Atrofia inflamatoria proliferativa: potencial lesión precursora de adenocarcinoma prostático

Atrofia inflamatoria proliferativa: potencial lesión precursora de adenocarcinoma prostático

Contenido principal del artículo

Inés Benedetti Padrón
Niradiz Reyes

Resumen

Introducción: la neoplasia intraepitelial prostática (PIN) es considerada actualmente como la única lesión precursora de cáncer de próstata (CaP); sin embargo se ha sospechado que lesiones atróficas podrían también estar involucradas en su carcinogénesis. En 1999 De Marzo propuso el término atrofia inflamatoria proliferativa (PIA) para denominar una lesión localizada en la zona periférica de la glándula,
con células epiteliales altamente proliferativas, frecuentemente acompañada de inflamación, que ha sido postulada como posible lesión precursora de PIN y CaP.
Objetivo: revisar los conceptos de atrofia inflamatoria proliferativa (PIA), características morfológicas, genéticas, moleculares y explicar la capacidad precursora de PIN y CaP.
Metodología: se revisaron las bases de datos Pubmed, Sciencedirect, EBSCOhost y OvidSP en búsqueda de estudios, revisiones sistemáticas, consensos y meta-análisis con las palabras clave: Proliferative Inflammatory Atrophy, Prostatic Atrophy, Prostatic Carcinoma, usando como fecha límite diciembre de 2012.
Resultados: las alteraciones moleculares descritas en la PIA apoyan el origen de ésta lesión en un contexto de estrés oxidativo, posiblemente originado por las células inflamatorias circundantes, que induce en algunas células epiteliales la expresión de genes de defensa contra el daño oxidativo del genoma, mientras que aquellas que fallan en expresar estos genes se tornan vulnerables a oxidantes y electrófilos,
lo que las hace propensas a desarrollar alteraciones genéticas que favorecerían su transformación en células cancerígenas. Esto, sumado a la asociación morfológica PIA-PIN/CaP, apunta a una relación progresiva entre estas lesiones.

Conclusiones: se ha observado asociación topográfica y transición morfológica de la PIA con la PIN y el CaP. Además se han reportado alteraciones genéticas, somáticas y moleculares en la PIA similares a las observadas en PIN y CaP, por lo que la primera ha sido postulada como posible lesión precursora de las dos últimas. Sin embargo es controversial, algunos estudios no han encontrado pruebas suficientes
para sustentar la postulación. Rev.cienc.biomed.2014;5(1):88-99

Palabras clave:

Descargas

Los datos de descargas todavía no están disponibles.

Detalles del artículo

Referencias (VER)

Shen MM, Abate-Shen M. Molecular genetics of prostate cancer: new prospects for old challenges. Genes & development. 2010;24(18):1967-2000.

De Marzo AM, Nakai Y, Nelson WG. Inflammation, atrophy, and prostate carcinogenesis. Urologic Oncology. 2007;25(5):398-400.

De Marzo AM, Platz E, Sutcliffe S, Xu J, Grönberg H, Dracke CH, et al. Inflammation in prostate carcinogenesis. Nature reviews. Cancer. 2007; 7(4): 256-69.

Reyes I, Reyes N, Iatropoulos M, Mittelman A, Geliebter J. Aging-associated changes in gene expression in the ACI rat prostate: Implications for carcinogenesis. The Prostate.

; 63(2):169-86.

Sfanos KS, De Marzo AM. Prostate cancer and inflammation: the evidence. Histopathology. 2012; 60(1):199-215.

Reyes N, Iatropoulos M, Mittelman A, Geliebter J. Microarray analysis of diet-induced alterations in gene expression in the ACI rat prostate. Eur J Cancer Prev. 2002. 11 Suppl 2: S37-42.

De Marzo AM, Meeker AK, Zha S, Luo J, Nakayama M, Platz EA, et al. Human prostate cancer precursors and pathobiology. Urology. 2003. 62(5 Suppl1): 55-62.

De Nunzio C, Kramer G, Marberger M, Montironi R, Nelson W, Schröder, et al. The controversial relationship between benign prostatic hyperplasia and prostate cancer: the role of inflammation. European Urology. 2011. 60(1):106-17.

Gurel B, Iwata T, Koh CH, Yegnasubramanian S, Nelson WG, De Marzo AM. Molecular alterations in prostate cancer as diagnostic, prognostic, and therapeutic targets. Adv

Anat Pathol. 2008.15(6):319-31.

Nelson WG, De Marzo AM, Isaacs WS. Prostate cancer. N Engl J Med. 2003. 349(4):366-81.

Vis AN, Van Der Kwast TH H. Prostatic intraepithelial neoplasia and putative precursor lesions of prostate cancer: a clinical perspective. BJU international. 2001; 88(2):147-57.

Klink JC, Miocinovic R, Galluzzi CM, Klein E. High-grade prostatic intraepithelial neoplasia. Korean J Urol, 2012. 53(5):297-303.

Bostwick DG, Cheng L. Precursors of prostate cancer. Histopathology. 2012. 60(1):4-27.

Bostwick DG, Liu L, Brawer M, Qian J. High-grade prostatic intraepithelial neoplasia. Rev Urol. 2004. 6(4):171-9.

De Marzo, Platz EA, Epstein JI, Ali T, Billis A, Chan TY. A working group classification of focal prostate atrophy lesions. Am J Surg Pathol. 2006. 30(10):1281-91.

De Marzo AM, Marchi VL, Epstein JI, Nelson WG. Proliferative inflammatory atrophy of the prostate: implications for prostatic carcinogenesis. Am J Pathol. 1999;155(6):1985-92.

Putzi MJ, De Marzo AM. Morphologic transitions between proliferative inflammatory atrophy and high-grade prostatic intraepithelial neoplasia. Urology. 2000; 56(5): 828-32.

Billis A. Prostatic atrophy. Clinicopathological significance. Int Braz J Urol. 2010; 36(4):401-9.

Amin MB, Tamboli P, Varma M, Srigley JR. Postatrophic hyperplasia of the prostate gland: a detailed analysis of its morphology in needle biopsy specimens. American Journal of Surgical Pathology. 1999;23(8):925-31.

McNeal JE. Prostate. En: Sternberg SS, ed. Histology for Pathologists. Philadelphia: Lippincott-Raven; 1997. p. 997–1017.

Montironi R, Mazzucchelli R, Lopez-Beltran A, Cheng L, Scarpelli M. Mechanisms of disease: high-grade prostatic intraepithelial neoplasia and other proposed preneoplastic

lesions in the prostate. Nature Reviews Urology. 2007;4(6): 321-32.

De Marzo AM, Putzi MJ, Nelson WG. New concepts in the pathology of prostatic epithelial carcinogenesis. Urology. 2001; 57(4 Suppl 1):103-14.

Wang W, Bergh A, Damber JE. Morphological transition of proliferative inflammatory atrophy to high-grade intraepithelial neoplasia and cancer in human prostate. The Prostate. 2009; 69(13):1378-86.

Shah R, Mucci N, Amin A, Macoska JA, Rubin MA. Postatrophic hyperplasia of the prostate gland: neoplastic precursor or innocent bystander? Am J Pathol. 2001;158(5):1767-73.

Anton RC, Kattan MW, Chakraborty S, Wheeler TM. Postatrophic hyperplasia of the prostate: lack of association with prostate cancer. Am J Pathol.1999;23(8): 932-6.

Billis A. Prostatic atrophy: an autopsy study of a histologic mimic of adenocarcinoma. Mod Pathol. 1998;11(1):47-54.

Billis A, Magna LA. Inflammatory atrophy of the prostate. Prevalence and significance. Archives of Pathology & Laboratory Medicine. 2003; 127(7):840-4.

Franks LM. Atrophy and hyperplasia in the prostate proper. J Pathology and bacteriology. 1954; 68(2):617-21.

Liavag I. The localization of prostatic carcinoma. An autopsy study. Scandinavian J Urology and Nephrology. 1968;2(2):65-71.

Ruska KM, Sauvageot J, Epstein JI. Histology and cellular kinetics of prostatic atrophy. Am J Surg Pathol. 1998; 22(9):1073-7.

van Leenders GJ, Gage WR, Hicks JL, van Balken V, Aalders TW, Schalken JA, et al. Intermediate cells in human prostate epithelium are enriched in proliferative inflammatory atrophy. Am J Pathol. 2003; 162(5):1529-37.

De Marzo AM, Nelson WG, Meeker AK, Coffey DS. Stem cell features of benign and malignant prostate epithelial cells. J Urol. 1998; 160(6 Pt 2): 2381-92.

Nakayama M, Bennett JC, Hicks JL, Epstein JI, Platz EA, Nelson WG. Hypermethylation of the human glutathione S-transferase-pi gene (GSTP1) CpG island is present in a

subset of proliferative inflammatory atrophy lesions but not in normal or hyperplastic epithelium of the prostate: a detailed study using laser-capture microdissection. Am J

Pathol. 2003; 163(3): 923-33.

Tomas D, Krušlina B, Rogatschb H, Schäferb G, Beliczaa M, Mikuzb G. Different types of atrophy in the prostate with and without adenocarcinoma. European Urology. 2007; 51(1): 98-103.

Di Silverio F, Vincenzo Gentilea, Matteisb A, Mariottia G, Giuseppea V, Pastore Luigi PA. Distribution of inflammation, pre-malignant lesions, incidental carcinoma in histologically confirmed benign prostatic hyperplasia: a retrospective analysis. European Urology. 2003; 43(2):164-75.

Postma R, Schroder FH, van der Kwast TH. Atrophy in prostate needle biopsy cores and its relationship to prostate cancer incidence in screened men. Urology. 2005; 65(4):745-9.

Perletti G, Montanari E, Vral A, Gazzano G, Marras E. Inflammation, prostatitis, proliferative inflammatory atrophy: ‘Fertile ground’ for prostate cancer development? Molecular medicine reports. 2010; 3(1): 3-12.

Yildiz-Sezer S, Verdorfer I, Schäfer G, Rogatsch H, Bartsch G, Mikuz G. Assessment of aberrations on chromosome 8 in prostatic atrophy. BJU Int. 2006. 98(1):184-8.

Macoska JA, Trybus TM, Wojno KJ. 8p22 loss concurrent with 8c gain is associated with poor outcome in prostate cancer. Urology. 2000;55(5):776-82.

Bethel CR, Faith D, Li X, Guan B, Hicks JL, Lan F. Decreased NKX3.1 protein expression in focal prostatic atrophy, prostatic intraepithelial neoplasia, and adenocarcinoma: association with gleason score and chromosome 8p deletion. Cancer Research. 2006;66(22):

-90.

Koh CM, Bieberich CH, Dang CHV, Nelson WG, Yegnasubramanian S. MYC and Prostate Cancer. Genes & Cancer. 2010;1(6):617-28.

Gurel B, Iwata T, Koh ChM, Jenkins RB, Lan F, Dang ChV . Nuclear MYC protein overexpression is an early alteration in human prostate carcinogenesis. Modern pathology. 2008; 21(9):1156-67.

Tsujimoto Y, Takayama H, Nonomura N, Okuyama A, Aozasa K. Postatrophic hyperplasia of the prostate in Japan: histologic and immunohistochemical features and p53 gene mutation analysis. The Prostate. 2002;52(4):279-87.

Kristiansen G. Diagnostic and prognostic molecular biomarkers for prostate cancer. Histopathology. 2012; 60(1):125-41.

De Marzo AM, Meeker AK, Esptein JI, Coffey DS. Prostate stem cell compartments: expression of the cell cycle inhibitor p27Kip1 in normal, hyperplastic, and neoplastic cells. Am J Pathol.1998;153(3): 911-9.

Wang W, Bergh A, Damber JE. Chronic inflammation in benign prostate hyperplasia is associated with focal upregulation of cyclooxygenase-2, Bcl-2, and cell proliferation in the glandular epithelium. The Prostate. 2004;61(1):60-72.

Wang W, Bergh A, Damber JE. Increased expression of CCAAT/enhancer-binding protein beta in proliferative inflammatory atrophy of the prostate: relation with the expression of COX-2, the androgen receptor, and presence of focal chronic inflammation. The Prostate.

; 67(11):1238-46.

Parsons JK, Nelson ChP, Cage WR, Nelson WG, Kensler TW, De Marzo AM. GSTA1 expression in normal, preneoplastic, and neoplastic human prostate tissue. The Prostate. 2001; 49(1): 30-7.

Bastian PJ, Yegnasubramanian S, Palapattua GS, Rogers CG, Linb X, De Marzo AM. Molecular biomarker in prostate cancer: the role of CpG island hypermethylation. European Urology. 2004; 46(6):698-708.

Nelson WG, De Marzo AM, Yegnasubramanian S. Epigenetic alterations in human prostate cancers. Endocrinology. 2009;150(9):3991-4002.

Benedettini E, Nguyen P, Loda M. The pathogenesis of prostate cancer: from molecular to metabolic alterations. Diagnostic Histopathology. 2008;14(5):195-201.

Zha S, Gage GR, Sauvageot J, Saria EA, Putzi MJ, Ewing ChM. Cyclooxygenase-2 is up-regulated in proliferative inflammatory atrophy of the prostate, but not in prostate carcinoma. Cancer Research. 2001; 61(24):8617-23.

Zha S, Yegnasubramanianc V, Nelson WG, William B I, De Marzo AM. Cyclooxygenases in cancer: progress and perspective. Cancer Letters. 2004. 215(1):1-20.

Ortega S, Malumbres M, Barbacid M. Cyclin D-dependent kinases, INK4 inhibitors and cancer. Biochimica et Biophysica Acta. 2002;1602(1):73-87.

Faith D, Han S, Lee DK, Friedi A, Hicks JL, De Marzo AM. p16 Is upregulated in proliferative inflammatory atrophy of the prostate. The Prostate. 2005;65(1):73-82.

Billis A, Freitas LL, Magna LA, Ubirajara F. Inflammatory atrophy on prostate needle biopsies: is there topographic relationship to cancer? Int Braz J Urol. 2007;33(3):355-

Brasil AA, Favaro WJ, Cagnon VH, Ferreira U, Billis A. Atrophy in specimens of radical prostatectomy: is there topographic relation to high-grade prostatic intraepithelial neoplasia or cancer? International Urology and Nephrology. 2011; 43(2):397-403.

Asimakopoulos A, Miano R, Maurielo A, Costantini S, Pasqualetti P, Pasqualetti P, et al. Significance of focal proliferative atrophy lesions in prostate biopsy cores that test negative for prostate carcinoma. Urologic Oncology. 2011;29(6):690-7.

Citado por