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"Latar Belakang: Metilasi di area promoter berpotensi mengakibatkan gene silencing pada gen CDH1 yang berperan penting dalam adhesi antarsel dan morfogenesis kraniofasial.Tujuan: Mengetahui distribusi metilasi antara individu cleft dan non-cleft. Metode: 24 sampel DNA penderita orofacial cleft dan 24 sampel kontrol dianalisis menggunakan teknik methylation-specific PCR (MSP).Hasil: Dari kelompok cleft didapatkan 5 sampel (20,83%) berstatus fully methylated dan 19 sampel (79,17%) berstatus partially methylated, sedangkan dari kelompok kontrol didapatkan 24 sampel (100%) berstatus partially methylated.Kesimpulan: Terjadi metilasi CDH1 pada penderita orofacial cleft, namun secara statistik tidak terdapat perbedaan bermakna pada distribusi status metilasi CDH1 antara individu cleft dan non-cleft (p=0,05).

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Background: Methylation at promoter area potentially results in silencing of CDH1 gene which plays important role in cell adhesion and craniofacial morphogenesis.

Objective: To obtain the distribution of CDH1 methylation in cleft and non-cleft individuals.

Methods: 24 DNA samples of individuals with orofacial cleft and 24 control samples were analyzed with methylation-specific PCR (MSP) technique.

Results: From cleft group, 5 (20.83%) were fully methylated and 19 (79.17%) were partially methylated; while from control group, 24 (100%) were partially methylated.

Conclusion: CDH1 methylation was observed in orofacial cleft affected individuals but there is no significant difference in CDH1 methylation status between cleft and non-cleft individuals (p=0.05)."

"Latar Belakang: Karsinoma sel skuamosa (KSS) lidah merupakan kanker rongga mulut (KRM) yang paling banyak ditemukan. Diseksi leher dikerjakan bersamaan dengan eksisi luas tumor karena tingginya angka occult metastasis yaitu sebesar 30% pada kelenjar getah bening (KGB) leher yang secara yang klinis tidak teraba (N0). Berdasarkan penelitian sebelumnya penanda epitelial E-cadherin dan penanda sel punca kanker CD44 dapat digunakan sebagai alat diagnostik prabedah untuk mengidentifikasi pasien yang mengalami metastasis KGB sehingga dapat menjadi salah satu modalitas yang membantu ahli bedah dalam mengambil keputusan tipe diseksi leher yang akan dikerjakan agar memberikan manfaat terbaik bagi pasien. Tujuan: Penelitian ini bertujuan untuk mengetahui hubungan ekspresi E-cadherin dan CD44 dengan metastasis KGB leher pada KSS lidah. Metode: Penelitian ini merupakan penelitian analitik dengan desain studi potong lintang. Pengambilan sampel dilakukan dengan cara consecutive sampling sesuai kriteria inklusi dan eksklusi. Kriteria inklusi adalah pasien KSS lidah tanpa metastasis jauh, dilakukan operasi eksisi luas tumor dan diseksi KGB leher, dan blok parafin yang layak diperiksa. Data sosiodemografi dan klinikopatologis diambil dari rekam medis. Pewarnaan imunohistokimia dengan E-cadherin dan CD44 dilakukan pada jaringan KSS lidah yang sudah terdapat di blok parafin tersimpan kemudian tingkat ekspresi E-cadherin dan CD44 dikelompokkan menjadi tinggi dan rendah sesuai kepustakaan. Analisis statistik dilakukan dengan program SPSS 24.0. Hasil: Didapatkan 30 dengan 15 subjek KSS lidah dengan metastasis KGB dan 15 subjek tanpa metastasis KGB. Dari analisis data, didapatkan terdapat hubungan yang bermakna antara ekspresi E-cadherin dengan metastasis KGB (p=0.000) dan terdapat hubungan yang bermakna antara CD44 dengan metastasis KGB (p=0.003). Kesimpulan: Ekspresi E-cadherin yang rendah dan CD44 yang tinggi memiliki hubungan bermakna dengan metastasis KGB pada KSS lidah.

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Background: Squamous cell carcinoma (SCC) of the tongue is the most common oral cavity cancer. Neck dissection was done simultaneously with wide excision of the tumor because of occult metastases high rate (about 30%) in clinically non-palpable neck lymph nodes (N0). Based on previous research, the epithelial marker E-cadherin and cancer stem cell marker CD44 could be used as pre-surgical diagnostic tools to identify patients who have lymph node metastases so that it could be a modality that helps surgeons in making decisions about neck dissection type to be performed to provide the best benefit for patients. Objective: To evaluate the association between E-cadherin and CD44 expressions and neck lymph node metastasis in SCC of the tongue. Methods: This research was an analytical study with a cross-sectional design. Samples were taken through consecutive sampling according to inclusion and exclusion criteria. Inclusion criteria were patients with SCC of the tongue without distant metastases, post wide excision of the tumor with neck lymph node dissection, and eligible paraffin block for examination. Sociodemographic and clinicopathological data were obtained from medical records. Immunohistochemistry staining was performed with E-cadherin and CD44 from stored paraffin blocks, then the expression levels of E-cadherin and CD44 were grouped into high and low according to the literature. Statistical analysis was conducted with SPSS 24.0. Results: Thirty samples of SCC of tongue were collected, consist of 15 subject with neck lymph node metastasis tongue and 15 subject without neck lymph node metastasis. From data analysis, a significant difference was found between E-cadherin and CD44 expressions with neck lymph node metastasis (p value was 0.000 and 0.003, respectively). Conclusion: Low expression of E-cadherin and high expression of CD44 was significantly associated with the occurence of neck lymph node metastasis in SCC of the tongue."

"In this volume, a group of internationally recognized experts reviews AJ biology over a wide range of organization, from atoms to molecules, to protein complexes, molecular networks, cells, tissues, and overall animal development. AJs have also been an integral part of animal evolution, and play central roles in cancer development, pathogen infection and other diseases. This book addresses major questions encompassing AJ biology. How did AJs evolve? How do cadherins and catenins interact to assemble AJs and mediate adhesion? How do AJs interface with other cellular machinery to couple adhesion with the whole cell? How do AJs affect cell behaviour and multicellular development? How can abnormal AJ activity lead to disease?"