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"Latar Belakang: Adenokarsinoma duktal pankreas dan adenokarsinoma ampula vateri, tanpa melihat gambaran episentrum tumor, sulit dibedakan secara histopatologi. Gejala klinis tidak spesifik sehingga kasus yang ditemukan seringkali tidak memenuhi kriteria resectable. Gambaran radiologi juga tidak spesifik, padahal terapi dan prognosis keduanya berbeda. Adenokarsinoma duktal pankreas memiliki angka kesintasan rendah dibanding adenokarsinoma ampula vateri. Penentuan asal tumor, berasal dari duktal pankreas atau ampula vateri, sangat penting. SMAD4 diduga dapat menjadi salah satu panel diagnostik imunohistokimia. Penelitian ini dilakukan dengan melihat perbandingan ekspresi SMAD4 di adenokarsinoma ampula vateri dan adenokarsinoma duktal pankreas.Tujuan: Mengetahui perbandingan ekspresi SMAD4 pada adenokarsinoma duktal pankreas dan adenokarsinoma ampula vateri.Metode: Penelitian analitik observasional, desain potong lintang pada sediaan reseksi adenokarsinoma duktal pankreas dan adenokarsinoma ampula vateri, periode Januari 2013 hingga September 2021. Pengambilan sampel dilakukan secara total sampling. Adenokasinoma ampula vateri dengan subtipe pankreatobiliar dieksklusi. Pemeriksaan imunohistokimia menggunakan antibodi primer SMAD4. Data imunohistokimia dianalisis untuk melihat adakah perbedaan ekspresi SMAD4 pada adenokarsinoma di ampula vateri dan adenokarsinoma duktal pankreas.Hasil: Loss of SMAD4 didapatkan pada 12 kasus (60 %) adenokarsinoma duktal pankreas dan 8 kasus (44,4 %) adenokarsinoma ampula vateri. Tidak didapatkan hubungan loss of SMAD4 pada adenokarsinoma duktal pankreas dan adenokarsinoma ampula vateri (p=0,338).Kesimpulan: Tidak terdapat hubungan bermakna loss of SMAD4 pada adenokarsinoma duktal pankreas dan adenokarsinoma ampula vateri. Namun terdapat trend loss of SMAD4 lebih tinggi pada adenokarsinoma duktal pankreas dibanding adenokarsinoma ampula vateri subtipe intestinal dan mixed type dominansi intestinal.......ackground: Differentiating pancreatic ductal adenocarcinoma and ampullary adenocarcinoma without knowing the epicenter of the tumor is difficult. The clinical symptoms are non-specific. The cases found usually do not meet the operable criteria. Radiological examination is also non-specific, although the treatment and prognosis are different. Pancreatic ductal adenocarcinoma has lower survival rate than ampullary adenocarcinoma. It is very important to determine the origin of the tumor from pancreatic ductal or ampulla of Vater. SMAD4 is expected to be one of immunohistochemical diagnostic panel for the pancreatic ductal adenocarcinoma. This study compares the SMAD4 expression in pancreatic ductal adenocarcinoma and ampullary adenocarcinoma.Objective: Knowing the comparison of SMAD4 expression in pancreatic ductal adenocarcinoma and ampullary adenocarcinoma.Methods: Observational analytical study with cross sectional design, total sampling was performed on the resection specimens of pancreatic ductal adenocarcinoma and ampullary adenocarcinoma, period January 2013 to December 2021. Ampullary adenocarcinoma with pancreatobilliary subtype was excluded. Immunohistochemical examination using SMAD4 primary antibody. Immunohistochemical data will be analyzed to see SMAD4 expression difference between pancreatic ductal adenocarcinoma and ampullary adenocarcinoma.Results: Loss of SMAD4 was found in 12 cases (66,7 %) of pancreatic ductal adenocarcinoma and 6 cases (44,4 %) of ampullary adenocarcinoma. There was no significant relationship between loss of SMAD4 in pancreatic ductal adenocarcinoma and ampullary adenocarcinoma (p=0,338).Conclusions: There was no significant relationship between loss of SMAD4 in pancreatic ductal adenocarcinoma and adenocarcinoma of the ampulla of vater. However, there was a trend of higher SMAD4 loss in pancreatic ductal adenocarcinoma than ampullary vater adenocarcinoma of intestinal subtype and mixed type with intestinal dominance."

"Latar Belakang: Respons patologis kanker payudara terhadap terapi neoadjuvan masih relatif rendah, khususnya di RSCM. Intensitas sTIL dan ekspresi PD-L1 telah diteliti sebagai prediktor respons terapi neoadjuvan. Penelitian ini menilai peran intensitas sTIL dan ekspresi PD-L1 terhadap repons terapi neoadjuvan kanker payudara. Data tersebut dapat dimanfaatkan sebagai data awal di Indonesia, untuk perencanaan terapi pasien kanker payudara yang lebih baik, terlebih dengan sudah tersedianya imunoterapi anti-PD-1/PD-L1.Tujuan: Mengetahui intensitas sTIL dan ekspresi PD-L1 sebagai prediktor respons patologis kanker payudara terhadap terapi neoadjuvan di RSCM.Metode: Penelitian berdesain kohort retrospektif, analitik observasional, pada kasus kanker payudara yang mendapatkan terapi neoadjuvan dan mastektomi di RSCM periode Januari 2014-Desember 2021. Dilakukan total sampling sebanyak 60 kasus. Ekspresi PD-L1 (imunohistokimia, klon 22C3) dan intensitas sTIL (histopatologi) diperiksa pada spesimen biopsi. Dilakukan analisis multivariat regresi linear untuk mendapatkan prediktor independen respons terapi neoadjuvan.Hasil: Didapatkan 60 pasien perempuan, median usia 46 tahun, 91,7% karsinoma invasif no special type. Median intensitas sTIL 10% (1%-70%). Intensitas sTIL rendah (≤10%) pada 58,3% sampel. Ekspresi PD-L1 positif (CPS ≥1) pada 28,3% sampel. Hanya 8,3% sampel mencapai pCR, 90% tergolong RCB kelas II-III. Didapatkan prediktor independen skor RCB: Setiap peningkatan 1% intensitas sTIL, tidak adanya invasi limfovaskular, dan pemberian kemoterapi berbasis taksan diprediksi menurunkan skor RCB sebanyak 0,058 (0,039-0,078), 0,781 (0,241-1,321), dan 0,594 (0,037-1,152). Ekspresi PD-L1 yang positif berhubungan dengan tercapainya pCR-RCB kelas I (p=0,048), tetapi skor CPS bukan merupakan prediktor skor RCB pada analisis multivariat regresi linear.Kesimpulan: Intensitas sTIL merupakan prediktor respons patologis kanker payudara terhadap terapi neoadjuvan di RSCM. Ekspresi PD-L1 berhubungan dengan tercapainya pCR-RCB kelas I, tetapi skor CPS bukan prediktor skor RCB.Kata kunci: PD-L1, programmed-death ligand 1, sTIL, stromal tumour infiltrating lymphocyte, kanker payudara, kemoterapi neoadjuvan, respons patologis......Background: Pathological responses to neoadjuvant therapy were still relatively poor, especially in RSCM. Studies had been done to search for predictors of response such as sTIL intensity and PD-L1 expression, which is known to block sTIL action in killing cancer cells. This research assessed sTIL intensity and PD-L1 expression as predictors of response to neoadjuvant therapy in breast cancer. The preliminary data might be used to better tailored breast cancer patient therapy, considering the availability of anti-PD-1/PD-L1 immunotherapy nowadays.Objective: To assess TIL intensity, PD-L1 expressions, and their roles as pathological predictors of breast cancer reponse to neoadjuvant therapy in RSCM.Method: This was an observational analytic retrospective cohort study on breast cancer patients receiving neoadjuvant therapy and mastectomy in RSCM from January 2014 to December 2021. Total sampling was done. PD-L1 expression (immunohistochemistry, clone 22C3) and sTIL intensity (histopathology) was examined in the biopsy specimen. Linear regression analysis was done to determine the independent predictors of neoadjuvant therapy response (evaluated in the mastectomy specimen with residual cancer burden/RCB score).Results: There were 60 female patients, median age 46 years old. 91,7% had invasive carcinoma of no special type. Median sTIL intensity was 10% (1%-70%). 58,3% patients had low sTIL intensity (≤10%). 28,3% patients had positive PD-L1 expression (CPS ≥1). Only 8,3% patients had pCR, while 90% patients had RCB class II-III. Every 1% increase in sTIL intensity, no lymphovascular invasion, and taxane chemotherapy were predicted to lower RCB score by 0,058, 0,781, dan 0,594, respectively. PD-L1 expression associated with pCR-RCB class I (p=0,048), but CPS score was not a predictor of RCB score in linear regression analysis. Conslusion: sTIL intensity was an independent predictor of breast cancer response to neoadjuvant therapy in RSCM. PD-L1 expression associated with pCR-RCB class I, but CPS score was not a predictor of RCB score. Keywords: PD-L1, programmed death ligand 1, sTIL, stromal tumour infltrating lymphocyte, breast cancer, neoadjuvant therapy, pathological response"

"Latar belakang: Pemfigoid bulosa merupakan kelompok penyakit bula subepidermal autoimun terbanyak. Patogenesis yang mendasari timbulnya penyakit ini adalah adanya ikatan antibodi terhadap antigen BP180 NC16A yang merupakan komponen dari hemidesmosom. Ikatan antibodi-antigen ini selanjutnya mengaktivasi sistem komplemen. Deposit imun yang terbentuk kemudian dapat diperiksa menggunakan direct immunofluorescence (DIF). Salah satu molekul yang juga dihasilkan pada proses aktivasi komplemen adalah C4d. Molekul ini dianggap cukup stabil dan dapat digunakan sebagai penanda adanya kerusakan jaringan yang dimediasi oleh antibodi. Penelitian ini bertujuan untuk melihat ekspresi imunohistokimia (IHK) C4d menggunakan formalin-fixed paraffin-embedded (FFPE) pada kasus pemfigoid bulosa.Bahan dan cara kerja: Sampel penelitian terdiri atas 28 kasus pemfigoid bulosa yang terbukti mengandung deposit imun pada pemeriksaan DIF. Seluruh kasus dipulas menggunakan Complement C4d Rabbit Polyclonal Antibody. Penilaian ekspresi IHK C4d dilakukan secara tersamar dan dinyatakan sebagai positif atau negatif.Hasil: Sebanyak 25 dari total 28 kasus pemfigoid bulosa (89,3%) menunjukkan C4d terekspresi positif pada pemeriksaan IHK.Kesimpulan: Pulasan IHK C4d menggunakan FFPE dapat digunakan untuk mendeteksi deposit imun pada kasus pemfigoid bulosa.......Background: Bullous pemphigoid is the most frequent autoimmune subepidermal blistering disease. It is caused by the production of autoantibodies against BP180 NC16A, a component of hemidesmosome. Binding of autoantibodies to their target antigen lead to complement activation. Subsequently, immune deposits formation can be identified by direct immunofluorescence (DIF). One split product that also produced during complement activation is C4d. It is known as an inactive molecule that can be used as marker of antibody mediated tissue injury. The aim of this study was to investigate the expression of C4d immunohistochemically using formalin-fixed paraffin-embedded (FFPE) in bullous pemphigoid cases.Material and methods: Immunohistochemical (IHC) stain was performed on 28 bullous pemphigoid cases proven to have immune deposits by DIF. All of these cases were labeled immunohistochemically using Complement C4d Rabbit Polyclonal Antibody. The results were blindly reviewed and defined as positive or negative.Results: Immunoreactivity with C4d were identified in 25 out of 28 bullous pemphigoid cases (89.3%).Conclusion: C4d IHC stain using FFPE can be used to detect immunoreactant deposition in case of bullous pemphigoid."