• 제목/요약/키워드: cancer tissue

검색결과 2,009건 처리시간 0.031초

Superoxide Dismutase Isoenzyme Activities in Plasma and Tissues of Iraqi Patients with Breast Cancer

  • Hasan, Hathama Razooki;Mathkor, Thikra Hasan;Al-Habal, Mohammed Hasan
    • Asian Pacific Journal of Cancer Prevention
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    • 제13권6호
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    • pp.2571-2576
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    • 2012
  • Breast cancer is the first of the most common ten cancers in Iraq. Its etiology is multifactorial, oxidative stress and lipid peroxidation being suggested to play important roles in carcinogenesis. The purpose of this study was to investigate the oxidant-antioxidant status in breast cancer patients, by measuring SOD isoenzyme activities (total SOD, CuZn-SOD, Mn-SOD and EC-SOD) in plasma and breast tumors, and by estimating thiobarbituric reactive substances (TBRS) in tissue homogenates. General increase in total SOD activity was observed in plasma and tissue samples of breast tumors, greater in the malignant when compared to benign group (p<0.05). Mn-SOD showed a significant decrease in tissue malignant samples (p<0.05), and insignificant decrease in plasma malignant samples compared with control and benign samples. Plasma EC-SOD activity in both patient benign and malignant breast tumors demonstrated 3.5% and 22.8% increase, respectively. However, there was a decrease in tissue EC-SOD activity in malignant breast tumors when compared with benign. A similar tendency was noted for TBRS. We suggest that elevated total SOD might reflect a response to oxidative stress, and then may predict a state of excess reactive oxygen species in the carcinogenesis process. If there is proteolytic removal of the heparin binding domain, EC-SOD will lose its affinity for the extracellular matrix and diffuse out of the tissue. This will result in a decreased EC-SOD activity, thus leading to an increase in the steady-state concentration of $O^{2-}$ in this domain, and increase in EC-SOD activity in the extracellular fluid. This might explain the results recorded here concerning the decrease in tissue EC-SOD activity and increase in plasma of breast cancer patients.

Expression of bcl-2 and p53 in Induction of Esophageal Cancer Cell Apoptosis by ECRG2 in Combination with Cisplatin

  • Song, Hai-Yan;Deng, Xiao-Hui;Yuan, Guo-Yan;Hou, Xin-Fang;Zhu, Zhen-Dong;Zhou, Li;Ren, Ming-Xin
    • Asian Pacific Journal of Cancer Prevention
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    • 제15권3호
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    • pp.1397-1401
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    • 2014
  • Aim: To investigate the mechanisms of induction of apoptosis of esophageal cancer cells by esophageal cancer-related gene 2 (ECRG2) in combination with cisplatin (DDP). Methods: Hoechest staining was performed to analyze the effects of single ECRG2 and ECRG2 in combination with DDP on apoptosis of EC9706 cells. The expression levels of p53 and bcl-2 mRNA and protein were determined by RT-PCR and Western blotting, respectively. Results: The number of apoptotic cells after the treatment with ECRG2 in combination with DDP for 24 hours was more than that after the treatment with single ECRG2. RT-PCR and Western blotting showed that the expression levels of bcl-2 mRNA and protein were both down-regulated, while p53 mRNA and protein were both up-regulated in the cells treated with ECRG2 in combination with DDP compared with those given ECRG2 alone. Conclusion: ECRG2 in combination with DDP can enhance the apoptosis of EC9706 cells, possibly by down-regulating bcl-2 expression and up-regulating p53.

폐암환자의 객담 및 암 조직에서 MAGE A 1-6와 SSX 1-9 유전자의 발현 (Expression of MAGE A 1-6 and SSX 1-9 Genes in the Sputum and Cancer Tissue of the Lung Cancer Patients)

  • 이연재;이장훈;이정철;이관호
    • Tuberculosis and Respiratory Diseases
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    • 제70권4호
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    • pp.315-322
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    • 2011
  • Background: A variety of diagnostic modalities for lung cancer have been developed. To achieve efficient and early detection of lung cancer, we tried to measure the expression rates of the melanoma associated gene (MAGE) and synovial sarcoma on X chromosome (SSX) genes. Methods: We designed primers for the SSX gene. In addition to the pre-developed MAGE A primer, using an SSX gene primer was attempted to increase the detection rate. We obtained cancer tissues and cancer-free lung tissues from resected lung, sputum from lung cancer patients who had not undergone surgery, and sputum from healthy people and patients with benign intrathoracic diseases. Results: The sensitivity of the MAGE or SSX gene RT-PCR to identifying cancer tissue of the 69 lung cancer patients was 95.2% for squamous cell carcinoma (scc), 87.0% for adenocarcinoma, and 100% for small cell carcinoma. The mean sensitivity value was 94.2% (p=0.001). For adenocarcinoma, the additional use of the SSX gene resulted in a higher expression rate than MAGE alone (87% vs. 69.6%). The expression rate for the cancer-free lung tissue was 14.3% in scc, 17.4% in adenocarcinoma, and 25.0% in small cell carcinoma. In the induced sputum of 49 lung cancer patients who had not undergone surgery, the expression rate for one of the two genes was 65.5%. The expression rate for the sputum of healthy people and benign intrathoracic diseases by MAGE or SSX gene reverse transcription polymerase chain reaction (RT-PCR) was 3.8% and 17.7%. Conclusion: Detecting lung cancer using the expression of MAGE and SSX genes in lung cancer tissue has high sensitivity.

GSTT1 is Deregulated in Left Colon Tumors

  • Coskunpinar, Ender;Canbay, Emel;Oltulu, Yasemin Musteri;Tiryakioglu, Necip Ozan;Bugra, Dursun
    • Asian Pacific Journal of Cancer Prevention
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    • 제15권5호
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    • pp.2319-2321
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    • 2014
  • Our aim was to determine GSTT1 expression levels in left colon tumors and paired normal tissue in order to identify specific alterations in GSTT1 mRNA levels. Alterations in GSTT1 expression in twenty-four left-sided colon tumors and paired cancer free tissue were determined by qRT-PCR. Significant fold changes were determined with t-test. When compared with cancer free tissue, left colon cancers showed a significant decrease in GSTT1 expression. However, GSTT1 mRNA levels among different grades increased gradually in correlation with tumor grade. Our results suggest that downregulation of GSTT1 in left-sided colon cancers is an early event and is reversed with cancer progression, probably due to cellular defense mechanisms as a response to changes in the microenvironment.

CK2 Enzyme Affinity Against c-myc424-434 Substrate in Human Lung Cancer Tissue

  • Yaylim, Ilhan;Ozkan, Nazli Ezgi;Isitmangil, Turgut;Isitmangil, Gulbu;Turna, Akif;Isbir, Turgay
    • Asian Pacific Journal of Cancer Prevention
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    • 제13권10호
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    • pp.5233-5236
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    • 2012
  • CK2 is a serine threonine kinase that participates in a variety of cellular processes with more than 300 defined substrates. This critical enzyme is known to be upregulated in cancers, but the role of this upregulation in carcinogenesis is not yet fully understood but c-myc, one of the defined CK2 substrates, is a well-known proto-oncogene that is normally essential in developmental process but is also involved in tumor development. We evaluated the optimal enzyme and substrate concentrations for CK2 activity in both neoplastic and non-neoplastic human lung tissues using the c-$myc^{424-434}$ peptide (EQKLISEEDL) as a substrate. The activities measured for the neoplastic tissue were 600-750 U/mg protein while those for the control tissue was in the range of 650-800 U/mg. $K_m$ value for c-myc peptide was determined as $0.33{\mu}M$ in non-neoplastic tissue and $0.18{\mu}M$ in neoplastic tissue. In this study, we did not observe an increased activity in the neoplastic tissue when compared with the non-neoplastic lung tissue, but we recorded two times higher affinity for c-$myc^{424-434}$ in cancer tissue. Considering the metabolic position of c-$myc^{424-434}$, our results suggest that phosphorylation by CK2 may be important in dimerization and thus it might affect the regulation of c-myc in cancer tissues.

Somatic Mutaome Profile in Human Cancer Tissues

  • Kim, Nayoung;Hong, Yourae;Kwon, Doyoung;Yoon, Sukjoon
    • Genomics & Informatics
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    • 제11권4호
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    • pp.239-244
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    • 2013
  • Somatic mutation is a major cause of cancer progression and varied responses of tumors against anticancer agents. Thus, we must obtain and characterize genome-wide mutational profiles in individual cancer subtypes. The Cancer Genome Atlas database includes large amounts of sequencing and omics data generated from diverse human cancer tissues. In the present study, we integrated and analyzed the exome sequencing data from ~3,000 tissue samples and summarized the major mutant genes in each of the diverse cancer subtypes and stages. Mutations were observed in most human genes (~23,000 genes) with low frequency from an analysis of 11 major cancer subtypes. The majority of tissue samples harbored 20-80 different mutant genes, on average. Lung cancer samples showed a greater number of mutations in diverse genes than other cancer subtypes. Only a few genes were mutated with over 5% frequency in tissue samples. Interestingly, mutation frequency was generally similar between non-metastatic and metastastic samples in most cancer subtypes. Among the 12 major mutations, the TP53, USH2A, TTN, and MUC16 genes were found to be frequent in most cancer types, while BRAF, FRG1B, PBRM1, and VHL showed lineage-specific mutation patterns. The present study provides a useful resource to understand the broad spectrum of mutation frequencies in various cancer types.

Down-Regulation of CYP1A1 Expression in Breast Cancer

  • Hafeez, S.;Ahmed, A.;Rashid, Asif Z.;Kayani, Mahmood Akhtar
    • Asian Pacific Journal of Cancer Prevention
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    • 제13권5호
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    • pp.1757-1760
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    • 2012
  • Breast cancer is a major cause of death in women worldwide. Mammary tissue expressing xenobiotic metabolizing enzymes metabolically activate or detoxify potential genotoxic breast carcinogens. Deregulation of these xenobiotic metabolizing enzymes is considered to be a major contributory factor to breast cancer. The present study is focused on the expression of the xenobiotic metabolizing gene, CYP1A1, in breast cancer and its possible relationships with different risk factors. Twenty five tumors and twenty five control breast tissue samples were collected from patients undergoing planned surgery or biopsy from different hospitals. Semi-quantitative reverse transcriptase polymerase chain reaction (RT-PCR) and western-blotting were used to investigate the expression of CYP1A1 in breast cancer control and disease samples. mRNA expression of CYP1A1 was down-regulated in 40% of breast tumor samples. Down-regulation was also observed at the protein level. Significnat relations were noted with marital status and tumour grade but not histopathological type. In conclusion, CYP1A1 protein expression was markedly reduced in tumor breast tissues samples as compared to paired control tissue samples.

Tissue CA125 and HE4 Gene Expression Levels Offer Superior Accuracy in Discriminating Benign from Malignant Pelvic Masses

  • Fawzy, Amal;Mohamed, Mohamed R;Ali, Mohamed AM;El-Magied, Mohamed H Abd;Helal, Amany M
    • Asian Pacific Journal of Cancer Prevention
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    • 제17권1호
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    • pp.323-333
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    • 2016
  • Background: Ovarian cancer remains a major worldwide health care issue due to the lack of satisfactory diagnostic methods for early detection of the disease. Prior studies on the role of serum cancer antigen 125 (CA125) and human epididymis protein 4 (HE4) in detecting ovarian cancer presented conflicting results. New tools to improve the accuracy of identifying malignancy are urgently needed. We here aimed to evaluate the diagnostic utility of tissue CA125 and HE4 gene expression in comparison to serum CA125 and HE4 in discriminating benign from malignant pelvic masses. Materials and Methods: One-hundred Egyptian women were enrolled in this study, including 60 epithelial ovarian cancer (EOC) patients and 20 benign ovarian tumor patients, as well as 20 apparently healthy women. Preoperative serum levels of CA125 and HE4 were measured by immunoassays. Tissue expression levels of genes encoding CA125 and HE4 were determined by quantitative real time polymerase chain reaction (qRT-PCR). The diagnostic performance of CA125 and HE4, measured either as mRNA or protein levels, was evaluated by receiver operating characteristic (ROC) curves. Results: The serum CA125+HE4 combination and serum HE4, with area under the curve (AUC) values of 0.935 and 0.932, respectively, performed significantly better than serum CA125 (AUC=0.592; P<0.001). Tissue CA125 and HE4 (AUC=1) performed significantly better than serum CA125 (P<0.001), serum HE4 (P=0.016) and the serum CA125+HE4 combination (P=0.018). Conclusions: Measurement of tissue CA125 and HE4 gene expression not only improves discriminatory performance, but also broadens the range of differential diagnostic possibilities in distinguishing EOC from benign ovarian tumors.

A review on three dimensional scaffolds for tumor engineering

  • Ceylan, Seda;Bolgen, Nimet
    • Biomaterials and Biomechanics in Bioengineering
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    • 제3권3호
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    • pp.141-155
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    • 2016
  • Two-dimensional (2D) cell culture and in vivo cancer model systems have been used to understand cancer biology and develop drug delivery systems for cancer therapy. Although cell culture and in vivo model studies have provided critical contribution about disease mechanism, these models present important problems. 2D tissue culture models lack of three dimensional (3D) structure, while animal models are expensive, time consuming, and inadequate to reflect human tumor biology. Up to the present, scaffolds and 3D matrices have been used for many different clinical applications in regenerative medicine such as heart valves, corneal implants and artificial cartilage. While tissue engineering has focused on clinical applications in regenerative medicine, scaffolds can be used in in vitro tumor models to better understand tumor relapse and metastasis. Because 3D in vitro models can partially mimic the tumor microenvironment as follows. This review focuses on different scaffold production techniques and polymer types for tumor model applications in cancer tissue engineering and reports recent studies about in vitro 3D polymeric tumor models including breast, ewing sarcoma, pancreas, oral, prostate and brain cancers.