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Latar Belakang. Tingkat kekambuhan dan toksisitas terapi merupakan masalah pada kanker serviks. Antibodi monoklonal sebagai terapi target menunjukkan peran menjanjikan dalam pengobatan kanker. Penelitian ini bertujuan untuk menganalisis efek imunologis pada pemberian radiasi bersama mAb h-R3 pada pasien kanker serviks.

Metode. Penelitian ini merupakan penelitian eksperimental yang dilakukan dalam dua tahun. Subjek dibagi menjadi dua kelompok, mendapat terapi radiasi dengan/tanpa mAb h-R3. Uji terhadap sel imun (sel NK CD56⁺, sel T CD4⁺, dan sel T CD8⁺) dilakukan pada darah perifer dan jaringan tumor untuk menilai efek imunologis dan respons terapi pada masing-masing kelompok. Analisis dilakukan dalam tiga waktu: sebelum terapi (pre terapi) untuk menilai kondisi awal, satu minggu setelah pemberian mAb h-R3 yang pertama (saat terapi) untuk menilai pengaruh mAb h-R3, dan setelah radiasi eksterna selesai sebelum brakhiterapi I (pasca terapi) untuk menilai pengaruh pemberian radiasi dengan atau tanpa mAb h-R3.

Hasil. Terdapat 22 subjek, stadium IIB hingga IIIB dengan rerata usia 51,2 ± 7,7 tahun. Didapatkan rasio sel NK CD56⁺ pre dan saat terapi di jaringan tumor pada kelompok mAb h-R3 lebih tinggi (p<0,05), menunjukkan pengaruh mAb h-R3 terhadap sel NK CD56⁺. Pengaruh tersebut terlihat juga pada jumlah sel T CD4⁺ dan CD8⁺ pre dan saat terapi di sirkulasi dan jaringan tumor, kelompok mAb mengalami peningkatan dengan perbedaan yang signifikan di sirkulasi antar dua kelompok (p<0,05). Pengaruh pemberian radiasi bersama mAb h-R3 terlihat dalam perbandingan antara pre dan pasca terapi, walaupun sel imun dalam sirkulasi pada kedua kelompok menurun, namun kelompok mAb h-R3 tetap memiliki jumlah lebih tinggi. Terdapat korelasi antara peningkatan jumlah sel NK CD56⁺ dengan penurunan volume tumor. Berdasarkan RECIST, kelompok mAb h-R3 memiliki respons lebih baik (p<0,05) dengan complete response 63,6% vs 18,2% pada kelompok kontrol.

Kesimpulan. mAb h-R3 meningkatkan jumlah sel imun secara sistemik maupun lokal, pemberian radiasi bersama mAb h-R3 menghasilkan respons imunitas seluler yang lebih baik sehingga meningkatkan respons terapi.

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Introduction. Rate of recurrences and toxicity of therapy remain as problems in cervical cancer. Monoclonal antibody as targeted therapy has showed a promising role in cancer treatment. This study aims to analyze the immunological response of radiation and mAb h-R3 in cervical cancer treatment.

Methods. This was an experimental study conducted in two years. Subjects were divided into two groups, one group received radiation with mAb h-R3 and the other received radiation only. Cellular immunity tests (NK CD56⁺ cell, CD4⁺ T cell, and CD8⁺ T cell) were performed on peripheral blood and tumor tissue to determine the immunological effect and tumor response on each group. Analyses were performed at 3 period: before treatment (pre therapy) as baseline, one week after first administration of mAb h-R3 (during therapy) to measure effect of mAb h-R3, and after external radiation before first brachytherapy (after therapy) to measure effect of radiation with or without mAb h-R3.

Result. There were 22 subjects, stage IIB to IIIB, with the mean age of 51.2 ± 7.7 years. The ratio of tumor tissue NK CD56⁺ cells pre- and during-therapy in mAb h-R3 group were higher (p<0.05), showing the effect of mAb h-R3 to NK CD56⁺ cells. Number of T CD4⁺ and CD8⁺ cells pre- and during-therapy in peripheral blood and tumor tissue in mAb h-R3 group increased with significant difference in peripheral blood between two groups (p<0.05). Radiation and mAb h-R3 effect were shown in pre- and post-therapy ratio, although all immune cells were decreased, mAb h-R3 group still have higher number of cells. There was a correlation between the increment of NK CD56⁺ cells with tumor volume reduction. Based on RECIST criteria, mAb h-R3 group have better response (p<0.05) than control group (complete response: 63.6% vs 18.2%).

Conclusion. mAb h-R3 increases the number of immune cells both systemically and locally, radiotherapy and mAb h-R3 have better immune response which will increase the therapeutic response.

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"ABSTRAKIn the past 10 years, recent development of targeted therapy in metastatic renal cell carcinoma (mRCC) has provided a new hope and significantly enhanced the prognosis of the disease. Three class of targeted therapy were developed, including multi-targeted tyrosine kinase inhibitors (TKI), the mammalian target of rapamycin (mTOR) complex-1 kinase inhibitors, and the humanized antivascular endothelial growth factor (VEGF) monoclonal antibody. Hence, the objective of this article was to critically examine the current evidence of targeted therapy treatment for patients with mRCC. In the majority of trials evaluating targeted therapy, patients were stratified according to Memorial Sloan Kattering Cancer Center (MSKCC) risk model and the recommendation of targeted treatment based on risk features. In first-line setting (no previous treatment), sunitinib, pazopanib, or bevacizumab plus IFN-α were recommended as treatment options for patient with favorable- or intermediate- risk features and clear cell histology. Patients who progressed after previous cytokine therapy would have sorafenib or axitinib as treatment options. Clear-cell mRCC with favorable- or intermediate- risk features and failure with first-line TKI therapy might be treated with sorafenib, everolimus, temsirolimus or axitinib. However, the current evidence did not show the best treatment sequencing after first-line TKI failure. In patients with poor-risk clear-cell and non-clear cell mRCC, temsirolimus was the treatment option supported by phase III clinical trial. In addition, several new drugs, nowadays, are still being investigated and waiting for the result of phase II or III clinical trial, and this might change the standard therapy for mRCC in the future."

"This book provides an overview of critical components of cell signaling machinery and its role in epithelial morphogenesis, proliferation, invasions and angiogenesis in human cancer and discusses novel types of protein kinase pathways."