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KANKER TESTIS

Pendahuluan Kanker ktestis adalah kanker yang paling sering pada pria antara umur 20 dan 35 tahun. (Primary testicular tumors are the most common solid malignant tumor in men between the ages of 20 and 35 years- Referensi no 1 !erdapat kira-kira "000 kasus baru dan hanya sekitar 350 sampai #00 kematian terkait kanker testis setiap tahun.$ (%ppro&imately "'000 new cases ha(e been diagnosed in )nited *tates e(ery year' and only about 350 to #00 deaths ha(e occurred annually + Referensi no 1 . Pada lebih dari "0, pasien' kanker testis dapat ditangani. -eberapa pasien dengan massa testis solid' yang ditemukan dengan ultrasound' dianggap mengalami kanker testis' sampai terbukti sebaliknya' dan dapat men.alani orchiecctomy radikal untuk menegakkan diagnosis definitif. *ebelum operasi' penanda serum untuk kaker testis dapat diambil. /ua penanda yang rutin digunakan dalam praktek klinik adalah human chorionic gonadotropin (h01 dan follicle-stimulating hormone (2*3 .2 (2or more than "0, of patients' testicular cancer is curable. %ny patient with a solid testicular mass' which has been confirmed on ultrasound' is considered to ha(e testicular cancer until pro(en otherwise' and should undergo a radical orchiectomy to make a definiti(e diagnosis. Prior to surgery' serum markers for testicular cancer should be obtained. !he two markers used in routine clinical practice are human chorionic gonadotropin (h01 and follicle-stimulating hormone (2*3 Referensi 2) Radical orchiectomy' dilakukan dengan pendekatan inguinal daripada skrotal. Penyebaran metastasis dari kanker testikular dapat diprediksi. *isi metastasis primer untuk kanker testikuler kiri dan kanan adalah berturut-turut pada nodus para-aortic dan nodus interaortoca(al pada retroperitoneum. /ranase limfatik dari skrotum' dipihak lain' adalah nodus inguinal. 4ika pada orchictomy skrotal' skrotum terlibat' penyebaran metastasis ke nodus retroperitoneal dan inguinal mungkin ter.adi. *etelah orchiectomy untuk melokalisir sel tumor germinal' le(el h01 (waktu paruh 5 sampai 5 hari dan 2*3 (waktu paruh 2# sampai 36 .am yang mengalami peningkatan sebelum operasi akan men.adi normal.$'2

(7hen performing a radical orchiectomy' the surgery should be performed by an inguinal approach rather than a scrotal approach. !he metastatic spread of testicular cancer is ordered and predictable. !he primary metastatic landing sites for left and right testicular cancers are the para-aortic and the interaortoca(al nodes in the retroperitoneum' respecti(ely. !he lymphatic drainage of the scrotum' on the other hand' is to the inguinal nodes. 8f the scrotum is surgically (iolated by performing a scrotal orchiectomy' metastatic spread to both the retroperitoneal and the inguinal nodes becomes possible. 2ollowing an orchiectomy for locali9ed germ cell tumor' h01 (half-life of 5 to 5 days and 2*3 (half-life of 2# to 36 hours le(els that were ele(ated before surgery should normali9e + referensi no 2 /iagnosis kanker testis dibuat berdasarkan patologi spesimen orchiectomy. Kira-kira "5, dari kanker testis adalah germ cell tumors' sedangkan kira-kira #, adalah ongerm cell tumors seperti tumor Leydig cell da sel *ertoli. Germ cell tumor selan.utnya diklasifikasikan sebagai tumor seminoma dan nonseminoma. )ntuk seminioma yang terlokalisir secara klinik' penanganan standar adalah penanganan retroperitoneum dengan radiasi untuk mencegah rekurensi nodus' sedangkan obser(asi dan follow-up tetap dilakukan. )ntuk nonseminoma yang terlokalisir secara klinik' memiliki resiko tinggi rekurensi' pilihan penanganan meliputi diseksi limfo nodus retroperitoneal profilaksis' dua siklus kemoterapi profilaksis atau obser(asi dengan follow-up sangat ketat. Pasien yang men.alani obser(asi harus memahami bahwa resiko rekurensi retroperitoneal sebesar 30,. Penanganan metastatic germ cell tumor secara umum adalah kemoterapi. Kebanyakan protokol kemoterapi menerapkan kombinasi bleomycin' etoposide dan cis-platinum.$'2 (!he diagnosis of testicular cancer is made based on the pathology of the orchiectomy specimen. %ppro&imately "5, of testicular cancers are germ cell tumors' while appro&imately #, of testicular cancers are nongerm cell tumors such as :eydig cell tumors and *ertoli cell tumors. 1erm cell tumors are further classified as seminomas and nonseminomas. #5 2or clinically locali9ed seminomas' the standard of care is to treat the retroperitoneum with radiation to pre(ent nodal recurrence' although obser(ation and close follow-up are also reasonable. #6 2or clinically locali9ed nonseminomas that are at high risk for recurrence' #5 the options include a prophylactic retroperitoneal lymph node dissection' two cycles of prophylactic chemotherapy or obser(ation with (ery close follow-up. Patients electing obser(ation should understand that there is a 30, risk of retroperitoneal recurrence. !he treatment of metastatic germ cell tumor generally in(ol(es chemotherapy. ;ost chemotherapy protocols employ a combination of bleomycin' etoposide and cis-platinum + <eferensi no 2

Frekuensi
Kanker testis' walaupun .arang adalah keganasan yang paling sering ter.adi pada pria dengan kelompok umur $5-35 tahun dan menimbulkan banyak ketertarikan untuk berbagai alasan. Kanker testis adalah satu dari banyak neoplasma solid yang bisa sembuh. Perbaikan yang dramatik dalam survival yang dihasilkan dari kombinasi teknik diagnostik yang efektif' perbaikan penanda tumor' multidrug chemotherapeutic regimens yang efektif' dan modifikasi teknik operasi' telah menurunkan mortalitas pasien mulai lebih dari 50, sebelum tahun $"50 men.adi kurang dari 5, pada tahun $""5.3
Testicular cancer, although relatively rare, is the most common malignancy in men in the 15- to 35-year age group and evokes widespread interest for several reasons. Testicular cancer has become one of the most curable solid neoplasms and serves as a paradigm for the multimodal treatment of malignancies. The dramatic improvement in survival resulting from the combination of effective diagnostic techni ues, improved tumor markers, effective multidrug chemotherapeutic regimens, and modifications of surgical techni ue has led to a decrease in patient mortality from more than 5!" before 1#$! to less than 5" in 1##$ %&eferensi 3'.

Kanker testis ter.adi antara $, dan $.5, dari neoplasma pria dan 5, dari tumor orologi secara umum' dengan 3-6 kasus baru ter.adi per $00'000 pria=per tahun di negara barat. Peningkatan insiden kanker testis ter.adi selama tahun $"50an dan $">0an' khususnya di negara ?ropa )tara' dan kecenderungan peningkatan yang .elas pada insiden kanker testis di mayoritas negara-negara industri di %merika )tara' ?ropa dan @ceania' walaupun terdapat perbedaan yang menge.utkan dalam angka insiden diangara negara-negara bertetangga. /ata dari Surveillance Epidemiology and End Results Program selama tahun $"53 sampai $""> memperlihatkan peningkatan resiko yang berlan.ut diantara pria Kaukasia di %merika *erikat sendiri' hanya untuk seminoma. !ahun 200>' sekitar >000 pria di %merika *erikat didiagnosis kanker testis' dan 3>0 pria meninggal karenanya. /ibandingkan pada tahun $"50an' insiden kasus meningkat sebesar 5'6 kasus per $00.000 pria' dan kulit putih memiliki insiden tertinggi 6'3 kasus per $00.000 pria.$'#'5 !esticular cancer represents between $, and $.5, of male neoplasms and 5, of urological tumours in general' with 3-$0 new cases occurring per $00'000 males=per

year in 7estern society ($-3 . %n increase in the incidence of testicular cancer was detected during the $"50s and $">0s' particularly in Aorthern ?uropean countries' and there is a clear trend towards an increased testicular cancer incidence in the last 30 years in the ma.ority of the industrialised countries in Aorth %merica' ?urope and @ceania' although surprising differences in incidence rates are seen between neighbouring countries (#'5 . /ata from the *ur(eillance ?pidemiology and ?nd <esults Program during the years $"53 to $""> show a continuing increased risk among 0aucasian men in the )*% only for seminoma referensi !)" *tudies published between $">0 and 2002 showed a clear trend towards an increased testicular cancer incidence in the last 30 years in the ma.ority of industriali9ed countries in Aorth %merica' ?urope' and @ceania Referensi 1). 8n 200>' appro&imately >000 men in the )nited *tates recei(ed a diagnosis of testicular cancer' and 3>0 men died of it. !he o(erall incidence of testicular cancer is 5.# cases per $00 000 men' and white men ha(e the highest incidence' at 6.3 cases per $00 000 men referensi #).

3anya $-2, dari kasus didiagnosis bilateral. !ipe histologi ber(ariasi' walaupun terlihat .elas didominasi oleh germ cell tumour ("0-"5, . Puncak insiden adalah dekade ketiga kehidupan untuk nonseminoma' dan dekade keempat untuk seminoma murni. Kluster familial telah diobser(asi' khususnya diantara saudara.# @nly $-2, of cases are bilateral at diagnosis. !he histological type (aries' although there is a clear predominance ("0-"5, of germ cell tumours ($ . Peak incidence is in the third decade of life for nonseminoma' and in the fourth decade for pure seminoma. 2amilial clustering has been obser(ed' particularly among siblings Referensi !)

Etiologi Penyebab pasti dari banyak kanker testikuler tidak diketahui. Aamun para ahli menemukan bahwa penyakit ini terkait dengan se.umlah kondisi lain. *e.umlah faktor resiko telah diketahui' termasukB6 !10! sebelumnya pada testis kontralateral' $ryptorchidism' 1angguan (ertilitas' 1angguan perkembangan se&' riwayat keluarga'

2aktor resiko prenatal dan perinatal termasuk berat lahir' umur gestasional' umur maternal' dan maternal merokok.

!he etiology of !10! is still unclear. % number of risk factors ha(e been recogni9ed' including prior !10! in the contralateral testicle' cryptorchidism' impaired fertility' disorders of se& de(elopment' family history' and prenatal and perinatal risk factors including birth weight' gestational age' maternal age' and maternal smoking C2"' 30D. %lthough there is some e(idence for a difference in risk factors among the different histologic subtypes' the ma.ority of risk factor analyses support a shared etiology of !10! subtypes C2"' 3$D (referensi 6 .

Klasifikasi Germ cell tumor (10! ter.adi sekitar "5, dari kanker testis. Kanker ini bisa menun.ukkan satu pola histologi yang menon.ol' atau campuran dari berbagai tipe histologi. )ntuk tu.uan penanganan' dua kategori luas dari tumor testis telah diketahui yaituB pure seminoma (tidak terdapat elemen nonseminomatous ' dan semua yang lain' yang bersama-sama dikenal sebagai nonseminomatous germ cell tumor"$ Tabel 1 Klasifikasi tumor testis Germ ell Tumor Seminoma Klasik (khas !idak khas *permatocytic Nonseminomatous ?mbryonal carcinoma !eratoma ;atur 8mmatur ;atur atau immatur dengan transformasi ganas 0horiocarcinoma Eolk sac tumor (endodermal sinus tumor Se! ord dan Stromal Tumor !umor sel *ertoliFs cell tumor

!umor sel :eydig !umor sel 1ranular !ipe campuran (misalnya tumor *ertoli-:eydig "i!ed Germ ell dan elemen#elemen Stromal 1onadoblastoma Tumor Adne!al dan Paratesti$ular %denocarcinoma dari rete testis ;esothelioma Tumor "is$ellaneous 0arcinoid :ymphoma !esticular metastasis

Patogenesis Perubahan karakteristik genetik yang ditemukan adalah isokromosom dari lengan pendek kromosom $2 Ci($2p D' yang sering terlihat pada kanker-kanker sporadik. /iduga bahwa gen pada area ini memiliki peran penting dalam perkembangan germ cell tumors. *e.umlah gen lain yang relatif memiliki efek yang lemah .uga terlibat dalam perkembangan kanker testis.$ 2aktor-faktor genetik memiliki peran dalam perkembangan kanker testis

diperlihatkan melalui fakta bahwa resiko untuk penyakit lebih tinggi pada keluarga urutan pertama dari pasien kanker daripada populasi umum. Kira-kira 2, dari pasien kanker testis melaporkan memiliki keluarga yang mengalami hal yang sama. *audara kandung secara khusus memiliki resiko yang tinggi dengan resiko relatif >+$0. )ntuk anak laki-laki dari pasien kanker testis' resiko relatif adalah #+6.$ /ua model karsinoma testikular in situ telah diusulkan. 2akta pertama bahwa genosit fetal yang berkembang men.adi spermatogonia yang diblokade dapat mengalami

pembagian sel yang abnormal dan kemudian ter.adi pertumbuhan in(asif dan stimulasi pu%ertal gonadotropin.$ ;odel postulat kedua' bahwa sel target yang paling sering untuk ter.adinya transformasi adalah &ygotene-pachytene spermatocyte. *elama stadium perkembangan germ cell' ter.adi pertukaran kromatid yang dihubungkan dengan pertukaran yang menyimpang. Aormalnya' sel-sel ini mengalami eliminasi melalui apoptosis. Pada suatu keadaan' pertukaran meyimpang ini dapat memicu peningkatan .umlah kopian $2p dan ekspresi berlebihan dari gen cyclin '2 ($$('2 . *el-sel pembawa abnormalitas ini relatif diproteksi terhadap kematian apoptotik oleh karena efek onkogenik dari $$('2) hali ini memicu inisiasi ulang dari siklus sel dan ketidak stabilan genomik.$ !ransformasi malignan dari germ cells te.adi dari proses perubahan genetik dalam berbagai langkah. *atu dari ke.adian paling awal adalah peningkatan kopian .umlah $2p' apakah sebagai $ atau lebih kopian dari i($2p atau sebagai duplikasi tandem dari kromosom lengan $2p. %bnormalitas ini ditemukan pada lesi karsinoma in situ tersembunyi demikian .uga pada penyakit lan.ut. *tudi selan.utnya menun.ukkan bahwa $$('2 ada pada pita kromosom $2p$3 dan bahwa $$('2 mengalami ekspresi berlebihan pada banyak germ cell tumor' termasuk karsinoma in situ. Penguatan dari $$('2 mengakti(asi cd*!+,) memungkinkan sel berkembanng melalui titik poin 1$-*.$ !he cause of testicular cancer is not known. !he characteristic genetic change found is an isochromosome of the short arm of chromosome $2 Ci($2p D' which is often seen in sporadic cancers. !his suggests that genes in this region are important in the de(elopment of germ cell tumors. % number of other genes that ha(e a relati(ely weak effect are also in(ol(ed in the de(elopment of testicular cancer. !hat genetic factors ha(e a role in the de(elopment of testicular cancer is shown by the fact that the risk for the disease is higher in first-degree relati(es of cancer patients than in the general population. %bout 2, of testicular cancer patients report ha(ing an affected relati(e. *iblings are at particularly increased risk' with a relati(e risk of >+$0. 2or sons of affected men' the relati(e risk is #+6. !wo models of testicular carcinoma in situ ha(e been proposed. !he first posits that fetal gonocytes whose de(elopment into spermatogonia is blocked may undergo

abnormal cell di(ision and then in(asi(e growth mediated by postnatal and pubertal gonadotropin stimulation. !he second model postulates that the most likely target cell for transformation is the 9ygotene-pachytene spermatocyte. /uring this stage of germ cell de(elopment' aberrant chromatid e&change e(ents associated with crossing o(er can occur. Aormally' these cells are eliminated by apoptosis. @n occasion' this crossing o(er may lead to increased $2p copy number and o(ere&pression of the cyclin /2 gene ($$('2 . !he cell carrying this abnormality is relati(ely protected against apoptotic death because of the oncogenic effect of $$('2) leading to re-initiation of the cell cycle and genomic instability. ;alignant transformation of germ cells is the result of a multistep process of genetic changes. @ne of the earliest e(ents is the increased copy number of $2p' either as $ or more copies of i($2p or as tandem duplications of chromosome arm $2p. !his abnormality is found in occult carcinoma in situ lesions as well as more ad(anced disease. 2urther studies indicate that $$('2 is present at chromosome band $2p$3 and that $$('2 is o(ere&pressed in most germ cell tumors' including carcinoma in situ. %mplification of $$('2 acti(ates cd*!+,) allowing the cell to progress through the 1$-* checkpoint. (referensi $

%iagnosis 1& Pemeriksaan Klinik Kanker testis secara umum mempengaruhi pria muda pada dekade ketiga dan keempat kehidupan. Aormalnya terlihat sebagai massa unilateral dalam skrotum atau massa intracrotal yang tidak nyeri' unilateral. Pada kira-kira 20, kasus' ge.ala pertama adalah nyeri skrotum' dan hampir 25, pasien dengan kanker testis mengalami nyeri lokal. Kadang-kadang' trauma pada skrotum dapat memperlihatkan adanya massa testikuler. 1ynaecomastia terlihat pada 5, kasus dan lebih sering pada tumor non-seminomatous. Ayeri punggung dan flank terlihat pada $$, kasus. Penurunan ukuran testis dapat mendahului tumor testis.6 !esticular cancer generally affects young men in the third or fourth decade of life. 8t normally appears as a painless' unilateral mass in the scrotum or the casual finding of an intrascrotal mass (30 . 8n appro&imately 20, of cases' the first symptom is scrotal pain' and up to 25, of patients with testicular cancer may ha(e local pain ($ . @ccasionally' trauma to the scrotum may re(eal the presence of a testicular mass. 1ynaecomastia appears in 5, of cases and is more common in non-seminomatous

tumours. -ack and flank pain are present in about $$, of cases ($6 . <eduction in testis si9e can precede a testicular tumour (3$ (referensi 6 . *ekitar $0, kasus tumor testis dapat menyerupai orchioepididymitis' yang menyebabkan keterlambatan diagnosis yang benar. )ltrasound dapat dilakukan pada beberapa kasus yang meragukan. Pemeriksaan fisik menun.ukkan gambaran massa dan harus selalu dilakukan pemeriksan umum untuk menemukan kemungkinan mestastasis .auh (supracla(icular ' suatu massa abdominal yang teraba atau gynaecomastia. /iagnosis benar harus ditegakkan pada semua pasien dengan massa intraskrotal.6 8n about $0, of cases' a testicular tumour can mimic an orchioepididymitis' with conseGuent delay of the correct diagnosis ($' 2 . )ltrasound must be performed in any doubtful case. Physical e&amination re(eals the features of the mass and must always be carried out in con.unction with a general e&amination in order to find possible (supracla(icular distant metastases' a palpable abdominal mass or gynaecomastia. % correct diagnosis must be established in all patients with an intrascrotal mass (32 .

'& Imaging (ada testis *aat ini' diagnostik ultrasound memberikan konfirmasi adanya masa testikuler dan untuk mengeksplorasi testis kontralateral. )latrasound sensitif dalam mendeteksi tumor testikuler pada hampir $00, kasus' dan memiliki peranan penting dalam menentukan apakah massa terletak intra- atau e&tratesticular. )ltrasound merupakan tes yang tidak mahal' namun tes ini tidak perlu dilakukan bila secara klinik tumor testikuler ada. )ltrasound pada testis dapat dilakukan pada pria muda tanpa massa testikuler yang teraba' mereka dengan massa retroperitoneal atau (isceral atau peningkatan human chorionic gonadotrophin (h01 serum atau %2P. )ltrasound direkomendasikan untuk follow-up testis kontralateral pada pasien beresiko.6 -agnetic resonance imaging (;<8 menawarkan sensitifitas dan spesifitas yang lebih tinggi daripada ultrasound untuk mendiagnosis tumor dan mampu untuk membedakan tumor seminomatous dari non-seminomatous. ;<8 pada scrotum

memberikan sensitifitas $00, dan spesifitas "5-$00,' namun biaya untuk ;<8 cukup tinggi.6'5 0urrently' diagnostic ultrasound ser(es to confirm the presence of a testicular mass and to e&plore the contralateral testis. 8ts sensiti(ity in detecting a testicular tumour is almost $00,' and it has an important role in determining whether a mass is intra- or e&tratesticular (33 . )ltrasound is an ine&pensi(e test' but it is unnecessary when the presence of a testicular tumour is clinically e(ident (3# . )ltrasound of the testis has to be performed in young men without a palpable testicular mass who ha(e retroperitoneal or (isceral masses or ele(ated serum human chorionic gonadotrophin (h01 or %2P (35-3> . )ltrasound is recommended in the follow-up of the contralateral testis in the follow-up of patients at risk (3" . ;agnetic resonance imaging (;<8 offers higher sensiti(ity and specificity than ultrasound for diagnosing tumours (#0-#2 and may be able to differentiate seminomatous from non-seminomatous tumours. ;<8 of the scrotum offers a sensiti(ity of $00, and a specificity of "5-$00, (#3 ' but its high cost does not .ustify its use for diagnosis.

)& Penanda tumor serum (ada diagnosis Penanda tumor serum adalah faktor-faktor prognostik yang berkontribusi terhadap diagnsosi dan penentuan stadium. Penanda tumor berikut ini dapat ditentukanB6 H H Lactate %2P (diproduksi oleh sel yol* sac h01 (ekspresi dari tropho%lasts . dehydrogenase (:/3 merupakan penanda destruksi .aringan'

direkomendasikan bagi pasien dengan penyakit metastasis. *ecara global' penanda ini meningkat pada 5$, kasus kanker testis. .lphafetoprotein meningkat pada 5050, pasien dengan non-seminomatous germ cell tumour (A*10! ' dan peningkatan dalam h01 terlihat pada #0-60, pasien dengan A*10!. *ekitar "0, dari tumor non-seminomatous terihat dengan peningkatan satu atau dua dari penanda ini. 3ampir 30, seminomas dapat muncul atau berkembang suatu peningkatan le(el h01 selama rangkaian penyakit.6 :/3 adalah penanda yang kurang spesifik' dan konsentrasinya sebanding dengan (olume tumor. :e(el :/3 mungkin meningkat pada >0, pasien dengan kanker

1!

testikuler lan.ut. Perlu dicatat bahwa le(el penanda negatif tidak menyingkirkan diagnosis germ cell tumour. Penanda lain yang dipela.ari adalah placental al*aline phosphatase (P:%P ' yang mungkin bernilai dalam monitoring pasien dengan pure seminoma. Penanda sitogenik dan molekuler tersedia di center spesifik' tapi hanya digunakan untuk tu.uan penelitian.6

*erum tumour markers are prognostic factors and contribute to diagnosis and staging (## . !he following markers should be determinedB H %2P (produced by yolk sac cells H h01 (e&pression of trophoblasts . :actate dehydrogenase (:/3 (marker of tissue destruction is recommended for patients with metastatic disease. 1lobally' there is an increase in these markers in 5$, of cases of testicular cancer ($6' 30 . %lphafetoprotein increases in 50-50, of patients with non-seminomatous germ cell tumour (A*10! ' and a rise in h01 is seen in #0-60, of patients with A*10!. %bout "0, of non-seminomatous tumours present with a rise in one or two of the markers. )p to 30, of seminomas can present or de(elop an ele(ated h01 le(el during the course of the disease (#5' #6 . :/3 is a less specific marker' and its concentration is proportional to tumour (olume. 8ts le(el may be ele(ated in >0, of patients with ad(anced testicular cancer (#5 . 8t should be noted that negati(e marker le(els do not e&clude the diagnosis of a germ cell tumour. @ther markers studied include placental alkaline phosphatase (P:%P ' which may be of (alue in monitoring patients with pure seminoma. 0ytogenetic and molecular markers are a(ailable in specific centres' but at present only contribute to research studies. ;easurement of serum %2P' h01 and :/3 (in ad(anced tumours is mandatory' while that of P:%P is optional.

*& Eks(lorasi Inguinal dan or$hide$tom+ *etiap pasien dengan dugaan massa testikuler harus men.alani eksplorasi inguinal dengan eksteriorisasi testis didalam tunikanya. @rchidectomy segera dengan membagi dari spermatic cord pada internal inguinal ring harus dilakukan .ika tumor ditemukan. 4ika diagnosis tidak .elas' biopsi testis dilakuan untuk irisan beku untuk pemeriksaan histologi.6

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Pada kasus penyakit disseminata dan metastasis yang mengancam kehidupan' praktek yang dilakuan saat ini mulai dengan up-front chemotherapy' dan orchidectomy bisa ditunda sampai stabilisasi klinik ter.adi.6 ?(ery patient with a suspected testicular mass must undergo inguinal e&ploration with e&teriorisation of the testis within its tunics. 8mmediate orchidectomy with di(ision of the spermatic cord at the internal inguinal ring must be performed if a tumour is found. 8f the diagnosis is not clear' a testicular biopsy is taken for fro9en section histological e&amination. 8n cases of disseminated disease and life-threatening metastases' it is current practice to start with up-front chemotherapy' and orchidectomy may be delayed until clinical stabilisation has occurred.

,& Organ-sparing surgery 7alaupun organ-sparing surgery tidak diindikasikan pada adanya non-tumoural contralateral testis' operasi ini dapat dilakukan pada kasus-kasus khusus yang semuanya untuk tindakan pencegahan.6 Pada tumor testikuler bilateral synchronous' tumor etachronous contralateral' atau pada tumor pada testis soliter dengan kadar testosteron pre-operatif normal' organ preserving surgery dapat dilakukan bila (olume tumor kurang dari 30, dari (olume testikuler dan operasi dilakukan seperti biasanya. Pada kasus lain' angka yang berhubungan dengan !in tinggi (setidaknya mencapai >2, ' dan pada semua pasien dapat ditangani dengan radioterapi ad.u(an (20 1y pada beberapa titik.6'5 8nfertilitas akan ter.adi sesudah radioterapi dan resiko insufisiensi sel :eydig .angka pan.ang sesudah radioterapi dari testis sisa meningkat. Penanganan radioterapi dapat ditunda pada pasien fertil yang masih menginginkan anak. Pilihan harus didiskusikan pada pasien dengan hati-hati dan operasi dilakukan di pusat yang berpengalaman.6 %lthough organ-sparing surgery is not indicated in the presence of non-tumoural contralateral testis' it can be attempted in special cases with all the necessary precautions.

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8n synchronous bilateral testicular tumours' metachronous contralateral tumours' or in a tumour in a solitary testis with normal pre-operati(e testosterone le(els' organ preser(ing surgery can be performed when the tumour (olume is less than 30, of the testicular (olume and surgical rules are respected. 8n those cases' the rate of associated !in is high (at least up to >2, ' and all patients must be treated with ad.u(ant radiotherapy (20 1y at some point (#5 . 8nfertility will result after radiotherapy and the risk insufficiency after radiotherapy of a solitary testis is treatment may be delayed in fertile patients who wish to must be carefully discussed with the patient and surgery e&perience (#"' 50 . of long-term :eydig cell increased (#> . <adiation father children. !he option performed in a centre with

-& Pemeriksaan (atologik (ada testis Pemeriksaan patologik yang diperlukanB$'2 H H 1ambaran makroskopikB lokasi' ukuran testis' ukuran tumor maksimum dan gambaran makroskopik dari epididimis' spermatic cord dan tunica (aginalis. *amplingB irisan $ cm2 untuk tiap sentimeter dari diameter tumor maksimum' termasuk parenkim yang terlihat normal secara makroskopik (.ika ada ' albuginea dan epididimis' dengan seleksi dari area yang diduga. Pada sekurangnya satu irisan proksimak dan satu distal dari spermatic cord ditambah beberapa area yang diduga. H 1ambaran mikroskopik dan diagnosisB tipe histologi (menentukan komponen indi(idual components dan memperkirakan .umlah dalam persentase menurut 73@ 200#B %da atau tidaknya in(asi (enous peri-tumoural dan=atau limfatik %da atau tidaknya in(asi albuginea' tunica (aginalis' rete testis' epididimis atau spermatic cord %da atau tidaknya neoplasia intratu%ular germ cell (!in neoplasi non-tumour parenchyma intratubular germ cell H Kategori p! menurut /umour (ode -etastasis (!A; 2002 pada

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*tudi imunohistokimiaB pada seminoma dan mi0ed germ cell tumour' %2P dan h01.

*ebaiknya dilakuan pemeriksaan penanda imunohistokimia' pada kasus yang meragukan' yaituB6 H H H Pada seminomaB cytokeratin (0%; 5.2 ' P:%P' c-kit Pada intratu%ular germ cell neoplasiaB P:%P' c-kit Penanda lainB chromogranine % (0g % ' Ki-$ (;8--$ .

;andatory pathological reGuirementsB H ;acroscopic featuresB side' testis si9e' ma&imum tumour si9e and macroscopic features of epididymis' spermatic cord and tunica (aginalis. 6 :imited update march 200" H *amplingB a $ cm2 section for e(ery centimetre of ma&imum tumour diameter' including normal macroscopic parenchyma (if present ' albuginea and epididymis' with selection of suspected areas. %t least one pro&imal and one distal section of spermatic cord plus any suspected area. H ;icroscopic features and diagnosisB histological type (specify indi(idual components and estimate amount as percentage according to 73@ 200# (2" B - presence or absence of peri-tumoural (enous and=or lymphatic in(asion - presence or absence of albuginea' tunica (aginalis' rete testis' epididymis or spermatic cord 8n(asion - presence or absence of intratubular germ cell neoplasia (!in in non-tumour parenchyma intratubular germ cell neoplasia H p! category according to !umour Aode ;etastasis (!A; 2002 H 8mmunohistochemical studiesB in seminoma and mi&ed germ cell tumour' %2P and h01. %d(isable immunohistochemical markers' in cases of doubt' areB H in seminomaB cytokeratins (0%; 5.2 ' P:%P' c-kit H in intratubular germ cell neoplasiaB P:%P' c-kit H other ad(isable markersB chromogranine % (0g % ' Ki-$ (;8--$ . .& %iagnosis karsinoma in situ /Tin0

1(

-iopsi kontralateral telah dian.urkan untuk menyingkirkan adanya !in. 7alaupun ini merupakan kebi.akan rutin dari beberapa negara' insiden !in dan contralateral metachronous testicular tumours' rendah (masing-masing ", dan 2.5, . ;asih sulit untuk mencapai konsensus pada apakah eksistensi !in kontralateral harus diidentifikasi pada semua kasus. Aamun' biopsi dari testis kontralateral dapat dilakukan pada pasien resiko tinggi !in kontralateral dengan (olume testikuler kurang dari $2 m:' riwayat cryptorchidism' atau spermatogenesis rendah (4ohnson *core $-3 . -iopsi kontralateral tidak diperlukan bagi pasien yang berumur lebih dari #0 tahun.6 *ekali !in didiagnosis' radioterapi lokal (20 1y dalam fraksi tunggal 2 1y merupakan pilihan penanganan. @leh karena prosedur ini dapat menyebabkan infertilitas' pasien harus men.alani konseling hati-hati mengenai penanganan. *elain infertilitas' fungsi sel :eydig dan produksi testosteron dapat mengalami kerusakan .angka pan.ang setelah radioterapi !in. Penanganan radiasi dapat ditunda pada pasien fertil yang masih menginginkan anak.6'5 0ontralateral biopsy has been ad(ocated to rule out the presence of !in (5$ . %lthough this is routine policy in some countries' the low incidence of !in and contralateral metachronous testicular tumours (up to ", and appro&imately 2.5,' respecti(ely (52' 53 ' the morbidity of !in treatment' and the fact that most of these metachronous tumours are at a low stage at presentation make it contro(ersial to recommend a systematic contralateral biopsy in all patients (5#-56 . 8t is still difficult to reach a consensus on whether the e&istence of contralateral !in must be identified in all cases. 3owe(er' biopsy of the contralateral testis should be offered to high-risk patients for contralateral !in with a testicular (olume of less than $2 m:' a history of cryptorchidism' or poor spermatogenesis (4ohnson *core $-3 . % contralateral biopsy is not necessary for patients older than #0 years (55-62 . % double biopsy is preferred to increase sensiti(ity. @nce !in is diagnosed' local radiotherapy (20 1y in single fractions of 2 1y is the treatment of choice. -ecause this may produce infertility' the patient must be carefully counselled before treatment commences (5#' 63 . 8n addition to infertility' :eydig cell function and testosterone production may be impaired long-term following radiotherapy for !in (#" . <adiation treatment may be delayed in fertile patients who wish to father children (5" .

15

1&

S$reening

7alaupun tidak ada sur(ey yang menyediakan keuntungan program screening' telah diperlihatkan bahwa stadium dan prognosis secara langsung berhubungan dengan diagnosis dini. Pada situasi adanya faktor resiko klinik' pemeriksaan dini indi(idu yang dipengaruhi' dian.urkan.6 %lthough there are no sur(eys pro(ing the ad(antages of screening programmes' it has been demonstrated that stage and prognosis are directly related to early diagnosis. 8n the presence of clinical risk factors' selfphysical e&amination by the affected indi(idual is ad(isable.

Penanganan Penanganan kanker testis terdiri dari orchiectomy dan bisa melibatkan operasi lain' terapi radiasi dan kemoterapi' tergantung pada stadium penyakit dan tipe tumor. ;elihat stadim penyakit' lebih dari "0, dari semua yang baru didiagnosis kanker testis dapat sembuh.>'" H *tadium pertama dari penanganan biasanya orchidectomyB mengangkat testis yang mengalami kanker lewat insisi pada paha' dilakukan dibawah anestesi umum. H Penanganan selan.utnya tergantung pada diagnosis patologik (seminoma (s nonseminoma dan stadium penyakit dan bisa meliputi radioterapi' kemoterapi atau obser(asi aktif. + + Pria dengan seminoma stadium awal' ditangani dengan radiotherapy untuk limph nodus ipsilateral atau kemoterapi dosis tunggal. Pria dengan non-seminoma stadium awal biasanya men.alani pengawasan ketat (penanda tumor' &-ray thoraks dan 0! scan .ika tidak ada faktor resiko patologik. + Pria dengan penyakit stadium dini yang relaps dan mereka dengan penyakit lan.ut' secara umum diru.uk untuk men.alani kemoterapi. 4ika kemoterapi

1)

masih menyisakan massa' dan mengandung kanker' biasanya perlu operasi pengangkatan. H 4ika pria memiliki orchidectomy bilateral (.arang ' maka perlu terapi penggantian testosteron berkelan.utan. -eberapa orang memilih untuk implan testikuler sesudah penanganan untuk alasan kosmetik.$'2

;anagement of testicular cancer consists of orchiectomy and may include other surgery' radiation therapy' and chemotherapy' depending on the disease stage and tumor type. <egardless of disease stage' more than "0, of all newly diagnosed cases of testicular cancer will be cured (referensi " . H
H !he first stage of treatment is usually an orchidectomyB remo(al of the diseased testicle (ia an incision in the groin' performed under general anaesthetic 2urther treatment depends on the pathological diagnosis (seminoma (s nonseminoma and the stage of disease and may include radiotherapy' chemotherapy or acti(e sur(eillance ++;en with early stage seminoma are treated with radiotherapy to the ipsilateral lymph nodes or single dose chemotherapy ++;en with early stage non-seminoma usually undergo close sur(eillance (tumour markers' chest &-ray and 0! scans if no pathological risk factors ++;en with early stage disease who relapse and men with ad(anced disease are generally referred for chemotherapy. 8f chemotherapy lea(es residual masses' these may contain cancer and usually will need surgical remo(al 2H 8f a man has a bilateral orchidectomy (rare he will reGuire ongoing testosterone replacement therapy. *ome men choose to ha(e a testicular implant during or after treatment for cosmetic reasons referensi 1)

Prognosis /he 2nternational Germ $ell $onsensus $lassification (81000 ' merupakan suatu instrumen yang didasarkan pada prognosis yang mudah diaplikasikan' saat ini digunakan dalam praktek klinik untuk klasifikasi resiko dan standar yang digunakan saat ini untuk semua panduan praktek' termasuk (ational $omprehensive $ancer (et3or*"$

1$

81000 membedakan pasien A*10! dengan prognosis baik' sedang dan burukI dengan keseluruhan 5-year sur(i(al masing-masing "2,' >0,' dan #>,.$ Aonseminoma prognosis baik (56, sampai 6$, dari nonseminomas B #-year progression-free survival (P2* adalah >",I 5-year survival sebesar "2, sampai "#,.$

!estis=retroperitoneal primer' dan !idak ada metastasis (isceral non pulmonarius' dan Penanda tumor serum baikI semua dariB
o o

%lpha-fetoprotein (%2P kurang dari $'000 ng=m:' dan 3uman chorionic gonadotropin (h01 kurang dari 5'000 8)=m: ($'000 ng=m: ' dan

:actate dehydrogenase (:/3 kurang dari $.5 kali per batas atas dari normal.

*eminoma prognosis baik ("0, dari seminoma B #-year P4S adalah >2,I #-year survival adalah >6,

-eberapa tempat primer' dan !idak ada metastasis (isceral nonpulmonarius' dan %2P' beberapa h01' beberapa :/3' normal

Aonseminoma prognosis sedang ($3-2>, dari nonseminoma B #-year P4S adalah 55,I 5-year sur(i(al adalah >0, sampai >3,

!estis=retroperitoneal primer' dan !idak ada metastasis (isceral nonpulmonarius' dan Penanda tumor serum intermediateI beberapa dari B

1*

o o o

%2P $'000 sampai $0'000 ng=m:' atau h01 5'000 8)=: sampai 50'000 8)=:' atau :/3 $.5 sampai $0 kali normal.

2ntermediate-prognosis seminoma ($0, dari seminoma B 5-year P2* adalah 65,I 5year sur(i(al adalah 52,

-eberapa tempat primer' dan ;etastasis (isceral nonpulmonarius' dan %2P' beberapa h01' beberapa :/3' normal

Poor-prognosis nonseminoma ($6,+26, dari nonseminoma B 5-year P2* adalah #$,I 5-year sur(i(al adalah 5$,

;ediastinal primer' atau ;etastasis (isceral nonpulmonarius' atau Penanda tumor serum burukI beberapa dariB
o o o

%2P lebih dari $0'000 ng=m:' atau h01 lebih dari 50'000 8)=m: ($0'000 ng=m: ' atau :/3 lebih dari $0 kali batas atas normal.

Poor-prognosis seminomaB !idak ada pasien seminoma yang diklasifikasikan prognosis buruk. !he 8nternational 1erm 0ell 0onsensus 0lassification (81000 'C5D an easily applicable' clinically based prognostic instrument' is now used in clinical practice for risk classification and is the current standard for all practice guidelines' including that of the Aational 0omprehensi(e 0ancer Aetwork.

1#

!he 81000 is based on a retrospecti(e analysis of 5'202 patients with metastatic nonseminomatous germ cell tumor (A*10! and 660 patients with metastatic seminomatous germ cell tumors from $0 countries' who were treated between $"55 and $""0. %ll patients recei(ed treatment with cisplatin- or carboplatin-containing therapy as their first chemotherapy course. ;edian followup was 5 years. 2or A*10!' independent ad(erse factors were identifiedB mediastinal primary siteI degree of ele(ation of alpha-fetoprotein' human chorionic gonadotropin (301 ' and lactate dehydrogenase (:/3 I and presence of nonpulmonary (isceral metastates (APJ; ' such as li(er' bone' and brain. 2or seminoma' the predominant ad(erse feature was the presence of APJ;. !he 81000 distinguishes A*10! patients with a good' intermediate' or poor prognosisI these ha(e reported 5-year o(erall sur(i(al of "2,' >0,' and #>,' respecti(ely. % subseGuent meta-analysis of sur(i(al of patients with A*10!' treated after $">" and classified according to the 8100 classification' included $0 papers describing $555 patients with A*10! with good (n K $0>5 ' intermediate (n K 232 ' or poor (n K #56 prognosis. Pooled 5-year sur(i(al estimates were "#,' >3,' and 5$,' respecti(ely. !here was a small increase in sur(i(al for good-prognosis and intermediate-prognosis patients' and a large increase in sur(i(al for patients with a poor prognosis. !he researchers suggested that the impro(ed sur(i(al was most likely due to both more effecti(e treatment strategies and more e&perience in treating A*10! patients.C$5D 1ood-prognosis nonseminoma (56, to 6$, of nonseminomas B 5-year progressionfree sur(i(al (P2* is >",I 5-year sur(i(al is "2, to "#,

Testis+retroperitoneal primary, and ,o nonpulmonary visceral metastases, and -ood serum tumor markers. all of/
o o o

0lpha-fetoprotein %012' less than 1,!!! ng+m3, and 4uman chorionic gonadotropin %h5-' less than 5,!!! 67+m3 %1,!!! ng+m3', and 3actate dehydrogenase %384' less than 1.5 times the upper limit of normal

1ood-prognosis seminoma ("0, of seminomas B 5-year P2* is >2,I 5-year sur(i(al is >6,

0ny primary site, and ,o nonpulmonary visceral metastases, and ,ormal 012, any h5-, any 384

2!

8ntermediate-prognosis nonseminoma ($3-2>, of nonseminomas B 5-year P2* is 55,I 5-year sur(i(al is >0, to >3,

Testis+retroperitoneal primary, and ,o nonpulmonary visceral metastases, and 6ntermediate serum tumor markers. any of/
o o o

012 1,!!! to 1!,!!! ng+m3, or h5- 5,!!! 67+3 to 5!,!!! 67+3, or 384 1.5 to 1! times normal

8ntermediate-prognosis seminoma ($0, of seminomas B 5-year P2* is 65,I 5-year sur(i(al is 52,

0ny primary site, and ,onpulmonary visceral metastases, and ,ormal 012, any h5-, any 384

Poor-prognosis nonseminoma ($6,+26, of nonseminomas B 5-year P2* is #$,I 5year sur(i(al is 5$,

9ediastinal primary, or ,onpulmonary visceral metastases, or 2oor serum tumor markers. any of/
o o o

012 more than 1!,!!! ng+m3, or h5- more than 5!,!!! 67+m3 %1!,!!! ng+m3', or 384 more than 1! times the upper limit of normal

Poor-prognosis seminomaB Ao seminoma patients are classified as poor prognosis.

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Daftar Pustaka $. *achde(a K' 3arris 4?. !esticular cancer. ;edscape refference. 20$2. 2. -runicardi 20' %ndersen /K' -iliar !<' /unn /:' 3unter 41' Pollock <?. !estis and epiddimis. %natomy. 8nB *chwart9Ls. Principles of surgery. 2005I>. 3. %costa 4' %dams 0%' %larcon :3' %naya /%' %shley *7' %uerbach P*' et all. )rologic malignancy. 8nB !ownsend. *abiston. !e&tbook of surgery. 200>I$>. #. %lbers P' %lbrecht 7' %lgaba 2' -okemeyer 0' 0ohn-0edermark 1' 2i9a9i K' et all. 1uidelines on testicular cancer. ?uropean %ssociation of )rology. 20$2. p $-32. 5. :in K' *harangpani <. *creening for testicular cancerB an e(idence re(iew for the )* pre(enti(e ser(ices task force. %nn intern med. 20$0I$53B3"6-". 6. *heikine E' 1enega ?' ;elamed 4' :ee P' <euter P?' Ee 3. ;olecular genetics of testicular germ cell tumors. %m 4 cancer res. 20$2I2B$53-$65. 5. %merican 0ancer *ociety. !esticular cancer. %0*. 20$3. >. %ndrology %ustralia. !esticular cancer. /iagnosis and management. 0linical summary guide. ;onash )ni(ersity. 20$0I6. ". )* Pre(enti(e !ask 2orces. *creening for !esticular 0ancerB ).*. Pre(enti(e *er(ices !ask 2orce <eaffirmation <ecommendation *tatement. %nn intern med. 20$$I$5#B#>3-6.

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