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[en] It is presently believed that radiotherapy is one of the promising treatments of pancreatic adenocarcinoma. However, irradiation in humans produces both acute and chronic effects. The effects of radiation therapy on pancreatic beta-cell function are not fully documented. Thus, changes induced by radiation on pancreatic islet function should be considered. In the present study, the effect of radiation on pancreatic beta-cell function in rats is investigated. (author). 8 refs.; 1 fig
[en] Purpose: Pancreatic neuroendocrine tumors (PNTs) are rare malignant neoplasms considered to be resistant to radiotherapy (RT), although data on efficacy are scarce. We reviewed our institutional experience to further delineate the role of RT for patients with PNTs. Methods and Materials: Between 1986 and 2006, 36 patients with PNTs were treated with RT to 49 sites. Of these 36 patients, 23 had radiographic follow-up data, which were used to determine the tumor response rate and freedom from local progression. Long-term toxicity was graded according to the National Cancer Institute Common Terminology Criteria for Adverse Events. Results: The overall response rate to RT was 39% (13% complete response, 26% partial response, 56% stable disease, and 4% progressive disease). A significant difference in the freedom from local progression between the groups receiving either greater than or less than the median 2 Gy/fraction biologically equivalent dose of 49.6 Gy was found, with all radiographic progression occurring in patients who had received ≤32 Gy. The actuarial 3-year local freedom from progression rate was 49%. Palliation was achieved in 90% of patients, with either improvement or resolution of symptoms after RT. Of 35 patients, 33 had metastatic disease at their referral for RT, and the median overall survival for this patient population was 2 years. Three long-term Grade 3 or greater toxicities were recorded. Conclusion: RT is an effective modality for achieving local control in patients with PNTs. RT produces high rates of symptomatic palliation and freedom from local progression. Prospective trials of radiotherapy for PNTs are warranted.
BackgroundSOX9, a progenitor cell marker, is important for pancreatic ductal development. Our goal was to examine SOX9 expression differences in intraductal papillary mucinous neoplasms (IPMNs) and ductal adenocarcinoma (PDAC) compared with benign pancreatic duct (BP).
MethodsSOX9 expression was evaluated by immunohistochemistry performed on 93 specimens: 37 BP, 24 low grade (LG) IPMN, 12 high grade (HG) IPMN, and 20 PDAC. A linear mixed-effects model was used to compare the percentage of cells expressing SOX9 by specimen type. A separate linear mixed-effects model evaluated differences in SOX9 expression by staining intensity in pancreatic epithelial cells.
ResultsNuclear SOX9 expression was detected in the epithelial cells of 98% HG IPMN, 93% LG IPMN, 83% PDAC, and 60% BP. Compared with BP, SOX9 was expressed from a significantly greater percentage of cells in LG IMPN, HG IMPN, and PDAC (p < 0.001 for each). BP and PDAC showed greater variability in SOX9 expression in epithelial cells compared with IPMNs which showed strong, homogenous SOX9 expression in almost all cells. Compared with BP, both LG and HG IPMN showed significantly greater SOX9 expression (p < 0.001 for each), but there was no significant difference in SOX9 expression between LG and HG IPMN (p > 0.05). PDAC had significantly higher expression of SOX9 compared with BP but significantly lower SOX9 expression compared with LG or HG IPMN (p < 0.001 for each).
ConclusionsIPMNs demonstrated the highest expression levels of SOX9. SOX9 expression in BP and PDAC demonstrated much more heterogeneity compared with the strong, uniform expression in IPMN.
[en] The ability to escape apoptosis or programmed cell death is a hallmark of human cancers, for example pancreatic cancer. This can promote tumorigenesis, since too little cell death by apoptosis disturbs tissue homeostasis. Additionally, defective apoptosis signaling is the underlying cause of failure to respond to current treatment approaches, since therapy-mediated antitumor activity requires the intactness of apoptosis signaling pathways in cancer cells. Thus, the elucidation of defects in the regulation of apoptosis in pancreatic carcinoma can result in the identification of novel targets for therapeutic interference and for exploitation for cancer drug discovery
[en] Purpose: The current IGRT repositioning cannot fully account for the organ deformation and rotation. We introduce a comprehensive solution using gated IMRT with online adaptive replanning to manage both inter- and intra-fractional variations. Methods and materials: The solution includes (1) generating respiration-gated IMRT plans based on 4DCT, (2) acquiring daily gated CT in treatment position prior to the treatment using a diagnostic-quality in-room CT (CTVision, Siemens) with the same gating window as that for the planning CT, (3) performing online repositioning or adaptive replanning based on the gated CT of the day, and (4) delivering the treatment with gating. The entire solution is demonstrated with RT data from 10 selected pancreatic cancer cases. The dosimetric impact of various advanced delivery technologies was investigated. Results: The online adaptive replanning based on the CT of the day combining with gating significantly improves normal tissue sparing during RT for pancreatic cancer. As the complexity of the delivery technology increases from no IGRT to with IGRT, gating and online adaptive replanning, the inter- and intra-fractional variations can be accounted for with increased adequacy. Conclusion: The online adaptive replanning technique based on daily respiration-gated diagnostic-quality CT combined with gated delivery can effectively correct for inter- and intra-fraction variations during radiation therapy.
[en] TO THE EDITOR: The recent article by Demir et al. in your esteemed journal provided for highly stimulating and interesting reading. Interestingly, over the past few years artemin has been identified as a significant player in the enhancement of oncogenicity of various other tumors besides pancreatic cancers.