Adenocarcinoma
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Publication
Journal: BMC cancer
December/5/2018
Abstract
Agarose encapsulated murine renal adenocarcinoma cells (RENCA macrobeads) are currently being investigated in clinical trials as a treatment for therapy-resistant metastatic colorectal cancer. We have previously demonstrated the capacity of RENCA macrobeads to produce diffusible substances that markedly inhibit the proliferation of epithelial-derived tumor cells outside the macrobead environment. This study examined the molecular mechanisms underlying the observed inhibition in targeted tumor cells exposed to RENCA macrobeads.We evaluated changes in transcription factor responses, participating intracellular signaling pathways and the involvement of specific cellular receptors in targeted tumor cells exposed to RENCA macrobeads.Factors secreted by RENCA macrobeads significantly up-regulated the activity of the MEF2 transcription factor as well as altered the transcription of MEF2b and MEF2d isoforms in targeted tumor cells. Suppression of individual or multiple MEF2 isoforms in target tumor cells markedly reduced the growth inhibitory effects of RENCA macrobeads. Furthermore, these effects were linked to the activation of the EGF receptor as attenuation of EGFR resulted in a substantial reduction of the cancer cell growth-inhibitory effect.Since interruption of the EGFR signaling cascade did not eliminate RENCA macrobead-induced growth control, our data suggests that RENCA macrobeads exert their full growth inhibitory effects through the simultaneous activation of multiple signaling pathways. In contrast to a precision medicine approach targeting single molecular abnormalities, the RENCA macrobead functions as a biological-systems therapy to re-establish regulation in a highly dysfunctional and dysregulated cancer system.
Publication
Journal: Annales de pathologie
March/2/2010
Abstract
Apoptosis detection in histological section is very important, but usual methods (TUNEL and morphologic changes) are controversial. Immunohistochemical stains of activated proteins during apoptosis improve detection of cell death in tissue sections. Activated caspase-3 and cleaved cytokeratin-18 are more and more used.
OBJECTIVE
This study compared immunohistochemical markers (activated caspase-3, cleaved cytokeratin-18 and two antibodies not yet evaluated: activated caspase-7 and cleaved PARP-1), cellular morphology and TUNEL.
METHODS
Tumour xenografts of the human colon cancer cell line HT29 were used, treated by photodynamic therapy, to obtain large numbers of cells undergoing apoptosis. Apoptotic cells were quantified and apoptotic indices were determined for each marker.
RESULTS
Comparison of apoptosis index indicated statistically best sensibility with activated-caspase-3 and cleaved-cytokeratin-19.
CONCLUSIONS
Immunohistochemistry for activated caspase-3 and cleaved cytkeratin-18 appear to be an easy, sensitive, and reliable method for detecting and quantifying apoptosis in this model. There are therefore recommended for the detection and quantification of apoptosis in tissue sections. Other markers as cleaved PARP-1 and activated caspase-7 can be an interessant solution: advantages and inconvenience for each methods are exposed.
Publication
Journal: Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie
May/4/2014
Abstract
Tumor infiltrating lymphocytes (TIL), as a microenvironment component were studied in various epithelial tumors, with contradictory results. Recent data about regulatory T-cells (Treg) revealed new explanations for pro- and anti-tumor implications of TIL. Tregs immunoprofile was recently completed with Foxp3 expression. A T-cell fraction (Th) is producing cytokine IL17 and is now considered acting in tumor progression. Our study aimed to analyze immunohistochemically (IHC) Foxp3+ and IL17 expression in resected lung adenocarcinomas, since they could become possible targets in the antitumor immunotherapy. The studied material was represented by paraffin-embedded tumor fragments from 59 patients with TIL identified on HE staining. The antibodies used were Foxp3 and IL17. The statistical analysis used logistical regression on SPSS19 software (Chicago, IL, USA). TIL was usually mild or scarce. A positive statistic correlation resulted between the amounts of TIL in peritumoral and intratumoral location but without correlation to histopathological grading. Foxp3 and IL17 were present in TIL lymphocytes, tumor cells and fibroblasts; IL17 was expressed also in periendothelial cells (PEC). Foxp3 positivity was significantly correlated for lymphocytes÷tumor cells, lymphocytes÷fibroblasts and tumor cells÷fibroblasts, suggesting their concerted action. Tumor cells and lymphocytes Foxp3 expression was inversely correlated with the amount of TIL. Between lymphocytic Foxp3 and PEC IL17, we found a weak negative correlation. The TIL had a quite positive correlation with PEC IL17. In these conditions, Foxp3 could be a mediator of the tumor cells inhibitory aggression upon the immune system and could be used as a molecular target for biological antitumor therapy.
Publication
Journal: Breast cancer research : BCR
November/3/2004
Abstract
BACKGROUND
Pregnancy protects against breast cancer development in humans and rats. Parous rats have persistently reduced circulating levels of growth hormone, which may affect the activity of the growth hormone/insulin-like growth factor (IGF)-I axis. We investigated the effects of IGF-I on parity-associated protection against mammary cancer.
METHODS
Three groups of rats were evaluated in the present study: IGF-I-treated parous rats; parous rats that did not receive IGF-I treatment; and age-matched virgin animals, which also did not receive IGF-I treatment. Approximately 60 days after N-methyl-N-nitrosourea injection, IGF-I treatment was discontinued and all of the animal groups were implanted with a silastic capsule containing 17beta-estradiol and progesterone. The 17beta-estradiol plus progesterone treatment continued for 135 days, after which the animals were killed.
RESULTS
IGF-I treatment of parous rats increased mammary tumor incidence to 83%, as compared with 16% in parous rats treated with 17beta-estradiol plus progesterone only. Tumor incidence and average number of tumors per animal did not differ between IGF-I-treated parous rats and age-matched virgin rats. At the time of N-methyl-N-nitrosourea exposure, DNA content was lowest but the alpha-lactalbumin concentration highest in the mammary glands of untreated parous rats in comparison with age-matched virgin and IGF-I-treated parous rats. The protein levels of estrogen receptor-alpha in the mammary gland was significantly higher in the age-matched virgin animals than in untreated parous and IGF-I-treated parous rats. Phosphorylation (activation) of the extracellular signal-regulated kinase-1/2 (ERK1/2) and expression of the progesterone receptor were both increased in IGF-I-treated parous rats, as compared with those in untreated parous and age-matched virgin rats. Expressions of cyclin D1 and transforming growth factor-beta3 in the mammary gland were lower in the age-matched virgin rats than in the untreated parous and IGF-I-treated parous rats.
CONCLUSIONS
We argue that tumor initiation (transformation and fixation of mutations) may be similar in parous and age-matched virgin animals, suggesting that the main differences in tumor formation lie in differences in tumor progression caused by the altered hormonal environment associated with parity. Furthermore, we provide evidence supporting the notion that tumor growth promotion seen in IGF-I-treated parous rats is caused by activation of estrogen receptor-alpha via the Raf/Ras/mitogen-activated protein kinase cascade.
Publication
Journal: The Biochemical journal
November/3/2004
Abstract
We have demonstrated previously that the EGFR (epidermal growth factor receptor) is a calmodulin (CaM)-binding protein. To establish whether or not the related receptor ErbB2/Neu/HER2 also binds CaM, we used human breast adenocarcinoma SK-BR-3 cells, because these cells overexpress this receptor thus facilitating the detection of this interaction. In the present paper, we show that ErbB2 could be pulled-down using CaM-agarose beads in a Ca2+-dependent manner, as detected by Western blot analysis using an anti-ErbB2 antibody. ErbB2 was also isolated by Ca2+-dependent CaM-affinity chromatography. We also demonstrate using an overlay technique with biotinylated CaM that CaM binds directly to the immunoprecipitated ErbB2. The binding of biotinylated CaM to ErbB2 depends strictly on the presence of Ca2+, since it was prevented by the presence of EGTA. Moreover, the addition of an excess of free CaM prevents the binding of its biotinylated form, demonstrating that this was a specific process. We excluded any interference with the EGFR, as SK-BR-3 cells express considerably lower levels of this receptor, and no detectable EGFR signal was observed by Western blot analysis in the immunoprecipitated ErbB2 preparations used to perform the overlay assays with biotinylated CaM. We also demonstrate that treating living cells with W7 [N-(6-aminohexyl)-5-chloro-1-naphthalenesulphonamide], a cell-permeant CaM antagonist, down-regulates ErbB2 phosphorylation, and show that W7 does not interfere non-specifically with the activity of ErbB tyrosine kinases. We also show that W7 inhibits the phosphorylation (activation) of both ERK1/2 (extracellular-signal-regulated kinases 1 and 2) and Akt/PKB (protein kinase B), in accordance with the inhibition observed in ErbB2 phosphorylation. In contrast, W7 treatment increased the phosphorylation (activation) of CREB (cAMP-response-element-binding protein) and ATF1 (activating transcription factor-1), two Ca2+-sensitive transcription factors that operate downstream of these ErbB2 signalling pathways, most likely because of the absence of calcineurin activity. We conclude that ErbB2 is a new CaM-binding protein, and that CaM plays a role in the regulation of this receptor and its downstream signalling pathways in vivo.
Publication
Journal: Urology journal
November/12/2018
Abstract
Though previous major abdominal surgery and pelvic irradiation may be a significant drawback of subsequent laparoscopic procedure, technological advances such as better visualization and more controlled finer movementsof robotic arms allowing better dissection in robotic-assisted laparoscopic surgery may reduce some of these challenges. However, limited data are available on the effect and safety of robotic surgery in these patients. The aim of this case report is to present efficacy and safety of robot assisted radical prostatectomy in a patient who has rectal and concurrent prostate cancer with the history of abdominoperineal resection, pelvic irradiation and adjuvantchemotherapy.
Publication
Journal: International journal of surgical pathology
December/22/2008
Abstract
A wide range of pathologies may primarily affect the lymphatic vessels in the lungs. In this article, a unique case of pulmonary silicosis associated with a subtle lymphangitic carcinomatosis from an unknown prostate cancer is reported and discussed.
Publication
Journal: The Journal of toxicological sciences
December/6/2018
Abstract
SIRT1, an NAD+-dependent deacetylase, causes deacetylation and down-regulation of its target p53. Given that p53 is an upstream regulator of the transcription of the cyclin-dependent kinase inhibitor p21/Cip1, SIRT1 is hypothesized to play a stimulatory role in carcinoma cell proliferation. We previously reported that down-regulation of SIRT1 caused the increase in p21/Cip1 in a post-transcriptional manner, suggesting that p53 is not involved in the p21/Cip1 increase and raising the question whether SIRT1 exhibits the activity other than deacetylase. In the present study, we examined whether SIRT1 down-regulation and the inhibitor for SIRT1 deacetylase activity affects p21/Cip1 and p53 expression in renal adenocarcinoma cells and normal renal cells. SIRT1 knockdown caused an increase in p53 and p21/Cip1 protein levels in renal adenocarcinoma ACHN cells but not normal renal-derived HK-2 cells. The increase in p53 in ACHN cells is unlikely to contribute to the upregulation of p21/Cip1 expression, given that SIRT1 knockdown did not increase p21/Cip1 mRNA levels in these cells. In contrast to the SIRT1-knock down assay, SIRT1 deacetylase inhibitor did not affect p53 or p21/Cip1 protein levels in ACHN cells. Therefore, SIRT1-knockdown likely stimulates p53 and p21/Cip1 protein expression in a deacetylase-independent manner.
Publication
Journal: Archives of gynecology and obstetrics
February/23/2010
Publication
Journal: Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association
December/9/2008
Publication
Journal: Applied immunohistochemistry & molecular morphology : AIMM
October/13/2004
Abstract
Using differential display mRNA techniques, the authors found cDNA of the heat shock 70 protein known as GRP75 overexpressed in ovarian cancer cell lines. In the current study, the authors used immunohistochemistry to characterize the expression pattern of GRP75 in ovarian carcinomas and compared it with epithelial tumors originating from the female reproductive tract, epithelial neoplasms from non-gynecologic sites (colon, pancreas, breast, and lung), and various normal tissues. The authors also developed an antigen capture ELISA assay to determine if GRP75 can be detected in tumors, ascites, or sera of patients with advanced mullerian adenocarcinomas. All epithelial tumors from the ovary and the female reproductive tract were positive for GRP75 expression with moderate to strong staining intensity; stromal expression of GRP75 was generally weak or absent. Adenocarcinomas from the colon, lung, pancreas, and breast also stained strongly positive for GRP75. The epithelial cells of all normal tissues examined were positive for GRP75, and strong staining was also seen in the corpora lutea, hepatocytes, enteric neural plexus of the esophagus and colon, and placental cytotrophoblast and syncytiotrophoblast, and in subpopulations of pancreatic acinar cells. The ELISA assay detected GRP75 in tumor lysates and ascitic fluid, but not sera, of patients with mullerian adenocarcinomas. The authors conclude that GRP75 is highly expressed in both benign and malignant epithelium, as well as cells of specialized function from a variety of tissues.
Publication
Journal: Radiology
February/24/2010
Abstract
OBJECTIVE
To compare the local-regional staging accuracy of the conventional two-dimensional (2D) T2-weighted imaging protocol and of the three-dimensional (3D) T2-weighted imaging protocol for preoperative magnetic resonance (MR) imaging in rectal cancer patients.
METHODS
This retrospective study was approved by the institutional review board, and a waiver of informed consent was obtained. A review was conducted of 109 preoperative 3-T MR images obtained with 2D and 3D T2-weighted imaging protocols in rectal cancer patients. Two radiologists independently assessed the radiologic findings for T and N category lesions, conspicuity of tumor margin, and image quality of 2D and 3D data. Interactive multiplanar reconstruction was performed for 3D data analysis. The linear weighted kappa values for T2-weighted imaging staging results (2D and 3D data) and histopathologic staging results were calculated and compared. Wilcoxon signed rank test was performed to compare tumoral conspicuity and overall image quality.
RESULTS
T category lesion staging accuracy values for 2D and 3D data, respectively, were 66.0% and 67.0% for reviewer 1 (P = .465) and 63.3% and 56.9% for reviewer 2 (P = .402). N category lesion staging accuracy values for 2D and 3D T2-weighted images, respectively, were 64.2% and 57.8% for reviewer 1 (P = .427) and 47.7% and 62.4% for reviewer 2 (P = .666). Tumor conspicuity was better for 2D T2-weighted imaging, but no significant difference in image quality was observed.
CONCLUSIONS
Preoperative MR imaging in rectal cancer patients for staging with conventional 2D and multiplanar reconstruction 3D T2-weighted imaging protocols showed no significant differences in accuracy of T and N category staging and overall image quality, as determined by degree of artifact. However, the 3D T2-weighted imaging protocol had limitations in regard to lesion conspicuity.
Publication
Journal: Canadian journal of ophthalmology. Journal canadien d'ophtalmologie
December/8/2008
Publication
Journal: Journal of clinical rheumatology : practical reports on rheumatic & musculoskeletal diseases
July/22/2015
Publication
Journal: Japanese journal of clinical oncology
July/13/2015
Publication
Journal: International journal of oncology
December/20/2018
Abstract
Metformin (MET) is the first‑line treatment for type 2 diabetes mellitus. Several epidemiological studies have suggested the potential anti‑cancer effects of MET, including its activity against pancreatic ductal adenocarcinoma (PDAC). Gemcitabine (GEM) has become the standard chemotherapy for PDAC; however, acquired resistance to GEM is a major challenge. In this study, we evaluated the anti‑tumor effects of MET against GEM‑resistant PDAC in a mouse xenograft model. GEM‑resistant BxG30 PDAC cells were implanted into BALB/c nude mice. The mice were divided into 4 groups (control, GEM, MET, and combined treatment with GEM + MET) and treated with the drugs for 4 weeks. Compared with the control mice, the final tumor volumes were significantly decreased in the mice treated with GEM + MET. Treatment to control volume ratios (T/C%) were calculated as 80.2% (GEM), 54.0% (MET) and 47.2% (GEM + MET). The anti‑tumor activity of GEM alone against BxG30 tumor xenografts was limited. MET treatment alone exerted satisfactory anti‑tumor effects; however, the optimal T/C% was achieved by treatment with GEM + MET, indicating that this combined treatment regimen potently inhibited the growth of GEM‑resistant PDAC. The expression of hypoxia‑inducible factor 1α (HIF‑1α) and the phosphorylation of ribosomal protein S6 (S6), an important downstream effector of the mammalian target of rapamycin (mTOR) signaling pathway, were also assessed by western blot analysis. The phosphorylation of S6 was inhibited by incubation with MET, but not with GEM, and the expression of HIF‑1α under hypoxic conditions was significantly inhibited by MET treatment, but not by GEM treatment. The production of vascular endothelial growth factor was also suppressed by MET treatment, but not by GEM treatment, as determined by ELISA. Taken together, the data of this study demonstrate that the anti‑tumor activity of MET is mediated via the suppression of mTOR‑HIF‑1 signaling, reflecting a different underlying mechanism of action than that of GEM. These results may prove to be clinically significant and reveal the potential of MET as an effective therapeutic drug for PDAC.
Publication
Journal: Ophthalmic surgery, lasers & imaging retina
July/15/2015
Abstract
Retinal pigment epithelium (RPE) neoplasms are extraordinarily rare and have been infrequently described in the literature. Most RPE tumors are pigmented and may simulate choroidal melanoma. The best management of RPE tumors has not yet been elucidated. In the current case, a 36-year-old man presenting with visual disturbance is found to have biopsy-proven RPE adenocarcinoma with subfoveal fluid. He is treated with grid laser over the lesion with complete resolution of fluid. RPE adenocarcinoma can present as an amelanotic mass, and grid laser over the lesion may represent a novel approach for treating associated subretinal fluid.
Publication
Journal: Cancer
May/3/2006
Abstract
BACKGROUND
Telomerase activation, which is observed in most human cancers, plays an important role in carcinogenesis. Human telomerase reverse transcriptase (hTERT) is a subunit of telomerase that is essential for telomerase activity. The aim of the study was to investigate whether nonsteroidal antiinflammatory drugs (NSAIDs) inhibit telomerase activity and hTERT.
METHODS
Four colon carcinoma cell lines, HT-29, COLO205, CRL-2134, and SW1116, were used in the experiments. Polymerase chain reaction-based telomeric repeat amplification (TRAP) enzyme-linked immunosorbent assay (ELISA) was used to measure telomerase activity in the cells after treatment with aspirin, indomethacin, or SC-236 (a specific cyclooxygenase-2 [COX-2] inhibitor). Expression of hTERT mRNA and protein was detected by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting, respectively. The dual luciferase reporter assay was performed to identify the potential cis-response elements to NSAIDs in the promoter region of hTERT.
RESULTS
Aspirin, indomethacin, and SC-236 inhibited telomerase activity in HT-29, COLO205, and CRL-2134 cell lines, but not in the SW1116 cell line. NSAIDs inhibited hTERT mRNA and protein expression through suppression of hTERT transcriptional activity. The hTERT promoter fragment -145 to -330 basepairs (bp) upstream of the ATG starting site was sufficient to respond to the NSAID-induced inhibitory effect and the inhibition was COX-2-independent.
CONCLUSIONS
NSAIDs inhibit telomerase activity at hTERT transcriptional, mRNA, and protein levels in colon carcinoma cells. The hTERT promoter fragment -145 to -330 bp may be the cis-response element to NSAIDs.
Publication
Journal: Eksperimental'naia i klinicheskaia gastroenterologiia = Experimental & clinical gastroenterology
April/3/2011
Abstract
The aim of the study was to explore the possibilities of CT in evaluating resectability of pancreatic head adenocarcinoma, depending on the tumor.
METHODS
The results of CT and intraoperative findings in 62 patients with cancer of the head of the pancreas.
RESULTS
It was shown that the tumor localized in caudal glands, had higher resectability when compared with tumors of the cranial localization at tumor sizes of 3-4 cm in size tumor less than 3 cm, the probability that radical surgery was highest in patients with central localization of the tumor.
Publication
Journal: VideoGIE : an official video journal of the American Society for Gastrointestinal Endoscopy
March/22/2019
Publication
Journal: The American journal of gastroenterology
December/30/2008
Publication
Journal: Clinical cancer research : an official journal of the American Association for Cancer Research
January/4/2009
Abstract
OBJECTIVE
In pancreatic carcinoma, vascular endothelial growth factor (VEGF) expression at the primary site has been suggested to be a prognostic parameter. We quantitatively analyzed VEGF expression in liver metastases from pancreatic carcinoma and examined the correlation among VEGF expression in liver metastases, clinicopathologic factors, and clinical outcome.
METHODS
The subjects consisted of 23 patients with pancreatic adenocarcinoma who had liver metastases and were treated with S-1 and gemcitabine as the first-line treatment. VEGF expression was quantitated by enzyme immunoassay in biopsy specimens of liver metastases and nontumorous liver tissue, and in plasma. In 10 of the 23 patients, VEGF expression was also quantitated in biopsy specimens of the primary pancreatic tumor. All samples were collected before treatment.
RESULTS
The VEGF level in nontumorous liver tissue was 36.6 +/- 10.0 pg/mg protein versus 376.8 +/- 106.1 pg/mg protein in liver metastases (P = 0.0016). Pretreatment VEGF levels in plasma and in primary pancreatic carcinoma did not correlate with VEGF levels in the corresponding liver metastases. The median VEGF level in liver metastases (138.9 pg/mg protein) was used as the cutoff value between high and low VEGF expression in liver metastases. Patients showing high VEGF expression had a significantly longer progression-free survival and overall survival than patients showing low VEGF expression in liver metastases (P = 0.0219 and P = 0.0074, respectively).
CONCLUSIONS
Evaluation of VEGF levels in liver metastases might be useful in assessing the prognosis of patients with metastatic pancreatic carcinoma who are under systemic chemotherapy.
Publication
Journal: International journal of surgical pathology
November/15/2004
Abstract
Postradiation sarcomas are rare, and the most commonly reported ones are malignant fibrous histiocytoma, osteosarcoma, angiosarcoma, fibrosarcoma, malignant peripheral nerve sheath tumor, and high-grade pleomorphic sarcoma, not otherwise specified. There are a few case reports of postradiation rhabdomyosarcomas following treatment of retinoblastoma, breast cancer, endometrial adenocarcinoma, and Hodgkin's disease. Secondary neoplasms following radiation and surgical treatment of rectal adenocarcinomas have not been reported in the English literature. We report a case of pleomorphic rhabdomyosarcoma of the anterior abdominal wall following treatment of rectal carcinoma, and we review the literature.
Publication
Journal: Clinical nuclear medicine
March/1/2010
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