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"ABSTRAK Latar Belakang :Karsinoma kolorektal (KKR) merupakan penyebab kematian kedua di dunia dari seluruh jeniskanker. KKR dapat disebabkan oleh defek dari MMR DNA. Microsatellite instability (MSI)adalah penanda defek MMR DNA. KKR MSI-H memiliki gambaran karakteristik tertentu.Tumor-infiltrating-lymphocyte (TIL) merupakan faktor prognosis. Hilangnya ekspresi PMS2 danMSH6 dapat sebagai penanda MSI. Penelitian ini bertujuan untuk menilai terjadinya MSI padaKKR di sisi kiri dan sisi kanan kolon melalui Hilangnya ekspresi PMS2 dan MSH6, sertamengetahui hubungan antara TIL dengan MSI-H.Bahan dan Metode :Dilakukan pulasan IHK PMS2 dan MSH6, serta penghitungan TIL. Penilaian dilakukan denganmenghitung hilangnya ekspresi PMS2 dan MSH6 pada inti sel dan dikelompokkan ke dalamkelompok mutasi dan tidak mutasi .Penghitungan TIL juga dikelompokkan ke dalam TIL tinggidan rendah, berdasarkan nilai titik potong Hasil : Didapatkan 27,8% kasus menunjukkan hilangnya ekspresi PMS2 dan MSH6 dengan 14,4%kasus di distal kolon. TIL terbanyak di distal kolon 30% kasus. Tidak terdapat perbedaanbermakna antara mutasi PMS2 dan MSH6 dengan lokasi (p=0,829) dan TIL (p=0,187). Terdapatperbedaan bermakna antara usia dan lokasi (p=0,020) serta peningkatan ekspresi PMS2 denganMSH6 (p=0,06).Kesimpulan :MSI-H ditemukan pada 27,8% kasus. Penggunaan PMS2 dan MSH6 pada penelitian ini belumdapat menggantikan 4 panel IHK. Terdapat kecenderungan dimana adenokarsinoma NOSmemiliki frekuensi mutasi lebih tinggi dari adenokarsinoma musinosum.ABSTRACT Background : Colorectal carcinoma (CRC) is the world second leading cause of death from all types of cancer.CRC can be caused by a defect of MMR DNA. Microsatellite instability (MSI) is a marker ofDNA MMR defect. CRC MSI-H has a certain characteristic figures. Tumor-infiltratinglymphocytes (TIL) isone of prognostic factor. Loss expression of the PMS2 and MSH6 can beuse as a marker of MSI. This study aims to assess the occurrence of MSI in CRC on the left sideand the right side of the colon through the loss of expression of PMS2 and MSH6, anddetermine the relationship between TIL with MSI-H. Materials and Methods :Immunohistochemical staining using two marker, there is PMS2 and MSH6. We also countingthe number of TIL. Assessment by calculating the loss expression of PMS2 and MSH6 in the cellnuclei and divided into two groups, the mutations and non mutations . TIL result also groupedinto high and low, based on the cutoff point. Result :There are 27.8% of cases showed loss of expression of PMS 2 and MSH6 with 14.4% of cases inthe distal colon. About 30% TIL cases located in distal colon. There were no significantdifferences between PMS2 and MSH6 mutation with the location (p = 0.829) and TIL (p =0.187). There are significant differences between age and location (p = 0.020) and increasedexpression of PMS2 with MSH6 (p = 0.06). \ Conclusion :MSI-H was found in 27.8% of cases. The use of PMS2 and MSH6 in this study have not beenable to replace 4 panels of IHC. There is a tendency where the adenocarcinoma NOS have ahigher mutation frequency than mucinous adenocarcinoma. ;Background :Colorectal carcinoma (CRC) is the world second leading cause of death from all types of cancer.CRC can be caused by a defect of MMR DNA. Microsatellite instability (MSI) is a marker ofDNA MMR defect. CRC MSI-H has a certain characteristic figures. Tumor-infiltratinglymphocytes (TIL) isone of prognostic factor. Loss expression of the PMS2 and MSH6 can beuse as a marker of MSI. This study aims to assess the occurrence of MSI in CRC on the left sideand the right side of the colon through the loss of expression of PMS2 and MSH6, anddetermine the relationship between TIL with MSI-H. Materials and Methods :Immunohistochemical staining using two marker, there is PMS2 and MSH6. We also countingthe number of TIL. Assessment by calculating the loss expression of PMS2 and MSH6 in the cellnuclei and divided into two groups, the mutations and non mutations . TIL result also groupedinto high and low, based on the cutoff point. Result :There are 27.8% of cases showed loss of expression of PMS 2 and MSH6 with 14.4% of cases inthe distal colon. About 30% TIL cases located in distal colon. There were no significantdifferences between PMS2 and MSH6 mutation with the location (p = 0.829) and TIL (p =0.187). There are significant differences between age and location (p = 0.020) and increasedexpression of PMS2 with MSH6 (p = 0.06). \ Conclusion :MSI-H was found in 27.8% of cases. The use of PMS2 and MSH6 in this study have not beenable to replace 4 panels of IHC. There is a tendency where the adenocarcinoma NOS have ahigher mutation frequency than mucinous adenocarcinoma. ;Background :Colorectal carcinoma (CRC) is the world second leading cause of death from all types of cancer.CRC can be caused by a defect of MMR DNA. Microsatellite instability (MSI) is a marker ofDNA MMR defect. CRC MSI-H has a certain characteristic figures. Tumor-infiltratinglymphocytes (TIL) isone of prognostic factor. Loss expression of the PMS2 and MSH6 can beuse as a marker of MSI. This study aims to assess the occurrence of MSI in CRC on the left sideand the right side of the colon through the loss of expression of PMS2 and MSH6, anddetermine the relationship between TIL with MSI-H. Materials and Methods :Immunohistochemical staining using two marker, there is PMS2 and MSH6. We also countingthe number of TIL. Assessment by calculating the loss expression of PMS2 and MSH6 in the cellnuclei and divided into two groups, the mutations and non mutations . TIL result also groupedinto high and low, based on the cutoff point. Result :There are 27.8% of cases showed loss of expression of PMS 2 and MSH6 with 14.4% of cases inthe distal colon. About 30% TIL cases located in distal colon. There were no significantdifferences between PMS2 and MSH6 mutation with the location (p = 0.829) and TIL (p =0.187). There are significant differences between age and location (p = 0.020) and increasedexpression of PMS2 with MSH6 (p = 0.06). \ Conclusion :MSI-H was found in 27.8% of cases. The use of PMS2 and MSH6 in this study have not beenable to replace 4 panels of IHC. There is a tendency where the adenocarcinoma NOS have ahigher mutation frequency than mucinous adenocarcinoma. "

"ABSTRAKLatar Belakang :Karsinoma kolorektal (KKR) merupakan salah satu kanker tersering di duniadan menjadi beban kesehatan global. KKR dapat muncul melalui 4 jalur patogenenis yangberbeda, salah satu di antaranya adalah serrated pathway. Pengaktifan jalur ini mengakibatkanperubahan progresif lesi-lesi prekursor seperti polip serrated, termasuk di dalamnya sessileserrated adenoma (SSA) dan tradisional serrated adenoma (TSA), menjadi karsinoma,diantaranya adenokarsinoma serrated (AS). AS diduga memberikan prognosis yang burukterhadap pengobatan. Gambaran histomorfologi adenokarsinoma serrated lebih banyakdidasarkan pada kemiripan dengan lesi prekursor SSA atau TSA, sehingga sulit dikenali.Penelitian ini bertujuan mengetahui persentasi AS diantara kasus KKR di Departemen PatologiAnatomik FKUI/RSCM, dan mengetahui gambaran histomorfologi yang bermakna dalammenandakan AS.Bahan dan Metode :Dilakukan review slide dari kasus-kasus KKR yang tercatat di arsipDepartemen Patologi Anatomik FKUI/RSCM. Penilaian histomorfologi dilakukan berdasarkankriteria yang diajukan oleh Tuppurainen et al, meliputi epithelial serration, sitoplasmaeosinofilik, inti vesikuler, anak inti nyata, nekrosis, produksi musin, dan adanya cell balls. Kasusdikategotikan ke dalam ?Pasti? dan ?Samar? AS, serta ?Klasik?. Dilakukan juga penilaian faktorprognostik, berupa invasi limfovaskular, invasi perineural, infiltrasi limfosit, dan tumor budding.Hasil :Didapatkan 41 kasus (35%) tergolong kategori ?Pasti? AS, 11 kasus (9.4%) tergolong?Samar? AS, dan sisanya sebanyak 65 kasus (55.6%) tergolong kategori adenokarsinoma?Klasik?. Didapatkan pula bahwa kriteria histomorfologi yang dapat dijadikan penanda serratedadalah epithelial serration (p=0.029), anak inti nyata (p=0.041), dan nekrosis <10% (p=0.014).Selain itu, didapatkan pula bahwa faktor-faktor yang berhubungan dengan morfologi serratedadalah yaitu lokasi tumor (p=0.010), infiltrasi limfosit (p=0.000), dan tumor budding (p=0.012).Kesimpulan :Adenokarsinoma serrated ditemukan 35% dari kasus-kasus adenokarsinoma kolondi Departemen Patologi Anatomik FKUI/RSCM. Gambaran histomorfologi yang menandakanadenokarsinoma serrated adalah adanya epithelial serration, anak inti nyata, dan nekrosis yangsedikit.Kata Kunci :Adenokarsinoma serrated, serrated pathway, histomorfologi, karsinomakolorektal.

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ABSTRACTBackground: Colorectal carcinoma (CRC) is one of the most common cancers in the world andbecome a global health burden nowadays. CRC may arise through 4 different pathways, one ofwhich is serrated pathway. Activation of this pathway results in progressive changes of precursorlesions such as sessile serrated adenomas (SSA) and traditional serrated adenomas (TSA), intocarcinoma. One type of carcinomais serrated adenocarcinoma (SA), in which known to give apoor prognosis to patient. Histomorphology overview shows that SA has similarity with SSA orTSA, making it difficult to recognize. This study aims to determine the percentage of the SAamong cases of CRC in Department of Anatomical Pathology Faculty of Medicine UniversitasIndonesia/Cipto Mangunkusumo Hospital, and to know histomorphological features that aremeaningful in indicating SA.Materials and Methods: CRC cases were collected from archive, and review slide wasconducted using morphological criteria proposed by Tuppurainen et al. This criteria includesepithelial serration, eosinophilic cytoplasm, vesicular nuclei, prominent nucleolei, necrosis,mucin production, and cell balls. Case were categorized into the "Definite" and "Pausy" SA, aswell as the "Classic". Assessment of prognostic factors, such as limfovascular invasion,perineural invasion, infiltration of lymphocytes and tumor budding, were also conducted.Results: There were 41 cases (35%) belong to the category of "Definite" SA, 11 cases (9.4%)classified as "Pausy? SA, and 65 cases (55.6%) belong to the category of "Classic"adenocarcinoma. Histomorphological analysis found that criteria showing significancy to SAwere epithelial serration (p = 0.029), prominent nucleolei (p = 0.041), and necrosis <10% (p =0.014). Several factors showed relation to serrated morphology were location of the tumor (p =0.010), infiltration of lymphocytes (p = 0.000), and tumor budding (p = 0.012).Conclusion: Serrated adenocarcinoma were found approximately 35% among cases of colorectaladenocarcinoma in the Department of Anatomical Pathology, Faculty of Medicine/CiptoMangunkusumo Hospital. Histomorpoholigical features that indicates SA includesepithelial serration, prominent nucleolei, and scanty necrosis.Keywords: Serrated adenocarcinoma, serrated pathway, histomorphological features, colorectalcarcinoma"

"Latar Belakang: Pemeriksaan histopatologi pada apendisitis akut dianggap sebagaipemeriksaan baku emas, walaupun tidak selalu dapat membuktikan adanyaperadangan akut. Hal tersebut menimbulkan dugaan adanya patogenesis lain yangbelum diketahui. Beberapa penelitian menemukan adanya korelasi antara sel mastdengan saraf enterik pada apendisitis akut. Tujuan penelitian ini adalah melihatkepadatan sel mast dan jaringan saraf, serta korelasi derajat kepadatan sel mastdengan derajat kepadatan jaringan saraf pada dinding apendisitis akut. Bahan dancara kerja: Penelitian observasional analitik potong lintang dilakukan pada 97sediaan histopatologi apendisitis akut yang dikelompokkan menjadi apendisitis akutfokal, supuratif, gangrenosa dan perforatif. Penilaian sel mast menggunakan pulasanToluidine blue dan penilaian jaringan saraf menggunakan pulasan IHK S100.Kemudian dilakukan penilaian korelasi derajat kepadatan sel mast dengan derajatkepadatan saraf enterik yang masing-masing dikelompokkan menjadi 4 derajat, padalapisan submukosa dan muskularis, menggunakan uji Sommers'd. Hasil: Kepadatansel mast/lpb lebih tinggi pada apendisitis akut fokal (3,9±1,3) dibandingkanapendisitis akut supuratif-gangrenosa. Sedangkan kepadatan jaringan saraf enterik/lpblebih tinggi pada apendisitis akut supuratif-gangrenosa (3,7±0,9). Terdapat korelasikuat antara derajat kepadatan sel mast dengan derajat kepadatan jaringan saraf enterikpada lapisan muskularis apendisitis akut (p<0,05; r=0,733). Sedangkan pada lapisansubmukosa terdapat korelasi lemah antara kedua variabel tersebut (p>0,05; r=0,118).Tidak terdapat perbedaan kepadatan sel mast dan kepadatan jaringan saraf yangbermakna pada kelompok apendisitis akut (p>0,05). Kesimpulan: Kepadatan selmast tertinggi terdapat pada apendisitis akut fokal, sedangkan kepadatan jaringansaraf tertinggi pada apendisitis akut supuratif-gangrenosa. Terdapat korelasi kuatantara derajat kepadatan sel mast dengan derajat kepadatan jaringan saraf enterikpada lapisan muskularis, sedangkan korelasi lemah terdapat pada lapisan submukosa apendisitis akut.

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Background: Histopathologic examination is the gold standard for diagnosis of acute

appendicitis, although no obvious histopathological signs of acute inflamation shown.

Therefore other unknown pathogenesis is suspected. Several studies prove there is

correlation between mast cells and enteric nerve system on acute appendicitis. The

aims of this study are to see the density of mast cell and enteric nerve and to evaluate

correlation between grade of mast cell density and enteric nerve density on

histopathologically acute appendicitis. Material and methods: A cross-sectional

retrospective study was conducted on 97 histopathologically acute appendicitis which

grouped as acute focal, acute suppurative, gangrenous (phlegmonous) and

perforative. All sections were subjected to toluidine blue stain for mast cell and S100

stain for enteric nerve. The density of mast cell and enteric nerve were designed into

4 grades. A correlation test between grade of mast cell density and grade of enteric

nerve density were studied in submucosa and muscularis using Somers?d correlation

test. Results: The highest densities of mast cell/hpf (3,9±1,3) and enteric nerve/hpf

(3,7±0,9) were found in acute focal appendicitis and suppurative-gangrenous

appendicitis respectively. There was strong correlation between grade of mast cell

density and enteric nerve density in muscularis (p<0,05; r=0,733), whereas the

submucosal layer had the weak one (p>0,05; r=0,118). There was no significant

difference for mast cell and enteric nerve density on each group (p>0,05).

Conclusion: The highest densities of mast cell and enteric nerve were found in acute

focal appendicitis and suppurative-gangrenous appendicitis respectively. There was

strong correlation between grade of mast cell density and grade of enteric nerve

density in muscularis layer of acute appendicitis, meanwhile the weak correlation was

on submucosa."

"Latar Belakang: Karsinoma gaster merupakan tumor ganas yang paling sering di daerah gastrointestinal atas. Menurut data epidemiologi adenokarsinoma gaster menunjukkan perkembangan kanker tipe intestinal dan kanker tipe difus melalui jalur kausa yang berbeda dan juga akhir-akhir ini pengobatan terapi target untuk adenokarsinoma telah diketahui dan dikembangkan. Penelitian ini bertujuan untuk mengetahui hubungan antara ekspresi HER2 dengan tipe histopatologik menurut klasifikasi Lauren dan derajat diferensiasi pada adenokarsinoma gaster.Bahan dan cara kerja: Penelitian dilakukan di Departemen Patologi Anatomik FKUI RSCM Jakarta, dengan melakukan analisis ekspresi HER2 untuk melihat hubungannya dengan tipe histopatologik dan derajat diferensiasi adenokarsinoma gaster yang diperoleh secara reseksi dan biopsi sejak tahun 2007-2011. Penilaian tipe histopatologik dengan menggunakan pulasan Hematoxillin Eosin dan penilaian ekspresi HER2 dengan menggunakan pulasan imunohistokimia HER2.Hasil: Dari tahun 2007-2011 diperoleh 55 kasus (76,4% laki-laki dan 23,6% wanita). Rata-rata umur penderita 50,55 tahun (rentang umur 29-73 tahun). Ekspresi HER2 3+, 2+, dan 1+ didapatkan pada 14,5%, 34,5%, dan 25,5% sampel. Sebanyak 25,5% sampel tidak menunjukkan ekspresi HER2. Ekspresi berlebih HER2 (3+) didapatkan pada 8 kasus (14,5%) adenokarsinoma gaster, yang seluruhnya adalah tipe intestinal .Kesimpulan: Terdapat hubungan yang bermakna antara ekspresi HER2 dengan tipe histopatologik (p= 0,021). Tidak terdapat hubungan yang bermakna antara ekspresi HER2 dengan derajat diferensiasi tumor (p=0,253).

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Background: Gastric carcinoma is the most common malignant tumor in upper gastrointestinal. According to epidemiologic data, gastric adenocarcinoma intestinal type and diffuse type showed different carcinogenesis. Recently, targeting therapy for adenocarcinoma has established. The aim of the study to know the relationship between HER2 expression and histopathologic type according to Lauren's classification and grading of gastric adenocarcinoma.Patient and method: This study has done in Anatomical Pathology department of medicine University Indonesia/ Cipto Mangunkusumo National Hospital, Jakarta. HER2 expression is analyzed to see the relationship with histopathologic type and differentiation of gastric adenocarcinoma. The specimens were from resection and biopsy (2007-2011). Histopathologic type evaluated with Hematoxylin Meyer's staining. HER2 expression evaluated with immunostaining with HER2 antibody.Results: We found 55 cases from 2007 until 2011 (76,4% men and 23,6% women). The mean age is 50,55 years (the range of age 29-73 years). HER2 expression 3+,2+ and 1+ are 14,5%, 34,5%, and 25,5% sampling. 25% sample did not show HER2 expression. We found overexpression HER2 (3+) in 8 cases (14,5%) of adenocarcinoma gastric intestinal type.Conclusion: There is a significant relation between HER2 expression with histopathologic type (p=0,021). There is no significant relation between HER2 with grading (p=0,253)."

"Latar Belakang : Ameloblastoma merupakan tumor odontogenik yang dijumpai pada tulang rahang. Tumbuh lambat dan berpotensi agresif terlihat dari mekanisme ekspansi kedalam tulang rahang. Receptor activator of nuclear factor-ĸB ligand (RANKL) dan Osteoprotogerin (OPG) merupakan protein yang mengatur osteoklastogenesis dimana kedua agen diklasifikasikan kedalam superfamili TNF. Tujuan : Menganalisis sifat invasif local ameloblastoma melalui ekspresi RANKL dan OPG pada berbagai tipe ameloblastoma. Metode Penelitian : 40 sampel ameloblastoma terdiri dari 9 sampel ameloblastoma tipe pleksiform, 15 sampel tipe folikular, dan 16 sampel tipe campuran. Sampel dipulas secara imunohistokimia dengan antibody RANKL dan OPG poliklonal kelinci. Hasil: Perbandingan RANKL dengan OPG pada ameloblastoma tipe pleksiform dan campuran memiliki nilai RANKL lebih besar OPG yang cukup besar, dibandingkan tipe folikular, sehingga kedua tipe tersebut dapat di katagorikan lebih dekstruktif dibandingkan tipe folikular. Perbandingan RANKL lebih kecil OPG pada tipe folikular sebesar 66,67 %. Hal ini mengambarkan pada tipe folikular lambat dalam perkembangannya, sedangkan perbandingan antara RANKL sama dengan OPG skor terbesar pada tipe campuran yakni sebesar 37,5 % hal ini berarti pada tipe campuran meskipun memilik kecendrungan dekstruktif namun dapat bersifat hemostasis. Kesimpulan : Terdapat perbedaan ekspresi RANKL dan OPG pada ke tiga tipe ameloblastoma dimana pada tipe pleksiform memiliki rasio RANKL dan OPG yang lebih tinggi dibandingkan kedua tipe yang lainnya. Ketidak seimbangan tersebut dapat menyebabkan kerusakan tulang dapat berlangsung lebih cepat.

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Background: Ameloblastoma is an odontogenic tumor is slow growing and aggressive of expansion into the jaw bone. Receptor activator of nuclear factor-ĸB ligand (RANKL) and Osteoprotogerin (OPG) protein that regulates osteoclastogenesis, both agents are TNF superfamily. Although benign, the ameloblastoma is destrutive tumor, locally invasive and presents a high rate of recurrence despite adequate surgical removal.

Objective: To analyze the nature of local invasive ameloblastoma through the expression of RANKL and OPG

Methods : 40 samples plexiform type ameloblastoma (n = 9), follicular type (n = 15), and mixed type (n = 16) by immunohistochemistry.

Results : Comparison of RANKL and OPG in ameloblastoma plexiform type, follicular type, and mixed type values had greater expression of ​​RANKL than OPG substantial plexiform type and mixed type, 66.67% of cases showed a greater expressin of OPG than RANKL type of follicular. RANKL same OPG biggest score of 37.5% on a mixed type.

Conclusion : There are differences in the expression of RANKL than OPG in plexiform type and mixed type has a higher ratio than the follicular type. Imbalances can cause locally invasive will go faster to resorption in jaw."

"Ameloblastoma merupakan tumor jinak yang berkembang lambat, bersifat invasif secara lokal dan sering terjadi rekurensi. Ameloblastoma tipe multikistik/padat merupakan tipe yang paling sering ditemukan. Cell adhesion molecules (CAMs) mempunyai peranan penting dalam proses morfogenesis jaringan pada saat perkembangan dan mempertahankan diferensiasi jaringan pada organisme dewasa. Faktor adhesi seluler dan motility merupakan mekanisme yang bertanggung jawab terhadap inisiasi dan perkembangan tumor. E-cadherin adalah molekul adhesi antar sel paling berpengaruh dalam adherens junction yang menjaga sel epitel melekat satu sama lain. Hilangnya fungsi protein E-cadherin sebagai tumor suppresor berhubungan dengan meningkatnya sifat invasif dan metastasis tumor. Tujuan penelitian ini adalah untuk menganalisis ekspresi Ecadherin pada ameloblastoma multikistik/padat pola folikuler, pola pleksiformis, dan pola campuran. Metode penelitian : 52 kasus ameloblastoma multikistik/padat dilakukan pemeriksaan ekspresi E-cadherin secara imunohistokimia. Hasil penelitian dievaluasi secara semikuantitatif, dengan melihat persentase sel tumor yang terpulas dan intensitas pulasan. Hasil : sampel penelitian berjumlah 52 (18 pola folikuler, 14 pola pleksiformis, dan 20 pola campuran). Secara imunohistokimia E-cadherin terekspresi pada lebih dari 50% sel tumor. Analisis secara statistik menunjukkan tidak terdapat perbedaan yang bermakna antara ketiga pola ameloblastoma multikistik/padat (p>0,05). Kesimpulan : pada hasil penelitian tampak bahwa ekspresi E-cadherin antara ketiga pola ameloblastoma multikistik/padat tidak menunjukkan perbedaan bermakna.

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Ameloblastoma is a benign tumor that slow-growth, locally invasive and high rate of recurrence. Ameloblastoma multicystic/solid is the most commonly found. Cell adhesion molecules (CAMs) have an important role, in the process of tissue morphogenesis during development and maintaining tissue differentiation in the adult organism. Cellular adhesion and motility factor is the mechanism responsible for tumor initiation and progression. E-cadherin is the most important cell adhesion molecules in the adherens junctions that maintain epithelial cells attached to one another. Loss of function of E-cadherin as tumor suppresor protein associated with increased invasive and metastatic behavior of tumor.

The purpose of this study was to analyze the expression of E-cadherin of multicystic/solid ameloblastoma in the follicular pattern, plexiform pattern, and mixed pattern.

Method : E-cadherin expression of 52 cases of multicystic/solid ameloblastoma investigated by immunohistochemical. The results were evaluated semiquantitatively, by investigating the percentage immunopositive of tumor cells and intensity of staining.

Results: 52 sample (18 follicular pattern, 14 plexiform pattern and 20 mixed pattern). E-cadherin expressed on more than 50% of tumor cells. Statistical analysis showed no significant difference among the three patterns ameloblastoma multicystic (p>0,05).

Conclusion: The expression of Ecadherin among the three patterns ameloblastoma multicystic/solid showed no significant difference."

"Latar Belakang: Ekspresi TIMP-2 (Tissue Inhibitor of Metalloproteinase-2) secara imunohistokimia digunakan untuk menentukan sifat invasif lokal ameloblastoma yang berkaitan dengan kemampuan rekurensi. Tujuan: Mengevaluasi ekspresi TIMP-2 secara imunohistokimia pada ameloblastoma pleksiform dan folikuler. Metode: Dilakukan pemeriksaan imunohistokimia pada sampel ameloblastoma pleksiform (n=16) dan folikuler (n=14) dengan antibodi monoklonal TIMP-2. Ekspresi imunohistokimia TIMP-2 dinilai dengan software Image J. Hasil: Tidak terdapat perbedaan bermakna ekspresi TIMP-2 pada ameloblastoma pleksiform dan folikuler pada uji Chi-Square dengan nilai signifikan p=0.072 (p>0.05). Pembahasan: Ekspresi TIMP-2 yang lemah berkaitan dengan meningkatnya kemampuan invasif lokal ameloblastoma. Kesimpulan: Ameloblastoma pleksiform dan folikuler sama-sama memiliki kemampuan invasif lokal yang sama.

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Background: Expression of TIMP-2 (Tissue Inhibitor of Metalloproteinase-2) immunohistochemically was used to evaluate local invasive characteristic of ameloblastomas which contributed to recurrence.

Objective: To evaluate expression of TIMP-2 in plexiform and follicular ameloblastoma.

Method: Plexiform (n=16) and follicular (n=14) ameloblastoma?s samples were immunohistochemically examined with monoclonal antibody TIMP-2. Expression of TIMP-2 was evaluated with Image J software.

Result: No significant difference of immunohistochemical expression of TIMP-2 between plexiform and follicular ameloblastoma p=0.072 (p>0.05), that was analyzed with Chi-Square test.

Discussion: Low grade TIMP-2 expression was contributed to local invasive capacity of ameloblastomas.

Conclusion: Plexiform and follicular ameloblastoma have similarity in capacity of local invasiveness."

"[ABSTRAKLatar Belakang: Kanker kolorektal merupakan tumor ganas ketiga di dunia.Sembilan puluh lima persen kanker kolorektal merupakan adenokarsinoma yangberasal dari lesi prekursor adenoma. Dilaporkan 15%-20% kanker terkait denganinfeksi virus. Virus yang diduga berhubungan dengan kanker kolorektal adalahhuman papilloma virus (HPV) dan tipe tersering adalah 16 dan 18. Hubunganantara HPV dan kanker kolorektal masih menjadi perdebatan. Penelitian inibertujuan untuk mengetahui perbedaan prevalensi infeksi HPV pada adenoma danadenokarsinoma kolorektal di Departemen Patologi Anatomik FKUI/RSCMJakarta dengan menggunakan teknik polymerase chain reaction (PCR). Bahandan Metode: Pemeriksaaan DNA HPV pada 33 kasus adenoma dan 33 kasusadenokarsinoma kolorektal dengan teknik nested PCR MY/GP dan elektroforesis.Pada kasus dengan hasil HPV positif, dilanjutkan PCR menggunakan primerspesifik HPV 16 dan HPV 18. Subjek penelitian berasal dari Departemen PatologiAnatomik FKUI/RSCM. Hasil: Satu dari 33 kasus (3,0%) adenoma dan 3 dari 33kasus (9,1%) adenokarsinoma positif infeksi HPV. Satu kasus adenoma positifHPV bukan merupakan tipe 16 dan 18. Satu kasus adenokarsinoma denganpositif, HPV merupakan tipe 16, 2 kasus merupakan gabungan tipe 16 dan 18.Kesimpulan: Prevalensi infeksi HPV pada adenokarsinoma lebih tinggidibandingkan adenoma kolorektal. Tipe HPV pada kasus adenokarsinomakolorektal merupakan tipe 16 dan 18.

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ABSTRACTBackground : Colorectal cancer is the third malignant tumor in the world.Ninety-five percent of colorectal cancers are adenocarcinomas derived fromprecursor lesions adenoma. There are 15% -20% of cancers associated with viralinfections. Virus are suspected associated with colorectal cancer is the humanpapilloma virus (HPV) and the most common types are 16 and 18. Therelationship between HPV and colorectal cancer is still being debated. This studypurpose to determine the prevalence differences of HPV infection in colorectaladenomas and adenocarcinomas in the Department of Anatomic Pathology,FKUI/RSCM Jakarta by using the polymerase chain reaction (PCR). Materialsand Methods : HPV DNA examination on 33 cases of adenoma and 33 cases ofcolorectal adenocarcinoma by nested MY/GP PCR technique and electrophoresis.In the cases with positive HPV results, continue by specific primers HPV 16 andHPV 18 PCR. The subject of the study came from the Department of AnatomicPathology, FKUI/RSCM. Result : One (3.0%) adenomas and 3 (9.1%)adenocarcinoma from 33 cases adenoma and adenocarcinoma are HPV positive.One case of HPV positive adenomas are not types 16 and 18. HPV positiveadenocarcinoma, 1 case was type 16, two cases are combination of types 16 and18. Conclusion : The HPV prevalence in adenocarcinoma was higher thancolorectal adenoma. HPV types on positive colorectal adenocarcinoma cases aretypes 16 and 18., Background : Colorectal cancer is the third malignant tumor in the world.Ninety-five percent of colorectal cancers are adenocarcinomas derived fromprecursor lesions adenoma. There are 15% -20% of cancers associated with viralinfections. Virus are suspected associated with colorectal cancer is the humanpapilloma virus (HPV) and the most common types are 16 and 18. Therelationship between HPV and colorectal cancer is still being debated. This studypurpose to determine the prevalence differences of HPV infection in colorectaladenomas and adenocarcinomas in the Department of Anatomic Pathology,FKUI/RSCM Jakarta by using the polymerase chain reaction (PCR). Materialsand Methods : HPV DNA examination on 33 cases of adenoma and 33 cases ofcolorectal adenocarcinoma by nested MY/GP PCR technique and electrophoresis.In the cases with positive HPV results, continue by specific primers HPV 16 andHPV 18 PCR. The subject of the study came from the Department of AnatomicPathology, FKUI/RSCM. Result : One (3.0%) adenomas and 3 (9.1%)adenocarcinoma from 33 cases adenoma and adenocarcinoma are HPV positive.One case of HPV positive adenomas are not types 16 and 18. HPV positiveadenocarcinoma, 1 case was type 16, two cases are combination of types 16 and18. Conclusion : The HPV prevalence in adenocarcinoma was higher thancolorectal adenoma. HPV types on positive colorectal adenocarcinoma cases aretypes 16 and 18.]"