Clinicopathological features and prognostic factors for survival in patients with primary appendiceal adenocarcinoma

Objective: Primary appendiceal adenocarcinoma accounts for 1% of colorectal tumors and is a rare malignancy. Peritoneal dissemination commonly occurs as part of the natural course of disease, following the sequence of luminal wall invasion, obstruction, and perforation. Patients and Methods: Twenty patients with appendiceal adenocarcinoma were surgically treated in our hospital between 1990 and 2021. The clinicopathological features, preoperative diagnosis, intraoperative diagnosis, surgical techniques, postoperative adjuvant chemotherapy, chemotherapy, outcome, and prognostic factors for survival of patients with primary appendiceal adenocarcinoma were reviewed. Results: Patients (8 males, 12 females), with an age from 35 to 94 years (mean: 72.8 years), were involved in the study. Before surgery, 7 (35%) patients were diagnosed with primary appendiceal adenocarcinoma and 13 were diagnosed with other conditions. 10 patients had stage I or II disease and 10 patients had stage III or IV disease. Sixteen patients received curative resection, while 4 received non-curative resection. The cumulative five-year survival rate was 62.1%. The preoperative and intraoperative diagnoses, pathological stage, and curative resection had a significant impact on survival. Conclusions: The preoperative and intraoperative diagnoses, pathological stage, and curative resection had an important impact on survival of patients with primary appendiceal adenocarcinoma

Primary myxofibrosarcoma of the parotid: case report

<p>Abstract</p> <p>Background</p> <p>Myxofibrosarcoma is common in the extremities of elderly people and is characterized by a high frequency of local recurrence.</p> <p>Case presentation</p> <p>We report a 37 year old female who presented with a 4-month history of facial pain and a 3-month history of painful progressive swelling in the preauricular area. She underwent a total parotidectomy. The tumor was histopathologically and immunohistochemically diagnosed as a low-grade myxofibrosarcoma. The patient was free of disease 9 months after surgery with uneventful post-operative clinical course.</p> <p>Conclusions</p> <p>Parotid area swelling should always alert doctors. To our knowledge, this is the first case of parotid myxofibrosarcoma. It should be added to the differential diagnosis of diseases of the parotid. We have to recognize this disease and seek adequate treatment for it.</p

Connexin-43 upregulation in micrometastases and tumor vasculature and its role in tumor cell attachment to pulmonary endothelium

<p>Abstract</p> <p>Background</p> <p>The modulation of gap junctional communication between tumor cells and between tumor and vascular endothelial cells during tumorigenesis and metastasis is complex. The notion of a role for loss of gap junctional intercellular communication in tumorigenesis and metastasis has been controversial. While some of the stages of tumorigenesis and metastasis, such as uncontrolled cell division and cellular detachment, would necessitate the loss of intercellular junctions, other stages, such as intravasation, endothelial attachment, and vascularization, likely require increased cell-cell contact. We hypothesized that, in this multi-stage scheme, connexin-43 is centrally involved as a cell adhesion molecule mediating metastatic tumor attachment to the pulmonary endothelium.</p> <p>Methods</p> <p>Tumor cell attachment to pulmonary vasculature, tumor growth, and connexin-43 expression was studied in metastatic lung tumor sections obtained after tail-vein injection into nude mice of syngeneic breast cancer cell lines, overexpressing wild type connexin-43 or dominant-negatively mutated connexin-43 proteins. High-resolution immunofluorescence microscopy and Western blot analysis was performed using a connexin-43 monoclonal antibody. Calcein Orange Red AM dye transfer by fluorescence imaging was used to evaluate the gap junction function.</p> <p>Results</p> <p>Adhesion of breast cancer cells to the pulmonary endothelium increased with cancer cells overexpressing connexin-43 and markedly decreased with cells expressing dominant-negative connexin-43. Upregulation of connexin-43 was observed in tumor cell-endothelial cell contact areas <it>in vitro </it>and <it>in vivo</it>, and in areas of intratumor blood vessels and in micrometastatic foci.</p> <p>Conclusion</p> <p>Connexin-43 facilitates metastatic 'homing' by increasing adhesion of cancer cells to the lung endothelial cells. The marked upregulation of connexin-43 in tumor cell-endothelial cell contact areas, whether in preexisting 'homing' vessels or in newly formed tumor vessels, suggests that connexin-43 can serve as a potential marker of micrometastases and tumor vasculature and that it may play a role in the early incorporation of endothelial cells into small tumors as seeds for vasculogenesis.</p

Discovery of novel targets for multi-epitope vaccines: Screening of HIV-1 genomes using association rule mining

© 2009 Paul and Piontkivska; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution Licens

Expression of Ixodes scapularis Antifreeze Glycoprotein Enhances Cold Tolerance in Drosophila melanogaster

Drosophila melanogaster experience cold shock injury and die when exposed to low non-freezing temperatures. In this study, we generated transgenic D. melanogaster that express putative Ixodes scapularis antifreeze glycoprotein (IAFGP) and show that the presence of IAFGP increases the ability of flies to survive in the cold. Male and female adult iafgp-expressing D. melanogaster exhibited higher survival rates compared with controls when placed at non-freezing temperatures. Increased hatching rates were evident in embryos expressing IAFGP when exposed to the cold. The TUNEL assay showed that flight muscles from iafgp-expressing female adult flies exhibited less apoptotic damage upon exposure to non-freezing temperatures in comparison to control flies. Collectively, these data suggest that expression of iafgp increases cold tolerance in flies by preventing apoptosis. This study defines a molecular basis for the role of an antifreeze protein in cryoprotection of flies

Cancer Genomics Identifies Regulatory Gene Networks Associated with the Transition from Dysplasia to Advanced Lung Adenocarcinomas Induced by c-Raf-1

Background: Lung cancer is a leading cause of cancer morbidity. To improve an understanding of molecular causes of disease a transgenic mouse model was investigated where targeted expression of the serine threonine kinase c-Raf to respiratory epithelium induced initialy dysplasia and subsequently adenocarcinomas. This enables dissection of genetic events associated with precancerous and cancerous lesions. Methodology/Principal Findings: By laser microdissection cancer cell populations were harvested and subjected to whole genome expression analyses. Overall 473 and 541 genes were significantly regulated, when cancer versus transgenic and non-transgenic cells were compared, giving rise to three distinct and one common regulatory gene network. At advanced stages of tumor growth predominately repression of gene expression was observed, but genes previously shown to be upregulated in dysplasia were also up-regulated in solid tumors. Regulation of developmental programs as well as epithelial mesenchymal and mesenchymal endothelial transition was a hall mark of adenocarcinomas. Additionaly, genes coding for cell adhesion, i.e. the integrins and the tight and gap junction proteins were repressed, whereas ligands for receptor tyrosine kinase such as epi- and amphiregulin were up-regulated. Notably, Vegfr- 2 and its ligand Vegfd, as well as Notch and Wnt signalling cascades were regulated as were glycosylases that influence cellular recognition. Other regulated signalling molecules included guanine exchange factors that play a role in an activation of the MAP kinases while several tumor suppressors i.e. Mcc, Hey1, Fat3, Armcx1 and Reck were significantly repressed. Finally, probable molecular switches forcing dysplastic cells into malignantly transformed cells could be identified. Conclusions/Significance: This study provides insight into molecular pertubations allowing dysplasia to progress further to adenocarcinoma induced by exaggerted c-Raf kinase activity

Glucose transporter expression in developing fetal lungs and lung neoplasms

Glucose uptake and metabolism are essential for proliferation and survival of cells, and are supposed to be enhanced in actively proliferating cell systems such as embryonic and cancer tissues. Glucose uptake is usually carried out through glucose transporters.In the developing fetal lung, metabolism of glucose is thought to be an important process in cell proliferation, differentiation and maturation. Active glucose uptake could result in accumulation of glycogen in epithelial cells, and utilization of glycogen could be a critical phenomenon for lung epithelia1 development. In hamsters, although facilitative glucose transporter isoform 1 (GLUTl) and isoform 4 (GLUT4) are not detected in adult lungs, expression of them is detected with immunohistochemical and Western blot analyses in the developing fetal lungs.In human lung carcinomas, GLUTl expression is seen in most cases of lung carcinoma, and is seen especially frequently in squamous cell carcinoma. GLUTl expression in adenocarcinoma of the lung is correlated with reduced cell differentiation, larger tumor size and positive lymph node metastasis. A few cases of lung carcinoma show positive staining for GLUT3 and GLUT4.Thus, expression of some facilitative glucose transporter isoforms is detected in developing fetal epithelium and in lung carcinomas. Overexpression of them could enhance uptake of glucose into these cells, and the increased influx of glucose could be involved in active cell proliferation, which is a common character of the developing lung epithelium and carcinoma