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"Latar Belakang: Perubahan genetik pada p53 menyebabkan imortalisasi dan kecenderungan sel bertransformasi menjadi neoplasma. Imortalisasi ini berhubungan dengan pemeliharaan panjang telomer oleh telomerase. hTERT adalah komponen kunci telomerase yang aktivitasnya ditekan oleh p53.Tujuan: Menganalisis profil protein hTERT pada sel galur KSSRM HSC-3 dan HSC-4 serta jaringan mukosa mulut normal. Metode: Profil protein hTERT dianalisis menggunakan teknik SDS-PAGE dan Gel Doc, Quantity One.Hasil: Protein hTERT diekspresikan oleh sel galur KSSRM mulut tipe HSC 3 dan HSC 4 serta 2 dari 17 sampel protein jaringan mukosa mulut normal.Simpulan: Protein hTERT yang diekspresikan oleh sel galur KSSRM berhubungan dengan kondisi mutan p53. Adanya ekspresi protein hTERT pada jaringan mukosa mulut normal diperkirakan karena adanya sel keratinosit dan infiltrasi sel hematopoietik.

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Backround: Genetic alteration on p53 allows cellular immortalization and predisposes cells to neoplastic transformation. This immortalization is related to telomere length maintenance by telomerase. hTERT is a key component of telomerase, which activity is suppressed by p53.Objectives: To analyze the hTERT protein profile in HSC-3 and HSC-4 OSCC cell lines and normal human oral mucosa tissue. Methods: SDS-PAGE and Gel Doc, Quantity One were used for analyzing hTERT protein profile.Results: hTERT protein expressed in HSC-3 and HSC-4 OSCC cell lines and 2/17 protein samples of normal human oral mucosal tissues.Conclusion: hTERT protein that was expressed by OSCC cell lines is related to their status of mutant p53. The existing of hTERT protein on normal human oral mucosas tissue may be caused by keratinocyte cells and infiltrated hemapoietic cells."

"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 berdasarkanberat 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.

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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."

"Latar belakang: Karsinoma urotelial merupakan keganasan kandung kemih tersering pada laki-laki. Faktor risikonya adalah merokok, pajanan bahan kimia, radiasi, infeksi Schistosoma hematobium. Mutasi p53 merupakan mutasi tersering pada karsinoma urotelial kandung kemih yang menyebabkan akumulasi protein p53 di inti dan terlihat dengan imunohistokimia. Tujuan penelitian adalah untuk melihat perbedaan ekspresi p53 pada karsinoma urotelial kandung kemih derajat rendah dan derajat tinggi serta hubungan ekspresi p53 dengan^{: "}stadium tumor. Bahan dan cara: Penelitian menggunakan desain potong lintang. Sampel terdiri atas 47 kasus yang terbagi menjadi 22 kasus karsinoma urotelial derajat rendah dan 25 kasus karsinoma urotelial derajat tinggi di Departemen Patologi Anatomik Fakultas Kedokteran Universitas Indonesia/Rumah Sakit Cipto Mangunkusumo (FKUI/RSCM) tahun 2009-2017. Dilakukan pulasan imunohistokimia p53 dengan menggunakan cut off positif ≥ 20% berdasarkan penelitian Thakur et al, Ong et al, dan Saint et al. Hasil: Ekspresi p53 positif pada 33 sampel (70,21%), terbanyak pada karsinoma urotelial derajat tinggi 20 kasus (80%), sedangkan pada karsinoma urotelial derajat rendah terdapat 13 kasus (59,1%). Sebanyak 22 kasus (68,8%) Nonmuscle invasive bladder cancer dan 11 kasus (73,3%) Muscle invasive bladder cancer menunjukkan ekspresi positif. Ekspresi p53 cenderung lebih banyak ditemukan pada karsinoma urotelial derajat tinggi dan stadium tinggi. Kesimpulan: Tidak ada perbedaan ekspresi p53 pada karsinoma urotelial kandung kemih derajat rendah dan derajat tinggi. Tidak ada hubungan antara ekspresi p53 dengan stadium tumor.Kata kunci: Karsinoma urotelial, kandung kemih, p53, imunohistokimia.

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Background : Urothelial carcinoma is the most common malignancy in the bladder and mainly occurs in older men. Risk factors for bladder cancer include smoking, exposure to chemicals, radiation and schistosoma hematobium infection. P53 is a tumor suppressor gene that is involved in the cell cycle and plays a role in the occurrence of apoptosis in response to DNA damage. P53 gene mutation is one of the most common genetic changes in urothelial bladder carcinoma. The p53 gene mutation will cause accumulation of p53 protein in the nuclei which can be detected through immunohistochemical examination. The aim of this study is to see differences of p53 expression in low grade and high grade urothelial carcinoma and to see the association of p53 expression with tumor stage. Material and method : This study uses a cross sectional study design. The sample consisted of 47 cases of urothelial bladder carcinoma divided into 22 cases of low grade urotelial carcinoma and 25 cases of high grade urotelial carcinoma originating from the archives of the Anatomical Pathology Department Faculty Medicine of Universitas Indonesia/Cipto Mangunkusumo Hospital (FKUI/ RSCM) in 2009-2017. The study was carried out by p53 immunohistochemical examination and assessment of p53 expression using a percentage with a positive cut off value of ≥ 20%. Result : This study obtained positive p53 expression in 33 samples from 47 samples studied (70,21%). Most are found in high grade urothelial carcinoma as many as 20 cases (80%). Whereas in low grade urothelial carcinoma there are 13 cases (59,1%) with positive p53 expression. As many as 22 cases (68,8%) of Non muscle invasive bladder cancer (NMIBC) and 11 cases (73,3%) of Muscle invasive bladder cancer (MIBC) showed positive p53 expression. There was no difference between p53 expression in low grade and high grade bladder urothelial carcinoma (p=0,118). This study also showed no association between p53 expression with tumor stage (p=1,000). Conclusion : P53 expression was not significantly different with tumor grade. P53 expression was not significantly associated with the tumor stage."

"Cellular responses to stress including DNA damage show multiple options involving the mechanisms of growth arrest, DNA repair and programmed cell death or apoptosis. Failures in these mechanisms can result in oncogenesis or accelerated senescence. Much of the response is coordinated by p53, a nuclear phosphoprotein with a central role in the defences against physical, chemical and pathogenic agents which challenge the DNA integrity. The p53 pathways for mobilising the cellular defences are linked to the pRb/E2F pathways regulating the cell cycle progression. This paper aims to review the current understanding on the networks and main molecular machinery of these processes. In addition, the implications on cellular decision making for the defences as well as evolutionary aspects of these mechanisms are discussed in brief."

"Bacterial lipopolysaccharide (LPS) is impacted in the etiology of inflammatory periodontal disease. Aside from immunopathologic reactions which may be involved in the pathogenesis of the disease, the possibility exist that direct cytotoxic effect on cultured human gingival fibroblasts may be equally destructive. The expression of P53 protein can be one of markers to examine the state of impaired DNA. The purpose of this study was to investigate the effect of LPS toward expression of P53 protein on cultured human gingival fibroblasts. Cultured human gingival fibroblasts were exposed to LPS in concentrations of 50 and 200 ug/ml and untreated medium for a period of 24 and 48 hours. Cells were harvested and prepared for immunohistochemical evaluation. After exposure for 24 and 48 hours, the fraction of P53-positive cells was 81.7% in case of 50 ug/ml LPS, and 88.8% in case of 200 ug/ml LPS. After exposure for 48 hours, the fraction of P53-positive cells was 32.2% in case of 50 ug/ml LPS, and 21.1% in case of 200 ug/ml LPS. None of untreated group showed p53-positive cells. Up-regulation of p53 protein during the initial logarithmic phase of growth may be a consequence of on-going DNA damage."

"Beberapa studi epidemiologi maupun studi metaanalisis menunjukkan beberapa faktor pada DM tipe 2 memiliki hubungan dengan risiko terjadinya kanker. Mutan p53 yang terbukti berkontribusi terhadap perkembangan tumor sementara insulin yang diketahui berperan dalam mengendalikan kadar gula tubuh, dipilih menjadi biomarker yang akan diteliti pada penelitian ini. Penelitian ini bertujuan untuk mempelajari hubungan kadar mutan p53 dan insulin pada kelompok pasien DM tipe 2 + kanker (n=51) dan pasien DM tipe 2 (n=51). Penelitian ini merupakan penelitian cross-sectional dengan teknik pengambilan sampel consecutive sampling. Pada penelitian, diketahui tidak terdapat perbedaan yang bermakna (p=0,774) pada nilai mutan p53 antara kelompok pasien DM tipe 2 + kanker (1,65±0,10 ng/mL) dan kelompok pasien DM tipe 2 (1,62±0,09 ng/mL). Terdapat perbedaan bermakna (p<0,001) pada kadar insulin antara kelompok pasien DM tipe 2 + kanker (19,33±2,68 µIU/mL) dan kelompok pasien DM tipe 2 (37,31±2,68 µIU/mL). Tidak terdapat korelasi bermakna antara kadar mutan p53 dengan kadar insulin pada kelompok pasien DM tipe 2 + kanker (r=0,191; p= 0,179) dan pada kelompok pasien DM tipe 2 (r=-0,081; p= 0,574). Berdasarkan hasil penelitian, dapat disimpulkan bahwa tidak ada perbedaan bermakna pada kadar mutan p53 antara kelompok pasien DM tipe 2 + kanker dan kelompok pasien DM tipe 2, namun terdapat perbedaan pada kadar insulin pada kedua kelompok. Selain itu, tidak ada korelasi bermakna antara kadar mutan p53 dan insulin pada kedua kelompok.

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Epidemiological studies and meta-analysis have shown that several factors in type 2 DM are related to cancer incidents. Mutant p53 is scientifically proven to contribute in tumor development while insulin that known well to play an important role in controlling body glucose levels, therefore those two biomarkers were chosen to be investigated in this study. This research aimed to study the correlation of mutant p53 and insulin in type 2 DM + cancer (n=51) and type 2 DM patients (n=51). This research was a cross-sectional study with consecutive technique sampling. This study showed that there was no significant difference (p=0.774) of mutant p53 value between type 2 DM + cancer patients group (1.65±0.10 ng/mL) and type 2 DM patients group (1.62±0.09 ng/mL). However, it was significant difference (p<0.001) of insulin value in type 2 DM + cancer patients group (19.33±2.68 µIU/mL) and type 2 DM patients group (37.31±2.68 µIU/mL). There was also no significant correlation between mutan p53 and insulin value in type 2 DM + cancer patients group (r=0.191; p=0.179) and type 2 DM patients group (r=-0.081; p=0.574). Based on the results, we concluded that there was no significant difference of mutant p53 value in type 2 DM + cancer patients group and in type 2 DM patients group but there was significant difference of insulin value in both groups. There was also no significant correlation between mutan p53 and insulin value in both groups."

"Latar belakang: Kanker esofagus dilaporkan sebagai penyebab kematian keenam dari seluruh jenis kanker yang ada di seluruh dunia. Salah satu faktor risiko terjadinyakeganasan esofagus, terutama adenokarsinoma esofagus adalah gastroesophageal reflux disease (GERD). Diagnosis dini GERD sangat penting karena esofagitis refluks kronismerupakan faktor risiko utama terjadinya Barret esofagus, yang merupakan lesi prekursor terjadinya adenokarsinoma esofagus.Tujuan penelitian ini adalah untuk mengetahui ekspresi p53 dan Ki67 pada esofagitis refluks derajat ringan, esofagitis refluks derajat berat dengan kriteria Esohisto dan Barret esofagus. Bahan dan cara: Penelitian ini merupakan penelitian deskriptif dengan desainpenelitian potong lintang, dengan melakukan pulasan imunohistokimia p53 dan Ki67 pada 76 kasus sampel yang terbagi menjadi 30 kasus esofagitis refluks derajat ringan, 14 kasus esofagitis refluks derajat berat, dan 32 kasus Barret esofagus di Departemen Patologi Anatomik Fakultas Kedokteran Universitas Indonesia/Rumah Sakit Cipto mangunkusumo (FKUI/RSCM) tahun 2016-2018.Hasil: Ekspresi p53 positif pada 54 kasus sampel (71,1%), terbanyak pada Barret esofagus sebanyak 28 kasus (51,9%). Ekspresi Ki67 tinggi pada 46 kasus (60,5%), terbanyak pada esofagitis refluks derajat berat sebanyak 12 kasus (85,7%) Kesimpulan: Ekspresi p53 dan Ki67 pada esofagitis refluks derajat berrat dan Barret esofagus lebih tinggi dibanding dengan esofagitis refluks derajat ringan.

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Background: Esophageal cancer is reported as the sixth leading cause of death from all types of cancer worldwide. One of the risk factors for esophageal malignancy, especially esophageal adenocarcinoma is gastroesophageal reflux disease (GERD). Early diagnosis of GERD is very important because chronic reflux esophagitis is a major risk factor for Barrett esophagus, which is a precursor lesion to esophageal adenocarcinoma. The aim of this study was to determine p53 and Ki67 expression in mild reflux esophagitis, severe reflux esophagitis with the criteria of Esohisto and Barrett esophagus. Materials and methods: This study is a descriptive study with a cross-sectional design, by performing immunohistochemical results of p53 and Ki67 in 76 sample cases which were divided into 30 cases of mild reflux esophagitis, 14 cases of severe reflux esophagitis, and 32 cases of Barret esophagus in the Department Anatomical Pathology, Faculty of Medicine, University of Indonesia / Cipto Mangunkusumo Hospital (FKUI / RSCM) 2016-2018. Results: P53 positive expression in 54 sample cases (71.1%), most in Barret esophagus

as many as 28 cases (51.9%). Ki67 expression was high in 46 cases (60.5%), most in severe reflux esophagitis as many as 12 cases (85.7%) Conclusion: The expression of p53 and Ki67 in severe reflux esophagitis and Barrett esophagus was higher than in mild reflux esophagitis."

"Selama ini pengobatan kanker serviks hanya menggunakan vaksin profilaktik yang bersifat preventif. Pengembangan vaksin terapeutik yang bersifat kuratif perlu dilakukan untuk penderita yang berada dalam tahap terinfeksi HPV-16 pra-kanker dan kanker. Akan tetapi, efektifitas dan keamanan kandidat vaksin terapeutik perlu diuji terlebih dahulu dengan uji interaksi onkoprotein E6 dengan protein penekan tumor p53. Oleh karena itu, tujuan penelitian ini adalah melakukan ekspresi protein p53. Protein p53 merupakan salah satu komponen sistem pendeteksi interaksi antigen E6 dengan p53. Ekspresi p53 menggunakan sel E. coli transforman dilakukan dengan pemberian induksi IPTG 1 mM selama 4 jam. Plasmid rekombinan pQE-80L_p53 mampu mengekspresikan protein p53 di dalam sel E. coli BL21 cp dengan berat molekul 54 KDa. Hasil western blotting menunjukkan sebuah pita berukuran 54 KDa yang sesuai dengan berat protein p53.

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Over the last few years, cervix medication depends only on prophylactic vaccination. The development of therapeutic vaccination needs to be improved in order to treat HPV 16 infected patients. However, vaccines safety needs to be tested by examining interaction between E6 oncoprotein and p53 tumour suppressor protein. Therefore, p53 protein needs to be expressed as one of the system components. pQE 80L recombinant plasmid is capable to express p53 6xhis tagged using E. coli BL21 Codon Plus as a cell host. Western blot result showed that 4 hours of 1 mM IPTG induction produced a single band with the size of 54 kDa."

"Penderita Diabetes Melitus (DM) Tipe 2 mengalami peningkatan risiko kanker yang diduga diakibatkan oleh kondisi hiperglikemia, hiperinsulinemia, dan inflamasi. Ketiga faktor tersebut dapat menginduksi proses tumorigenesis melalui jalur glukotoksisitas, lipotoksisitas, dan stres oksidatif. Penelitian ini bertujuan untuk mengukur dan membandingkan mutan p53 sebagai tumor marker pada pasien DM tipe 2 dan pasien DM tipe 2 yang menderita kanker, mengukur dan membandingkan HbA1c pada kedua kelompok, serta melihat korelasi mutan p53 dengan HbA1c pada kedua kelompok. Desain studi yang digunakan adalah cross-sectional dengan teknik pengambilan sampel consecutive sampling. Kelompok yang diteliti pada penelitian ini adalah pasien DM tipe 2 (n = 51) dan pasien DM tipe 2 yang menderita kanker (n = 51). Analisis mutan p53 pada serum sampel dilakukan menggunakan ELISA, sedangkan pengukuran HbA1c dilakukan dengan Afinion Analyzer. Pada penelitian ini kadar serum mutan p53 pada kelompok pasien DM tipe 2 (1,62 ± 0,08 ng/ml) tidak berbeda bermakna dengan kelompok pasien DM tipe 2 yang menderita kanker (1,64 ± 0,09 ng/ml) (p = 0,774). Sementara itu, HbA1c pada kelompok DM tipe 2 (8,42 ± 0,25 %) berbeda bermakna dengan kelompok DM tipe 2 yang menderita kanker (7,02 ± 0,20 %) (p < 0,001). Tidak terdapat hubungan yang bermakna antara kadar mutan p53 dengan HbA1c, baik pada kelompok DM tipe 2 (r = 0,083; p = 0,561), maupun kelompok DM tipe 2 yang menderita kanker (r = 0,072; p = 0,617). Penelitian ini menunjukkan bahwa kadar mutan p53 pada kelompok DM tipe 2 dan DM tipe 2 yang menderita kanker tidak berbeda bermakna, namun HbA1c pada kedua kelompok berbeda bermakna. Sementara itu, tidak terdapat hubungan yang bermakna antara kadar mutan p53 dengan HbA1c pada kedua kelompok.

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Type 2 Diabetes Mellitus has been found to increase the risk of cancer which is caused by conditions of hyperglycemia, hyperinsulinemia, and inflammation. These three factors are able to induce tumorigenesis through mechanisms of glucotoxicity, lipotoxicity, and oxidative stress. This study aimed to measure and compare mutant p53 as tumor marker in Type 2 Diabetes Mellitus patients and Type 2 Diabetes Mellitus patients with cancer, to measure and compare HbA1c level in both groups, and to analyze the correlation between mutant p53 and HbA1c level in both groups. This study was a cross-sectional study with consecutive sampling technique in which two groups were involved, namely type 2 diabetes mellitus patients (n = 51) and type 2 diabetes mellitus patients with cancer (n = 51). Serological level of mutant p53 protein was analyzed using ELISA and HbA1c was measured with HbA1c Afinion Analyzer.

The serological level of mutant p53 in the type 2 diabetes mellitus patients (1.62 ± 0.08 ng/ml) showed no significant difference compared with type 2 diabetes mellitus patients with cancer (1.64 ± 0.09 ng/ml) (p = 0.774). Meanwhile, HbA1c level showed significant difference between type 2 diabetes mellitus patients (8.42 ± 0.25 %) and type 2 diabetes mellitus patients with cancer (7.02 ± 0.20 %) (p < 0.001). Mild correlations between mutant p53 and HbA1c level were found in both type 2 diabetes mellitus patients (r = 0.083; p = 0.561) and type 2 diabetes mellitus patients with cancer (r = 0.072; p = 0.617). Based on the result, there was no significant difference between mutant p53 in type 2 diabetes mellitus patients with and without cancer. HbA1c level was found to be significantly different in both groups. Meanwhile, there was no significant correlation between mutant p53 and HbA1c in both groups."

"Latar Belakang: Karsinoma sel sebasea adalah keganasan yang cukup sering ditemukan pada populasi Asia dan bersifat agresif dengan tingkat rekurensi lokal dan metastasis jauh yang tinggi. Peningkatan ekspresi pulasan imunohistokimia (IHK) tumor suppressor gene p53 dan Ki-67 sebagai penanda aktifitas proliferasi pada tumor kepala dan leher menunjukkan adanya korelasi antara aktivitas proliferasi dengan buruknya prognosis.Tujuan: Menilai ekspresi p53 dan Ki-67 pada karsinoma sel sebasea yang dihubungkan dengan faktor prognostik klinis dan histopatologi pada karsinoma sel sebasea yaitu ukuran tumor, keterlibatan kelenjar getah bening (KGB), metastasis jauh, diferensiasi, penyebaran pagetoid, dan invasi perineural.Metode: Pulasan IHK menggunakan antibodi p53 dan Ki-67 dilakukan pada jaringan karsinoma sel sebasea di blok parafin yang berasal dari data rekam medis sejak Juni 2017 – Juni 2022 di RSCM. Penilaian ekspresi dilakukan pada nukleus dengan metode manual dan semi-kuantitatif pada 1 lapang pandang dengan minimal jumlah sel sebanyak 500 sel dari hasil foto dan diproses ke dalam peranti lunak Qupath. Hasil penilaian selanjutnya di cek silang dengan data klinis pasien yang sudah dicatat di tabel induk dan kemudian dianalisa secara statistik untuk mengetahui hubungan keduanya.Hasil: Total 34 pasien dengan ketersediaan blok parafin dianalisa berdasarkan data klinis dan ekspresi p53 dan Ki-67. Tidak ditemukan adanya hubungan yang signifikan secara statistik antara kategori ekspresi p53 dengan faktor prognosis klinis dan histopatologi (p>0.05). Ekspresi p53 pada hasil penelitian menunjukkan proporsi faktor prognosis buruk lebih banyak ditemukan pada ekspresi tinggi yaitu adanya metastasis, invasi perineural, dan penyebaran pagetoid. Tidak ditemukan adanya hubungan yang signifikan secara statistik antara kategori ekspresi Ki-67 dengan faktor prognosis klinis dan histopatologi (p>0.05). Ekspresi Ki-67 pada penelitian ini menunjukkan proporsi faktor prognosis buruk lebih banyak ditemukan pada ekspresi tinggi yaitu ukuran tumor yang lebih besar, metastasis, diferensiasi buruk, dan invasi perineural.Kesimpulan: Tidak terdapat hubungan yang bermakna secara statistik antara ekspresi Ki-67 dan p53 dengan faktor prognosis klinis dan histopatologi buruk pada karsinoma sel sebasea. Terdapat proporsi sampel dengan ekspresi Ki-67 tinggi yang lebih banyak dan nilai tengah yang lebih tinggi pada faktor prognosis ukuran tumor, metastasis, berdiferensiasi buruk, serta invasi perineural, meskipun hasil yang didapatkan tidak jauh berbeda dan secara statistik tidak bermakna. Pada pulasan p53 terdapat perbedaan yang cukup besar dalam hal proporsi pulasan dengan ekspresi tinggi serta nilai tengah yang lebih tinggi pada faktor prognosis ukuran tumor.

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Sebaceous cell carcinoma is a relatively common malignancy in the Asian population, characterized by aggressive behavior with high rates of local recurrence and distant metastasis. Increased expression of immunohistochemical marker such as tumor suppressor gene p53 and Ki-67, a proliferation marker, in head and neck tumors suggests a correlation between proliferation activity and poor prognosis.

Objective: This study aims to evaluate the expression of p53 and Ki-67 in sebaceous cell carcinoma and its association with clinical and histopathological prognostic factors, including tumor size, lymph node involvement, distant metastasis, cell differentiation, pagetoid spread, and perineural invasion.

Methods: Immunohistochemical staining using p53 and Ki-67 antibodies was performed on paraffin-embedded sebaceous cell carcinoma tissues obtained from medical records between June 2017 and June 2022 at RSCM. Expression assessment was conducted on nuclei using manual and semi-quantitative methods on 500 cells per field processed with Qupath software. The results were cross-checked with patients' clinical data recorded in a master table and statistically analyzed to determine their relationship.

Results: A total of 34 patients were analyzed based on clinical data and p53 and Ki-67 expression. There was no statistically significant association between p53 expression and clinical and histopathological prognostic factors (p>0.05). However, high p53 expression was associated with a higher proportion of poor prognostic factors, such as metastasis, perineural invasion, and pagetoid spread. Similarly, there was no statistically significant association between Ki-67 expression categories and clinical and histopathological prognostic factors (p>0.05). High Ki-67 expression was more frequently observed in cases with larger tumor size, metastasis, poor differentiation, and perineural invasion.

Conclusion: This study found no significant statistical association between Ki-67 and p53 expression with poor prognostic factors in sebaceous cell carcinoma. Nonetheless, a higher proportion of samples with high Ki-67 expression and higher median values were observed in cases with bigger tumor size, metastasis, poor differentiation, and perineural invasion, although these differences were not statistically significant. For p53 expression, significant differences were found in terms of proportion and median values concerning tumor size prognostic factors.

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