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Abstrak :
Protein sel merupakan makromolekul yang terdiri dari satu atau beberapa polipeptida yang tersusun dari rangkaian asam amino yang saling berikatan. Terdapat perbedaan profil protein antara sel normal dengan sel kanker. Tujuan : Melihat ekspresi protein pada KSSRM dan mukosa mulut normal. Metode : Sel galur HSC-3 dan HSC-4 dikultur hingga confluent. Sel skuamosa mukosa normal diambil dari jaringan gingiva pasien odontektomi. Semua sampel dilakukan prosedur ekstraksi protein, Bradford protein assay, dan SDS PAGE. Hasil : KSSRM mengekspresikan protein dengan level cukup tinggi pada berat molekul 31-78 kDa. Namun, pada mukosa normal, kebanyakan mengekspresikan protein pada berat molekul antara 39 - 172 kDa. Kesimpulan : Terdapat perbedaan ekspresi protein pada sel galur KSSRM dibandingkan dengan mukosa mulut normal.

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Cells Proteins are macro molecules consist of one or several polypeptides which formed from amine acid chain that bound one another. There is a different of protein profile between normal and cancer cells. Objective : To observe the protein expression in OSCC and normal oral mucous. Method : Cell lines HSC-3 and HSC-4 were cultured until confluent. Normal squamous mucosa was taken from gingival tissues patient who had odontectomy procedure. Protein extraction, Bradford protein assay, and SDS PAGE procedure were performed for all samples. Results : Oral squamous cells carcinoma expressed rather high level of protein which have molecular weight of 31-78 kDa compared to normal gingival which express protein molecular weight ranging between 39 - 172 kDa. Conclusion : There are different protein expression between oral squamous cells carcinoma and normal oral mucous.

Abstrak :
Latar Belakang: p73, homolog p53, diketahui memiliki kemampuan serupa dalam menekan pertumbuhan tumor. Protein p73 diekspresikan dalam berbagai level pada sel kanker dan jaringan normal yang berbeda. Belum diketahui bagaimana pola ekspresi protein p73 pada KSSRM dan pada jaringan mukosa mulut normal. Tujuan: Mengetahui profil protein p73 pada KSSRM tipe mutant p53 dan jaringan mukosa mulut normal berdasarkan berat molekul protein. Metode: Ekstrak protein dari HSC-3 dan HSC-4 serta jaringan mukosa normal dianalisa dengan teknik SDS PAGE untuk mendeteksi protein p73 berdasarkan berat molekulnya. Hasil:. pita protein p73 pada HSC-3 lebih tebal daripada HSC- 4. Terdapat variasi profil protein p73 pada mukosa mulut normal dengan pita protein tebal (8/17) dan sedang (5/17). Simpulan: Terdapat perbedaan profil protein p73 antara HSC-3 dan HSC-4 berkaitan dengan tingkat protein p53 dan SNP pada kodon 72. Kebanyakan sampel jaringan mukosa memperlihatkan ketebalan pita protein p73 yang cukup tinggi. ......Backround: p73, the homolog of p53, has a similar ability in tumor suppression. p73 protein expressed at a different level in various cancer cells and normal tissues. Profile of p73 protein in mutant p53 OSCC cell line and normal human oral mucosa have not been known. Objectives: To observe p73 protein profile in mutant p53 OSCC cell lines and normal human oral mucosa. Methods: The extracted protein of HSC-3 and HSC-4 cell lines and normal mucosal tissues were analyzed with SDS PAGE to detect p73 protein based on the molecular weight. Results:. The band of p73 protein in HSC-3 shows a higher density compared to its density of HSC-4. A thick p73 protein band was shown on 8/17 of normal mucosal tissues while medium level of p73 protein band was shown on 5/17. Conclusion: The protein profile between HSC-3 and HSC-4 were different related with p53 protein and SNP on codon 72 of each samples. Most of mucosal tissues shows a quite high density of p73 protein bands.

Abstrak :
Indonesian Journal of Dentistry 2006; Edisi Khusus KPPIKG XIV: 353-357 Oral squamous cell carcinoma represents more than 90% of all oral cancers. Ten percent of the cases are found on the buccal mucosa and the gingiva. The World Health Organization defines a premalignant or precancerous lesion as a morphologically altered tissue in which cancer is more likely occur and includes oral leukoplakia, oral erythroplakia, and possibly oral lichen planus (OLP). The purpose of this study was to discuss the possibility of malignant transformation of OLP. The potency of OLP as a premalignant lesion is still an ongoing controversial discussion in the literature. The report a case of oral squamous cell carcinoma located on the left buccal mucosa accompanied by oral lichenoid lesions on the right buccal mucosa, lower labial mucosa, and left buccal mucosa. These findings led to a possibility of malignant transformation of the oral lichenoid lesions. Unfortunately, biopsy on the lichenoid lesions was not performed. Therefore, a definitive diagnosis of OLP could be established and the possibility of the lesions being dysplastic remained unclear. This study concluded that biopsy is mandatory to establish a definitive diagnosis of OLP and to investigate the possibility of dysplasia. It is necessary to perform examination of genetic alterations in dysplastic OLP in order to assess loss of heterozygosity (LOH), which may help to consider the risk of malignant transformation.

Abstrak :
Profil hTERT dan P73 pada kultur sel kanker mulut dibandingkan mukosa normal: studi pendahuluan. Perubahan genetik pada p53 memungkinkan terjadinya imortalisasi sel dan meningkatkan predisposisi terjadinya transformasi ke arah neoplasma. Hal ini terkait dengan aktivitas telomerase yang menjaga panjang telomer, yang aktivitasnya seharusnya dibatasi oleh p53. p73, yang merupakan homolog p53, mempunyai kemampuan supresi tumor yang mirip dengan p53. Tingkat ekspresi P73 dan human TERT kemungkinan berbeda pada berbagai jenis sel kanker dibandingkan dengan jaringan normalnya. Saat ini belum terdapat data tentang profil protein human TERT dan P73 pada sel lini karsinoma sel skuamosa oral (KSSO) dibandingkan dengan jaringan mukosa oral normal. Tujuan: Studi ini bertujuan untuk mendapatkan profil human TERT dan P73 pada sel lini KSSO dengan mutasi p53 dibandingkan dengan mukosa oral normal. Metode: Sel lini HSC-3 dan HSC-4 dengan mutasi p53 dikultur sedangkan mukosa oral normal dikumpulkan dari pasien tanpa kanker yang menjalani perawatan bedah mulut. Ekstraksi protein dan analisis profil human TERT dan P73 dilakukan dengan SDS-PAGE dan ditentukan berdasarkan perkiraan berat protein. Hasil: Pita human TERT jelas terlihat pada sel HSC-3 dan HSC-4 namun tidak pada mukosa oral normal. Densitas pita P73 pada sel HSC-3 terlihat lebih tebal dibandingkan pada sel HSC-4. Hanya 50% sampel mukosa oral normal memperlihatkan pita P73. Simpulan: Terlihat profil human TERT dan P73 yang berbeda pada sel kanker dan sel normal. Perbedaan ini kemungkinan bersifat spesifik tergantung jenis sel dan dipengaruhi oleh status p53. Perlu dilakukan penelitian lanjutan untuk menganalisis kemungkinan peran p73 dalam menggantikan fungsi p53 pada kanker mulut selanjutnya diperlukan.

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Genetic alteration on p53 allows cellular immortalization and predisposes cells to neoplastic transformation. This immortalization is related to telomere length maintenance by telomerase. Human TERT is a key component of telomerase, which activity is suppressed by p53. The p73, the homolog of p53, has a similar ability in tumor suppression. The P73 is expressed at a different level in various cancer cells and normal tissues. Profile of human TERT and P73 in mutant p53 OSCC cell line and normal human oral mucosa have not been known. Objective: To observe human TERT and P73 profile in mutant p53 OSCC cell lines and normal human oral mucosa. Methods: The extracted protein of HSC-3 and HSC-4 cell lines and normal mucosal tissues were analyzed with SDS PAGE to detect human TERT and p73 expression based on the molecular weight. Results: The HSC-3 cell line showed thicker band density of P73 compared to its density of HSC-4. Only 50% of normal oral mucosa tissue showed thick P73 band density. The human TERT band was clearly shown in HSC-3 and HSC-4 cell lines but not in normal oral mucosa. Conclusion: Different profile of human TERT and P73 in OSCC cell lines and normal oral mucosa might be cell-type specific and influenced by the status of p53. Analysis of the role of p73 in these cancers might need further research to determine possible p73 substitution for p53 function.