy (PD) and is associated with prolonged hospital stay, readmission, increased hospital costs and decreased quality of life. However, the pathophysiology of DGE remains unclear.
Methods: This is a retrospective study of patients who underwent PD for pancreatic or periampullary tumours.
Phys Imaging Radiat Oncol
January 2025
Department of Radiation Oncology, Hokkaido University Faculty of Medicine and Graduate School of Medicine, North 15 West 7, Kita-ku, Sapporo, Hokkaido 060-8638, Japan.
Background And Purpose: Radiation-induced lymphopenia (RIL) may be associated with a worse prognosis in pancreatic cancer. This study aimed to develop a normal tissue complication probability (NTCP) model to predict severe RIL in patients with pancreatic cancer undergoing concurrent chemoradiotherapy (CCRT).
Materials And Methods: We reviewed pancreatic cancer patients treated at our facility for model training and internal validation.
Ann Transl Med
December 2024
Institute for Tumor Immunology, Center for Tumor Biology and Immunology, Philipps-University Marburg, Marburg, Germany.
One of the most important targets for natural killer (NK) cell-mediated therapy is the induction of natural killer group 2D ligand (NKG2D-L) expression. APTO253 is a small molecule that selectively kills acute myeloid leukemia (AML) cells, and it has been reported that APTO253 can induce Krüppel-like factor 4 (KLF4) expression and downregulate c-MYC expression. Recently, we discovered a novel role of APTO253 in modulating the NK cell response by inducing surface expression of NKG2D-Ls, especially MHC class I polypeptide-related sequence A (MICA), in AML cells.
View Article and Find Full Text PDFAnn Transl Med
December 2024
Department of Clinical Oncology, The Christie NHS Foundation Trust, Manchester, UK.
World J Gastrointest Oncol
January 2025
Faculty of Medicine, Carol Davila University of Medicine and Pharmacy, Bucharest 050474, Romania.
Background: Pancreatic ductal adenocarcinoma (PDAC) is an aggressive lethal malignancy with limited options for treatment and a 5-year survival rate of 11% in the United States. As for other types of tumors, such as colorectal cancer, aberrant lipid synthesis and reprogrammed lipid metabolism have been suggested to be associated with PDAC development and progression.
Aim: To identify the possible involvement of lipid metabolism in PDAC by analyzing in tumoral and non-tumoral tissues the expression level of the most relevant genes involved in the long-chain fatty acid (FA) import into cell.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!