journal ca prostat-dr. amrizal spu

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  • 8/12/2019 JOURNAL CA Prostat-Dr. Amrizal SpU

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    The association between CaP and

    chronic prostatic inflammation

    In Cap, several key observations have

    supported the postulated relationship

    between chronic inflammation and prostate

    carcinogenesis.

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    Sexual transmitted diseases and CaP

    Penelitian epidemiologi hubungan antaraonkogenesis yang disebabkan oleh prosesiflamasi. Dimana penyakit menular seksualberperan dlm inisiasi dan progresi dari cap.

    Peningkatan resiko ca prostat pada pasien dgriwayat prostatitis klinis atau simtomatis telahdilaporkan. Juga beberapa metaanalisismenunjukkan resiko cap pada pasien dg infeksi

    hpv. Banyakanya partner seksual, usia pertamakali berhubungan, kebiasaan berhubunganseksual, dan frekuensi berhubungan seks menjadifaktor resiko terjadinya cap

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    Cytokine network and CaP

    IL-1

    IL-6

    IL-17

    IL-8

    TNF-a

    TGF-b

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    Cytokine network and CaP

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    Chemokines and CaP

    Chemokines juga terlibat pada pertumbuhan danpertahanan sel epitel prostat manusia. Hal inidibuktikan bahwa sel epitel prostat memproduksiprotein-1 kemotaktik makrofag dimanan melalui

    kemokin reseptor-2 dan phosphatidylinositol 3-kinase merangsang proliferasi dan invasi seltumor prostat. Pada penelitian lain menunjukkanbahwa kemokin ligand-5 dan reseptornya

    berekspresi pada permukaan sel CaP yang dapatberfungsi sebagai faktor autokrin danmengaktivasi banyak respon sel yang meng

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    Polymorphisms of proinflammatory

    genes and CaP

    Polimorfisme dari gen sitokin seperti TNF-B1,

    IL-1a/b, IL-8, IL-10 dan kemokinn reseptor 5

    dapat mempengaruhi tidak hanya pada

    inflamasi dan respon imun tapi seringkali

    berhubungan dengan

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    There is emerging evidence on the key role of COX-2 in prostatecarcinogenesis.99 COX-2 is considered a promoter of proliferation inCaP and its expression is associated with reactive oxygen speciesproduction and genomic damage induced by chronicinflammation.28 Its rapid induction results in enhanced synthesis of

    prostanoids at the tumor site with several procarcinogenic effectsincluding direct stimulation of prostate tumor growth and inhibitionof immune surveillance in the prostate. Several reports have shownthat COX-2, an early-response gene induced by a variety of cytokinesand growth factors, is involved in invasion and angiogenesis in vitroand in vivo and is upregulated in many human malignancies

    including CaP.28,67,98 This upregulation is seen throughout thetumorigenic process from early hyperplasia to metastaticdisease,100102 and has been described in many clinical cases withevolution of proliferative inflammatory atrophy (PIA) and PIN.103