scholarly journals Histopathological characteristics and coexpression of p53 and p16INK4a proteins in renal cancer

2008 ◽  
Vol 65 (11) ◽  
pp. 820-824
Author(s):  
Sladjana Zivkovic ◽  
Milos Kostov ◽  
Svetlana Pavlovic ◽  
Zaklina Mijovic
Keyword(s):  
Significant Positive Correlation ◽  
Renal Carcinoma ◽  
Malignant Tumors ◽  
Immunohistochemical Analysis ◽  
P53 Mutation ◽  
Clinicopathological Parameters ◽  
Tumor Differentiation ◽  
Tissue Samples ◽  
Protein P53 ◽  
P16 Expression

Background/Aim. Renal carcinoma represents histologically heterogeneous group of malignant tumors, with various clinical aggressiveness. The frequency of p53 mutation in primal renal carcinoma is rare, although there are information about its heterogeneous accumulation. The loss of protein p16 expression in primal renal carcinoma is detected in 20-30% of the cases. The aim of this paper was to determine frequency of mutated protein p53 and expression of protein p16INK4a in renal carcinoma, to analyze their correlative relation and relation with the examined clinicopathological parameters. Methods. The examination included 12 patients (66.7% men, 33.3% women), with patohistologically verified renal carcinoma. Expression of mutated form of protein p53 and protein p16 was determined in tissue samples, by immunohistochemical analysis using of mice monoclonical antibodies produced by DAKO, Denmark. Results. In 9 (75%) of the cases was detected mutated protein p53, of whom 66.6% had higher histological gradus of tumor (G3-4) and higher pathological stadium of the disease (pT3a-b) at the same time. In 7 (58.3%) and 5 (41.7%) of the cases expression of protein p16, the loss of expression of protein p16 were detected respectively. A statistically significant positive correlation was determined between pathological stadium of disease (TNM) and the degree of tumor differentiation (G) (? = 0.834; p < 0.001), as well as between TNM and mitotic index (? = 0.622; p = 0.031). Conclusion. A mutated form of protein p53 exists in 75% of the cases with the renal carcinoma and 66.6% of then have higher histological gradus of tumor and higher stadium of tumor disease at the same time. Coexpression of mutated protein p53 and protein p16INK4a in renal carcinoma is not statistically significant and it is not in correlation with clinicopathological parameters. Immunohistochemical analysis of mutated protein p53 in renal carcinoma can have predictive significance.

scholarly journals HER1R497K andHER2I655V Polymorphisms Are Linked to Development of Breast Cancer

2013 ◽  
Vol 34 (6) ◽  
pp. 407-417 ◽  
Author(s):  
Naglaa R. AbdRaboh ◽  
Hanan H. Shehata ◽  
Manal B. Ahmed ◽  
Fatehia A. Bayoumi
Keyword(s):  
Breast Cancer ◽  
Malignant Tumors ◽  
Immunohistochemical Analysis ◽  
Control Group ◽  
Breast Cancer Patients ◽  
Tissue Samples ◽  
Her2 Protein ◽  
Restriction Fragment Polymorphism ◽  
Epidermal Growth ◽  
Control Study

BACKGROUND: Polymorphism of the genes of Human Epidermal growth factor receptor1 (HER1) and receptor2 (HER2) have been reported to be linked to pathogenesis of several malignant tumors but still there is contradiction regarding their association with breast cancer.OBJECTIVE: In this case control study we aimed to analyze the frequency ofHER1R497K (rs 11543848) andHER2I655V (rs 1136201) Polymorphisms in breast cancer.SUBJECT AND METHOD: The frequency ofHER1Arg(R) 497Lys (K) andHER2Ile (I) 655Val (V) polymorphisms were tested in 64 breast cancer patients and 86 normal control by polymerase chain reaction followed by restriction fragment polymorphism detection. Immunohistochemical analysis was done for HER2 protein on the available 18 malignant tissue samples.RESULTS:HER1497K andHER2655V variant had significantly increased breast cancer risk (OR=2.6, 95% CI 1.6–4.2, OR=2.2, 95% CI 1.2–4.1, p< 0.05) respectively. Moreover, combinedHER1K497 andHER2V655 variant was detected in 26.6% malignant in comparison to 8.14% of control group (OR=4.1, 95% CI 1.58–10.57), but, no significant association was noticed between both Polymorphisms and clinicopathological features of the disease. As regard HER2 immunohistochemical expression no significant correlation was revealed with HER2 655V polymorphism.CONCLUSIONS: Our findings suggest thatHER1497K andHER2655V polymorphisms are potential risk factor for development of breast cancer.

scholarly journals ANALYSIS OF IMMUNOHISTOCHEMICAL EXPRESSION OF P16INK4a IN NEOPLASTIC SQUAMOUS CELL LESIONS OF CERVIX

2016 ◽  
Vol 1 (02) ◽  
Author(s):  
Dr. K.R. Mohan ◽  
Dr. S. Sasikala ◽  
Dr. S. Ravi ◽  
Dr. P. Sagunthala, ◽  
Dr. I.Vijay Sathish Kumar,
Keyword(s):  
Squamous Cell ◽  
Immunohistochemical Analysis ◽  
Cost Effective ◽  
Large Cell ◽  
Hpv Infection ◽  
Invasive Squamous Cell Carcinoma ◽  
Strong Reaction ◽  
Tissue Samples ◽  
Reaction Intensity ◽  
P16 Expression

Introduction: Cervical cancer is caused by persistent infection by high risk Human papilloma virus (HPV).Increasing expression of HPV viral oncogenes might be reflected by increased expression of p16. Hence immunohistochemical detection of p16INK4a is an easy and cost effective method than molecular detection of HPV. Aims: The purpose of this study were to evaluate the results of expression of p16INK4a in neoplastic squamous cell lesions of cervix in order to assess the association of HPV infection in those lesions and to study the pattern of expression of p16 and also to compare p16 expression in various histological types of cervical neoplastic squamous cell lesions by immunohistochemistry. Methods: Immunohistochemical analysis of p16 expression was performed on 26 paraffin embedded tissue samples, obtained from cervical biopsy including 2 early invasive squamous cell carcinoma (SCC), 6 large cell keratinizing SCC, 16 large cell non- keratinizing SCC and 2 cases small cell non-keratinizing SCC by using commercially available mouse monoclonal antibody to p16 (clone G175 – 405). Two parameters were evaluated in p16 expression: Percentage of p16 positive cells and reaction intensity of p16 immunostaining. The p16 expression was graded as negative; Grade 1, 2, 3 and its reaction intensity was graded as negative, weak, moderate and strong. Results: In the present study out of 26 cases, the incidence of large cell non- keratinizing SCC constituted majority of the neoplastic lesions of cervix (61.5%). Most of the SCC (96.15%) showed grade 3 scoring for p16 positivity except one case which showed grade 2 scoring. Majority of SCC cases (96%) showed strong reaction intensity for p16 immunostaining. Conclusion: In this study of 26 neoplastic sqaumous cell lesions, all patterns of cervical neoplasia showed p16 positivity. P16 may be useful as an adjunct in histological sections to detect HPV in those lesions.

Hepatocyte ultrastructural alterations in perimetastatic areas

1996 ◽  
Vol 54 ◽  
pp. 768-769
Author(s):  
H. J. Finol ◽  
M. E. Correa ◽  
L.A. Sosa ◽  
A. Márquez ◽  
N.L. Díaz
Keyword(s):  
Malignant Tumor ◽  
Malignant Tumors ◽  
Surrounding Tissue ◽  
Ultrastructural Changes ◽  
Pancreas Carcinoma ◽  
Duct Carcinoma ◽  
Tissue Samples ◽  
Primary Malignant Tumor ◽  
Transmission Electron ◽  
Remote Sites

In classical oncological literature two mechanisms for tissue aggression in patients with cancer have been described. The first is the progressive invasion, infiltration and destruction of tissues surrounding primary malignant tumor or their metastases; the other includes alterations produced in remote sites that are not directly affected by any focus of disease, the so called paraneoplastic phenomenon. The non-invaded tissue which surrounds a primary malignant tumor or its metastases has been usually considered a normal tissue . In this work we describe the ultrastructural changes observed in hepatocytes located next to metastases from diverse malignant tumors.Hepatic biopsies were obtained surgically in patients with different malignant tumors which metatastized in liver. Biopsies included tumor mass, the zone of macroscopic contact between the tumor and the surrounding tissue, and the tissue adjacent to the tumor but outside the macroscopic area of infiltration. The patients (n = 5), 36–75 years old, presented different tumors including rhabdomyosarcoma, leiomyosarcoma, pancreas carcinoma, biliar duct carcinoma and colon carcinoma. Tissue samples were processed with routine techniques for transmission electron microscopy and observed in a Hitachi H-500 electron microscope.

scholarly journals Comprehensive analyses of competing endogenous RNA networks reveal potential biomarkers for predicting hepatocellular carcinoma recurrence

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Ping Yan ◽  
Zuotian Huang ◽  
Tong Mou ◽  
Yunhai Luo ◽  
Yanyao Liu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Malignant Tumors ◽  
Expression Profiles ◽  
Clinical Information ◽  
Gene Expression Omnibus ◽  
The Cancer Genome Atlas ◽  
High Rate ◽  
Competing Endogenous Rna ◽  
Tissue Samples ◽  
Potential Biomarkers

Abstract Background Hepatocellular carcinoma (HCC) is one of the most common and deadly malignant tumors, with a high rate of recurrence worldwide. This study aimed to investigate the mechanism underlying the progression of HCC and to identify recurrence-related biomarkers. Methods We first analyzed 132 HCC patients with paired tumor and adjacent normal tissue samples from the Gene Expression Omnibus (GEO) database to identify differentially expressed genes (DEGs). The expression profiles and clinical information of 372 HCC patients from The Cancer Genome Atlas (TCGA) database were next analyzed to further validate the DEGs, construct competing endogenous RNA (ceRNA) networks and discover the prognostic genes associated with recurrence. Finally, several recurrence-related genes were evaluated in two external cohorts, consisting of fifty-two and forty-nine HCC patients, respectively. Results With the comprehensive strategies of data mining, two potential interactive ceRNA networks were constructed based on the competitive relationships of the ceRNA hypothesis. The ‘upregulated’ ceRNA network consists of 6 upregulated lncRNAs, 3 downregulated miRNAs and 5 upregulated mRNAs, and the ‘downregulated’ network includes 4 downregulated lncRNAs, 12 upregulated miRNAs and 67 downregulated mRNAs. Survival analysis of the genes in the ceRNA networks demonstrated that 20 mRNAs were significantly associated with recurrence-free survival (RFS). Based on the prognostic mRNAs, a four-gene signature (ADH4, DNASE1L3, HGFAC and MELK) was established with the least absolute shrinkage and selection operator (LASSO) algorithm to predict the RFS of HCC patients, the performance of which was evaluated by receiver operating characteristic curves. The signature was also validated in two external cohort and displayed effective discrimination and prediction for the RFS of HCC patients. Conclusions In conclusion, the present study elucidated the underlying mechanisms of tumorigenesis and progression, provided two visualized ceRNA networks and successfully identified several potential biomarkers for HCC recurrence prediction and targeted therapies.

scholarly journals Aspartame and cancer – new evidence for causation

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Philip J. Landrigan ◽  
Kurt Straif
Keyword(s):  
Public Health ◽  
Cancer Risk ◽  
Malignant Tumors ◽  
Daily Intake ◽  
Immunohistochemical Analysis ◽  
International Agency ◽  
Advisory Group ◽  
Malignant Neoplasms ◽  
Acceptable Daily Intake ◽  
New Findings

Abstract Background Aspartame is one of the world’s most widely used artificial sweeteners and is an ingredient in more than 5000 food products globally. A particularly important use is in low-calorie beverages consumed by children and pregnant women. The Ramazzini Institute (RI) reported in 2006 and 2007 that aspartame causes dose-related increases in malignant tumors in multiple organs in rats and mice. Increased cancer risk was seen even at low exposure levels approaching the Acceptable Daily Intake (ADI). Prenatal exposures caused increased malignancies in rodent offspring at lower doses than in adults. These findings generated intense controversy focused on the accuracy of RI’s diagnoses of hematopoietic and lymphoid tissue tumors (HLTs). Critics made the claim that pulmonary lesions observed in aspartame-exposed animals were inflammatory lesions caused by Mycoplasma infection rather than malignant neoplasms. Methods To address this question, RI subjected all HLTs from aspartame-exposed animals to immunohistochemical analysis using a battery of markers and to morphological reassessment using the most recent Internationally Harmonized Nomenclature and Diagnostic (INHAND) criteria. Findings This immunohistochemical and morphological re-evaluation confirmed the original diagnoses of malignancy in 92.3% of cases. Six lesions originally diagnosed as lymphoma (8% of all HLTs) were reclassified: 3 to lymphoid hyperplasia, and 3 to chronic inflammation with fibrosis. There was no evidence of Mycoplasma infection. Interpretation These new findings confirm that aspartame is a chemical carcinogen in rodents. They confirm the very worrisome finding that prenatal exposure to aspartame increases cancer risk in rodent offspring. They validate the conclusions of the original RI studies. These findings are of great importance for public health. In light of them, we encourage all national and international public health agencies to urgently reexamine their assessments of aspartame’s health risks - especially the risks of prenatal and early postnatal exposures. We call upon food agencies to reassess Acceptable Daily Intake (ADI) levels for aspartame. We note that an Advisory Group to the International Agency for Research on Cancer has recommended high-priority reevaluation of aspartame’s carcinogenicity to humans.

Abstract P195: No Functional Nerve Recovery To 6 Months Post Renal Denervation With Rf Energy In A Normotensive Pig Model

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Andrew Sharp ◽  
Stefan Tunev ◽  
Markus P Schlaich ◽  
David P LEE ◽  
Aloke Finn ◽  
...  
Keyword(s):  
Animal Studies ◽  
Renal Denervation ◽  
Blood Pressure Reduction ◽  
Immunohistochemical Analysis ◽  
Swine Model ◽  
Renal Nerve ◽  
Tissue Samples ◽  
Axon Density ◽  
Rf Energy

Background: The safety and efficacy of catheter-based radio frequency (RF) renal denervation (RDN) have been demonstrated in randomized, sham-controlled trials. Long-term durability of blood pressure reduction following RDN has also been demonstrated by all-comer registries, although published pre-clinical reports of functional renal nerve regrowth are not consistent. We quantified the processes that support RDN procedural durability utilizing animal models. Methods: Animal studies were conducted in accordance with published guidelines. RDN was performed (4 lesions in the main renal artery) in normotensive swine using the Symplicity Spyral™ RDN system (Medtronic, Santa Rosa, CA, USA). Two additional groups not undergoing RDN served as control. Serial histological tissue samples were obtained in separate groups at 7 (n=12/group) and 180 (N=16/group) days post-procedure in all animals followed by bioanalytical quantification of cortical norepinephrine (NE) levels and immunohistochemical analysis of renal cortical axon density in matched samples. Results: Renal cortical axon density and NE levels were significantly reduced at 7 days and persisted through 180 days following RDN compared with control ( Figure ). Nerve fibrosis and necrosis were observed in the region of ablation, while nerve body atrophy was apparent distal to ablation location at 180 days. Conclusions: Reductions in both NE and renal cortical axon density were sustained at 7 and 180 days post-RDN procedure using RF renal denervation in a normotensive swine model. These data confirm and extend other pre-clinical and clinical evidence of long-term durability of the RDN procedure using RF energy.

scholarly journals KLF2 Inhibits the Migration and Invasion of Prostate Cancer Cells by Downregulating MMP2

2018 ◽  
Vol 13 (1) ◽  
pp. 155798831881690 ◽  
Author(s):  
Binshuai Wang ◽  
Mingyuan Liu ◽  
Yimeng Song ◽  
Changying Li ◽  
Shudong Zhang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Tumor Suppressor ◽  
Cell Function ◽  
Malignant Tumors ◽  
Suppressor Gene ◽  
Migration And Invasion ◽  
Tissue Samples ◽  
Tumor Tissues ◽  
Luciferase Activity Assay

KLF2, a member of the Kruppel-like factor (KLF) family, is thought to be a tumor suppressor in many kinds of malignant tumors. Its functions in prostate cancer (PCa) are unknown. This study aimed to explore the role of KLF2 in the migration and invasion of PCa cells. The expression of KLF2 was measured by immunohistochemistry in PCa tissues and in paired non-tumor tissues. KLF2 and MMP2 expression in cells was measured by Western blot and RT-qPCR. Adenoviruses and siRNAs were used in cell function tests to investigate the role of KLF2 in regulating MMP2. Interactions between KLF2 and MMP2 were analyzed by a luciferase activity assay. The present study, for the first time, identified that KLF2 was downregulated both in PCa clinical tissue samples and in cancer cell lines. The overexpression of KLF2 inhibited the migration and invasion of PCa cells via the suppression of MMP2.This study demonstrates that KLF2 might act as a tumor suppressor gene in PCa and that the pharmaceutical upregulation of KLF2 may be a potential approach for treatment.

scholarly journals Increased STIP1 and Hsp90 Correlate with Progression and Prognosis of Lung Adenocarcinoma

2021 ◽  
Author(s):  
Biaoxue Rong ◽  
Youwen Zhang ◽  
Junye Wang ◽  
Shucheng Ye ◽  
Maoqing Guo ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Malignant Tumors ◽  
Clinical Stage ◽  
A549 Cells ◽  
Biological Behavior ◽  
Prognostic Indicators ◽  
Normal Lung ◽  
Clinicopathological Parameters ◽  
Strong Positive Correlation ◽  
Advanced Clinical Stage

Abstract Background: Stress-inducible phosphoprotein 1 (STIP1) and heat shock protein 90 (Hsp90) have been found to be correlated with malignant tumors. The aim of this investigation was to study the relationship between their expressions and lung adenocarcinoma (LAC). Methods: The expressions of STIP1and Hsp90 in LAC cells and tissues were tested by immunohistochemistry and western blot; the correlation between their expressions and clinicopathological parameters of LAC was analyzed by survival analysisand multiple regression analysis. Results: Expressions of STIP1 and Hsp90 were higher in A549 cells and LAC tissues than that in 16 human bronchial epithelial cells (16HBE cells) (P<0.05) and adjacent normal lung tissues (P < 0.05). The expression of STIP1 and Hsp90 in LAC showed a strong positive correlation (P < 0.05) and significantly correlated with lymph node metastasis (P < 0.05), advanced clinical stage (P < 0.05) and shorter survival (P < 0.05) of LAC. Conclusions: Increased expressions of STIP1 and Hsp90 were closely related to malignant biological behavior of LAC, suggesting that they could be used as potential biomarkers and prognostic indicators for LAC.

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