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The Role of Ageing, Inflammation and Maspin in the Early Stages of Prostatic Malignant Transformation

Received: 29 June 2017    Accepted: 26 July 2017    Published: 25 August 2017
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Abstract

Prostate cancer (PCa) progression is an intricate step-wise process, starting from malignant transformations in the benign prostatic epithelium. The hallmark of PCa is the long period of its development from premalignant transformations in the benign prostatic epithelium towards clinically active carcinoma. Along with the age, inflammation, race and genetics, which are well-recognized risk factors for prostatic carcinoma, epigenetics play also a significant role in the initiation and progression of prostatic carcinoma. DNA methylation in the CpG gene islands is a key player in the regulation of gene expression and silencing, and significantly contributes to the disease development. Progression of cancer is associated with the loss of several tumor suppressor genes such as Maspin through mutations or epigenetic silencing. Epigenetic silencing of Maspin seems to be one of the earliest somatic change, contributing to the development of prostatic carcinoma in the human prostate.

Published in International Journal of Clinical Oncology and Cancer Research (Volume 2, Issue 4)
DOI 10.11648/j.ijcocr.20170204.14
Page(s) 93-98
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2024. Published by Science Publishing Group

Keywords

Prostate Carcinogenesis, Field Effect, Epigenetics, Ageing, Chronic Inflammation, Maspin

References
[1] Siegel RL, Miller KD, Jemal A (2017) Cancer statistics. CA Cancer J Clin 67: 7-30.
[2] Fradet Y, Klotz L, Zlotta A, Trachtenberg J (2009) The burden of prostate cancer in Canada. Can Urol Assoc J 3: S92-S100.
[3] Botswick DG and Cheng L (2012) Precursors of prostate cancer. Histopathology 60: 4-27.
[4] Esfahani M, Ataei N, Panjehpour M (2015) Biomarkers for Evaluation of Prostate Cancer Prognosis. Asian Pac J Cancer Prev 16: 2601-2611.
[5] Chai M and Brown ER (2009) Field Effect in Cancer–An Update. Annals of Clinical & Laboratory Science 39: 4.
[6] Montironi R, Mazzucchelli R, Lopez-Beltran A, Scarpelli M, Liang Cheng L (2011) Prostatic intraepithelial neoplasia: its morphological and molecular diagnosis and clinical significance. BJU International 108: 1394-1399.
[7] Botswick DG and Cheng L (2012) Precursors of prostate cancer. Histopathology 60: 4-27.
[8] De Marzo AM, Marchi VL, Epstein JI, Nelson WG (1999) Proliferative inflammatory atrophy of the prostate: implications for prostatic carcinogenesis. Am J Pathol 155: 1985-1992.
[9] Vis AN, Van Der Kwast TH (2001) Prostatic intraepithelial neoplasia and putative precursor lesions of prostate cancer: a clinical perspective. BJU Int 88: 147-157.
[10] Garcia FU, Haber MH, Chen X (2007) Prostatic Basal Cells in the Peripheral and Transitional Zones: Zonal Variation in Morphology and in Immunophenotype. Prostate 67: 1686-1692.
[11] Qian J and Bostwick DG (1995) The Extent and Zonal Location of Prostatic Intraepithelial Neoplasia and Atypical Adenomatous Hyperplasia: Relationship with Carcinoma in Radical Prostatectomy Specimens. Path. Res. Pract 191: 860-867.
[12] Jung M and Pfeifer GP (2015) Aging and DNA methylation. BMC Biology 13: 7.
[13] Goeman l, Joniau S, Ponette D, Van Poppel H (2003) Is low-grade intraepithelial neoplasia a risk factor for cancer? Prostate Cancer and Prostatic Diseases 6: 305-310.
[14] Li LC, Okino ST, Dahia R (2003) DNA methylation in prostate cancer. Biochimia et Biophysica Acta 1704: 87-102.
[15] Richardson B (2003) Impact of aging on DNA methylation. Ageing Research Reviews (2003) 245-261.
[16] Bastian PJ, Yegnasubramanian S, Palapattu GS, Rogers CG, Lin X, et al. (2004) Molecular Biomarker in Prostate Cancer: The Role of CpG Island Hyper methylation. European Urology 46: 698-708.
[17] Feinberg AP and Vogelstein B (1983) Hypomethylation distinguishes genes of some human cancers from their normal counterparts. Nature 301: 89-92.
[18] Issa JP. CpG-island methylation in aging and cancer. Curr Top Microbiol Immunol (2000) 249: 101-118.
[19] Issa JP, Ottaviano YL, Celano P, Hamilton SR, Davidson NE, et al. (1994) Methylation of the oestrogen receptor CpG island links ageing and neoplasia in human colon. Nat Genet 7: 536-540.
[20] Bechis SK, Otsetov AG, Ge R, Wanq Z, Vanqel MG, et al. (2015) Age and obesity promote methylation and suppression of 5-alphareductase 2- implications for personalized therapy in BPH. J Urol 194: 1031-1037.
[21] Ge R, Wang Z, Bechis SK, Otsetov AG, Hua S, et al. (2015) DNA Methyl Transferase 1 Reduces Expression of SRD5A2 in the Aging Adult Prostate. The American Journal of Pathology 185: 170-182.
[22] Wang W, Bergh A, Damber JE (2007) Increased expression of CCA22. AT/enhancer-binding protein in proliferative inflammatory atrophy of the prostate: relation with the expression of COX-2, the androgen receptor, and presence of focal chronic inflammation. Prostate 67: 1238-1246.
[23] Wang W, Bergh A, Damber JE (2009) Morphological transition of proliferative inflammatory atrophy to high-grade intraepithelial neoplasia and cancer in human prostate. Prostate 69: 1378-1386.
[24] Liu L, Wylie RC, Andrews LG, Tollefsbol TO (2003) Aging, cancer and nutrition: the DNA methylation connection. Mechanisms of Ageing and Development 124: 989-998.
[25] Bachman KE, Rountree MR, Baylin SB (2001) Dnmt3a and Dnmt3b are transcriptional repressors that exhibit unique localization properties to heterochromatin. J Biol Chem 276: 32282-32287.
[26] Lopatina N, Haskell JF, Andrews LG, Poole JC, Saldanha S, et al. (2002) Differential maintenance and de novo methylating activity by three DNA methyltransferases in aging and immortalized fibroblasts. J Cell Biochem 84: 324-334.
[27] Yamanaka M, Watanabe M, Yamada Y, Takagi A, Murata T, et al. (2003) Altered methylation of multiple genes in carcinogenesis of the prostate. Int J Cancer 106: 382-387.
[28] Yegnasubramanian S, Kowalski J, Gonzalgo ML, Zahurak M, Piantadosi S, et al. (2004) Hypermethylation of CpG islands in primary and metastatic human prostate cancer. Cancer Res: 1975-1986.
[29] Nakayama M, Gonzalgo ML, Yegnasubramanian S, Lin X, De Marzo AM, et al. (2004) GSTP1 CpG island hypermethylation as a molecularbiomarker for prostate cancer. J Cell Biochem 91: 540-552.
[30] Pierson CR, McGowen R, Grignon D, Sakr W, Dey J, et al (2002) Maspin is Up-Regulated in Premalignant Prostate Epithelia. The Prostate 52: 255-262.
Cite This Article
  • APA Style

    Kalin Petrov Kalchev, Alexander Ivanov Hinev, Alkwin Wanders, Alexander Georgiev Otsetov. (2017). The Role of Ageing, Inflammation and Maspin in the Early Stages of Prostatic Malignant Transformation. International Journal of Clinical Oncology and Cancer Research, 2(4), 93-98. https://doi.org/10.11648/j.ijcocr.20170204.14

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    ACS Style

    Kalin Petrov Kalchev; Alexander Ivanov Hinev; Alkwin Wanders; Alexander Georgiev Otsetov. The Role of Ageing, Inflammation and Maspin in the Early Stages of Prostatic Malignant Transformation. Int. J. Clin. Oncol. Cancer Res. 2017, 2(4), 93-98. doi: 10.11648/j.ijcocr.20170204.14

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    AMA Style

    Kalin Petrov Kalchev, Alexander Ivanov Hinev, Alkwin Wanders, Alexander Georgiev Otsetov. The Role of Ageing, Inflammation and Maspin in the Early Stages of Prostatic Malignant Transformation. Int J Clin Oncol Cancer Res. 2017;2(4):93-98. doi: 10.11648/j.ijcocr.20170204.14

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  • @article{10.11648/j.ijcocr.20170204.14,
      author = {Kalin Petrov Kalchev and Alexander Ivanov Hinev and Alkwin Wanders and Alexander Georgiev Otsetov},
      title = {The Role of Ageing, Inflammation and Maspin in the Early Stages of Prostatic Malignant Transformation},
      journal = {International Journal of Clinical Oncology and Cancer Research},
      volume = {2},
      number = {4},
      pages = {93-98},
      doi = {10.11648/j.ijcocr.20170204.14},
      url = {https://doi.org/10.11648/j.ijcocr.20170204.14},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ijcocr.20170204.14},
      abstract = {Prostate cancer (PCa) progression is an intricate step-wise process, starting from malignant transformations in the benign prostatic epithelium. The hallmark of PCa is the long period of its development from premalignant transformations in the benign prostatic epithelium towards clinically active carcinoma. Along with the age, inflammation, race and genetics, which are well-recognized risk factors for prostatic carcinoma, epigenetics play also a significant role in the initiation and progression of prostatic carcinoma. DNA methylation in the CpG gene islands is a key player in the regulation of gene expression and silencing, and significantly contributes to the disease development. Progression of cancer is associated with the loss of several tumor suppressor genes such as Maspin through mutations or epigenetic silencing. Epigenetic silencing of Maspin seems to be one of the earliest somatic change, contributing to the development of prostatic carcinoma in the human prostate.},
     year = {2017}
    }
    

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    T1  - The Role of Ageing, Inflammation and Maspin in the Early Stages of Prostatic Malignant Transformation
    AU  - Kalin Petrov Kalchev
    AU  - Alexander Ivanov Hinev
    AU  - Alkwin Wanders
    AU  - Alexander Georgiev Otsetov
    Y1  - 2017/08/25
    PY  - 2017
    N1  - https://doi.org/10.11648/j.ijcocr.20170204.14
    DO  - 10.11648/j.ijcocr.20170204.14
    T2  - International Journal of Clinical Oncology and Cancer Research
    JF  - International Journal of Clinical Oncology and Cancer Research
    JO  - International Journal of Clinical Oncology and Cancer Research
    SP  - 93
    EP  - 98
    PB  - Science Publishing Group
    SN  - 2578-9511
    UR  - https://doi.org/10.11648/j.ijcocr.20170204.14
    AB  - Prostate cancer (PCa) progression is an intricate step-wise process, starting from malignant transformations in the benign prostatic epithelium. The hallmark of PCa is the long period of its development from premalignant transformations in the benign prostatic epithelium towards clinically active carcinoma. Along with the age, inflammation, race and genetics, which are well-recognized risk factors for prostatic carcinoma, epigenetics play also a significant role in the initiation and progression of prostatic carcinoma. DNA methylation in the CpG gene islands is a key player in the regulation of gene expression and silencing, and significantly contributes to the disease development. Progression of cancer is associated with the loss of several tumor suppressor genes such as Maspin through mutations or epigenetic silencing. Epigenetic silencing of Maspin seems to be one of the earliest somatic change, contributing to the development of prostatic carcinoma in the human prostate.
    VL  - 2
    IS  - 4
    ER  - 

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Author Information
  • Department of Pathology, Varna Medical University, Varna, Bulgaria

  • Department of Urology, Varna Medical University, Varna, Bulgaria

  • Department of Medical Biosciences, Pathology, Ume? University, Ume?, Sweden

  • Department of Medical Biosciences, Pathology, Ume? University, Ume?, Sweden

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