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"DNA damage can have particularly severe carcinogenic influence if it incapacitates the cellular machinery normally protecting the cell from the effects of genomic damage. The protective functions involve not only DNA repair and apoptosis (programmed cell death), but also regulation of the cell cycle and proliferation. Therefore, carcinogenesis can be promoted by inactivating or altering key regulatory proteins like p16INK4a, which has the capability to arrest the cell cycle in the G1 phase and prevent inappropriate proliferation. Functional cyclin-dependent kinase (Cdk) inhibitor p16INK4a binds to Cdk-4 and Cdk-6, thereby preventing the Cdk-cyclin complexes from promoting phosphorylation of pRb and releasing the transcription factor E2F needed for the cell cycle to proceed to the S phase. Arrest in G1 accounts for a minority of arresting cells after DNA damage, the majority of arrests taking place in G2 without recognized p16INK4a contribution. However, inactivating alterations of p16INK4a are common in cancers, possibly because of additional functions of p16INK4a in senescence and inhibition of the spreading and migration of cancer cells. Since oncogenic initiation is insufficient for growing significant tumors without spreading and angiogenesis, this could partly explain why inactivated p16INK4a is frequently exhibited in clinical tumors in spite of apparently less exclusive role in cell cycle arrest. On the other hand, multiple oncogenic events are usually necessary to develop cancer, and generally both pRb and p53 pathways are impaired in tumors. This suggests that growth regulation in G1 and therefore also its key molecular components including p16INK4a are important in carcinogenesis."

"Karsinoma kolorektal merupakan salah satu kanker dengan beban penyakit yang tinggi di dunia. Berbagai penelitian mengenai efek anti-tumor vitamin D telah dilakukan sejak hubungannya dengan kanker kolorektal terungkap. Studi ini bertujuan untuk mencari secara sistematis penelitian mengenai efek anti-tumor vitamin D pada kanker kolorektal untuk memahami mekanisme molekuler di balik aktivitasnya. Sebuah tinjauan sistematis dilakukan dengan mencari di database elektronik PubMed untuk penelitian asli yang mempelajari efek pemberian vitamin D pada kanker kolorektal. Studi yang menyelidiki mekanisme di balik efek tersebut memenuhi syarat untuk evaluasi. Dua puluh tujuh studi dimasukkan untuk analisis dengan rentang tanggal publikasi dari 1987 hingga 2017. Studi in vitro dan in vivo mengungkapkan bahwa pemberian vitamin D mampu menekan proliferasi, menginduksi apoptosis, mempertahankan diferensiasi sel, mengurangi respons proinflamasi, menghambat angiogenesis, dan menghambat perkembangan metastasis. Penambahan kalsium ke suplementasi vitamin D juga ditemukan meningkatkan aktivitas anti-tumor vitamin D melalui cross-talk antara jalur pensinyalan mereka. Vitamin D dapat menghambat pertumbuhan dan perkembangan kanker kolorektal melalui jalur genomik (mengatur transkripsi gen pro- dan anti-tumor) atau non-genomik (mencegah aktivasi jalur pensinyalan pro-tumor secara langsung).

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Colorectal carcinoma is one of the cancers with a high disease burden globally. Since its relationship with colorectal cancer has been revealed, various studies on the antitumor effect of vitamin D have been conducted. This study aims to systematically search for research on the anti-tumor effect of vitamin D on colorectal cancer to understand the molecular mechanism behind its activity. A systematic review was carried out by searching the PubMed electronic database for original research studying the effects of vitamin D administration on colorectal cancer. Studies investigating the mechanism behind these effects are eligible for evaluation. Twenty-seven studies were included for analysis with publication date ranges from 1987 to 2017. In vitro and in vivo studies revealed that administration of vitamin D could suppress proliferation, induce apoptosis, maintain cell differentiation, reduce pro-inflammatory responses, inhibit angiogenesis, and inhibit the development of metastases. The addition of calcium to vitamin D supplementation was also found to increase vitamin D anti-tumor activity through cross-talk between their signaling pathways. Vitamin D can inhibit the growth and development of colorectal cancer through genomic pathways (regulating transcription of pro- and anti-tumoral genes) or non-genomic (directly prevents activation of pro-tumor signaling pathways)."

"Latar belakang : Tumor ganas adneksa mata merupakan keganasan epitel yang berasal dari kelopak mata, konjungtiva dan kelenjar kelenjar yang berada pada jaringan tersebut. Tumor ini sebenarnya mempunyai prognosis baik bila diobati pada stadium dini.Metode : Dilakukan studi historical cohort dengan survival analysis. Subyek adalah penderita tumor ganas adneksa mata yang berobat ke poliklinik subbagian Tumor Mata FKUI/RSUPN Dr. Cipto Mangunkusumo pada periode 1 Januari 1996 sampai 31 Desember 2000 mendapat tindakan operasi. Analisis data menggunakan cara cox proportional hazard dan analisis life table menurut metode Kaplan-Meier.Hasil : Dari 74 penderita tumor ganas adneksa mata didapat angka harapan hidup 74.24%. Penderita terbanyak adalah karsinoma sel skuamosa (51.4%), karsinoma set basal (28.4%), adenokarsinoma (14.8%) dan melanoma maligna (5.4%). Metastasis memberikan resiko tertinggi terhadap kematian HR 51.69(9.72-274.76), kelompok tumor karsinoma sel skuarnosa - adenokarsinoma HR 4.91 (0.62-38.81), penderita mendapat tambahan radiasi HR 10.72(1.25-92.18), dan jenis operasi eksenterasi HR 7.63(1.59-36.48)Kesimpulan : Faktor resiko yang berhubungan dengan kematian adalah metastasis, kelompok tumor karsinoma sel skuamosa dan adenokarsinoma, dilakukan tindakan radiasi dan tindakan eksenterasi orbita.

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Background : Malignant eye adnexa tumor originates from epithelium of eye lid, conjunctiva, and nodes of those tissues. The prognosis of this tumor is good if it is treated during the initial stadium.

Method : A historical cohort study was carried out with survival analysis. The subject of the study were patients with malignant eye adnexa tumor who went to Sub-division of Eye Tumor FKUI/RSUPN Dr. Cipto Mangunkusumo from the period of January I, 1996 to December 31, 2000 and received surgical treatment. Data analysis used was cox proportional hazard and life table analysis with Kaplan Meier method.

Result : From 74 patients with malignant eye adnexa tumor we obtained a survival rate of 74.24%. Most of them suffer from squamous cell carcinoma (51.4%), basal cell carcinoma (28.4%), adenocarcinoma (14.8%) and melanoma maligna (5.4%). Metastasis contributes to a high risk of death HR 51.69 (9.72-274.76), squamous cell carcinoma - adenocarcinoma group type HR 4.91 (0.62-38.81), patients receiving additional radiation treatment HR 10.72 (1.25-92.18), and exenteration HR 7.63 (1.59-36.48).

Conclusion : The risk factor which causes death is metastasis, squamous cell carcinoma and adenocarcinoma group type, radiation treatment and exenteration of the orbit were done."

"Latar belakang dan tujuan: Pemeriksaan MRI standar terkadang sulit untuk membedakan tumor ganas dan jinak orbita karena karakteristik imaging yang nonspesifik, padahal biopsi pada lokasi tertentu seperti apeks orbita dan basis kranium periorbital sulit dilakukan dan memiliki risiko komplikasi yang tinggi sehingga klinisi memerlukan pemeriksaan MRI yang lebih spesifik untuk memperkirakan sifat tumor. Pada beberapa penelitian sebelumnya, nilai Apparent Diffusion Coefficient ADC baik menggunakan MRI 3Tesla T, 1,5T, dan gabungan keduanya, mampu membedakan tumor ganas dan jinak orbita, namun memiliki nilai ambang bervariasi. Penelitian ini bertujuan mencari rerata nilai ADC menggunakan MRI 1,5T pada kelompok tumor ganas dan jinak orbita serta mencari nilai ambang untuk membedakan keduanya. Metode: Sebanyak 33 pasien tumor orbita yang telah menjalani pemeriksaan MRI orbita dengan kekuatan 1,5T dan mendapatkan nilai ADC tumor, dikelompokkan berdasarkan hasil histopatologis menjadi kelompok ganas dan jinak. Analisis statistik nilai ADC antara kelompok ganas dan jinak dilakukan menggunakan uji nonparametrik. Selanjutnya, penentuan nilai ambang optimal untuk membedakan tumor ganas dan jinak dilakukan menggunakan kurva receiver-operating characteristic ROC. Hasil: Dari 33 sampel diperoleh 17 tumor ganas dan 16 tumor jinak. Hasil histopatologis mayoritas pada kelompok tumor ganas dan jinak masing-masing adalah limfoma 4/17 dan meningioma grade I 9/16. Median dan range nilai ADC pada kelompok tumor ganas adalah 0,8 0,6-2,1 10 minus;3 mm2/s yang berbeda bermakna dengan kelompok tumor jinak 1,1 0,8-2,6 10 minus;3 mm2/s p=0,001. Nilai ambang optimal ADC untuk membedakan tumor ganas dan jinak adalah 0,88 10 minus;3 mm2/s dengan perkiraan sensitivitas 76,5 dan spesifisitas 93,8. Simpulan: Nilai ADC pada kelompok tumor ganas orbita lebih rendah dibandingkan tumor jinak dan bisa digunakan untuk memperkirakan karakteristik suatu tumor orbita.

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Background and purpose: Differentiating between malignant and benign orbital tumor using standard MRI sometimes is difficult because of nonspecific imaging characteristics, meanwhile biopsy in certain area such as orbital apex and periorbital skull base is difficult to do with higher risk of complication so that ophthalmologist may need suggestion from MRI result to predict the characteristic of tumor. In previous studies, the Apparent Diffusion Coefficient ADC value using MRI 3Tesla T, 1,5T, and combination of both, are able to differentiate between them but with variable cut-off value. This study aims to find out the ADC value of malignant and benign orbital tumor using MRI 1,5T and calculate the optimum cut-off value to differentiate them.

Methods: Thirty-three patients with orbital tumor who has undergone MRI examination and get the ADC value of tumor are classified into malignant and benign group. ADC value between malignant and benign group is statistically analyzed using nonparametric test. The optimal cut off value between malignant and benign tumor is calculated receiver-operating characteristic ROC curve.

Results: Among all samples, 17 are malignant and 16 are benign. Majority of histopathological result in malignant group are lymphoma 4/17 while in benign group are meningioma grade I 9/16. The mean ADC value in malignant group 0,8 10 minus;3 mm2/s is significantly different from benign group 1,1 10 minus;3 mm2/s p=0,001. The optimum cut-off ADC value to differentiate between malignant and benign orbital tumor is 0,88 10 minus;3 mm2/s with prediction of sensitivity 76,5 and specificity 93,8.

Conclusion: ADC value in malignant orbital tumor is lower than benign tumor and it can be used to predict the characteristic of orbital tumor. "

"Respons tumor terhadap radiasi dipengaruhi oleh berbagai faktor yang dapat digolongkan ke dalam faktor intrinsik yang bersifat genetik dan faktor-faktor lingkungan mikro (microenvirontment) yang disebut faktor epigenetik. Faktor intrinsik dapat ditunjukkan dengan 'predictive assay' yang dapat memperlihatkan sensitivitas individual tumor. Faktor epigenetik terdiri dari berbagai faktor termasuk hipoksia, vaskularisasi dan fraksi pertumbuhan. Dan berbagai penelitian dapat ditunjukkan hubungan antara beberapa faktor itu dengan respons tumor, maupun antara ketiga faktor tersebut. Dapat diasumsikan bahwa faktor hipoksia, vaskularisasi dan fraksi pertumbuhan merupakan indikatorindikator Iingkungan tumor yang dapat merupakan prediktor terhadap respons radiasi pada jaringan tumor tersebut. Pada penelitian ini, fraksi pertumbuhan tumor akan diteliti kaitannya dengan respons tumor dan pemanfaatannya dalam pengobatan gabungan untuk meningkatkan respons pada tumor yang mempunyai prognosis buruk. Berdasarkan asumsi bahwa tumor dengan fraksi pertumbuhan rendah relatif hipoksik, maka dilakukan pengobatan gabungan radiasi dengan MMC, suatu sitostatika yang bekerja efektif dalam keadaan hipoksik pada kelompok-kelompok tumor yang sudah digolongkan ke dalam fraksi pertumbuhan yang rendah dan yang tinggi. Pemilahan pasien berdasarkan besarnya fraksi pertumbuhan dilakukan dengan pemeriksaan imunohistokimia pada jaringan biopsi segar penderita kanker leher rahim menggunakan antibodi monoklonal Ki-67. Penderita KLR yang diteliti adalah penderita stadium lanjut lokal (stadium II b sampai III b menurut FIGO) yang datang ke Sub Bagian Onkologi Bagian Obstetri dan Ginekologi FKUI/RSCM dan kemudian dikirim ke Sub Bagian Radioterapi Bagian Radiologi FKUI/RSCM

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Response of tumors toward radiation is affected by various factors that can be classified as intrinsic factors, which are genetic, and epigenetic factors, which are micro environment. The intrinsic factors can be demonstrated through a "predictive assay" which can show the sensitivity of individual tumor.Epigenetic factors consist of many factors including hypoxia, vascularization, and growth fraction. From results of many studies, can' be shown that there is a relation between these last factors with response of tumor. There is also relation among these three factors. We can assume that hypoxia, vascularization and growth fraction are indicators of tumor's environment which can also be predictors of response to radiation in tumor tissue.In this study, the rate of tumor growth will be studied in it's relation to tumor's response and the uses in combined treatment to increase the response of tumors with bad prognosis.Based on an assumption that tumors with low growth fraction are relatively hypoxic, combination of radiation with MMC is used, a cytostatic agent that effectively work on hypoxic condition in groups of tumors which have been classified as having low growth fraction. Patients grouping were performed based on the growth fraction as seen in immunohisto chemistry examination on fresh biopsy tissue of patients with cancer of cervix, using Ki-67 monoclonal antibody. Those patients of cancer of the cervix included in this study were patients in locally advanced stages (stage IIb - IIIb by FIGO classification), who came to Oncology Sub Department of the Department of Obstetric and Gynecology Faculty of Medicine University of Indonesia/Dr. Cipto Mangunkusumo Hospital, and referred to Radiotherapy Sub Department of the Department of Radiology at the same institute.After going through inclusion and exclusion criteria, 146 patients were found to be suitable for evaluation with the prescribed protocol. The patients were sorted into 4 groups according the growth fraction and type of treatment to be performed. Group I and Group II were patients with Ki-67 index less than 40% with a difference that Group I underwent radiation therapy only, while Group II was treated with combination of radiation therapy and MMC. Group III and IV were patients with Ki-67 index 40% or higher, with a difference that Group III underwent radiation therapy only, while Group IV was treated with combination of radiation therapy and MMC. The 40 % Ki-67 criterion was determined based on results of preliminary study which set the level around 40%.The radiation therapy consisted of external radiation to the pelvis area in 28 sessions with a dose of 180 cGy per sessions or 5040 cGy total dose given in around 5.5 weeks. After a 1 - 2 week rest, radiation therapy were continued in the form of intra cavitary radiation using High Dose Rate (HDR) system in 2 sessions, I week apart, each in a dose of 850 cGy, giving a total dose of 1700 cGy. A small number of patients (42 patients) were given with Low Dose Rate (LDR) intra cavitary system in similar session and interval with those patients with HDR system. The dose was 1300 cGy per session or total dose of 2600 cGy being equal to the total dose of 1700 cGy in HDR system. Mitomycin-C was given in the combined treatment groups, with a dose of 15 mglm2, as a bolus injection intravenously, at the first day of external radiation and the first intracavitary insertion.Routine blood examinations were performed to each patient before treatment and once a week until the radiation therapy were completed. Liver function tests were performed before treatment, at the end of external radiation and after all radiation therapy completion."

"Tumor otak merupakan jenis tumor yang sangat sulit ditangani dan menyebabkan mortalitas serta morbiditas yang berat. Saat ini, kombinasi radioterapi, kemoterapi (temozolomid dan agen lainnya), serta kortikosteroid menjadi terapi utama untuk berbagai jenis tumor, termasuk tumor otak. Walaupun demikian, data menunjukkan bahwa kombinasi terapi tersebut tidak memberikan perbaikan pada kondisi klinis pasien. Hal ini menyebabkan perlunya dilakukan pencarian senyawa baru atau repurposing terapi yang sudah ada yang dapat memperbaiki prognosis pasien tumor otak. Metformin, suatu agen antidiabetes yang telah dikenal, belakangan ini banyak diteliti potensinya sebagai antineoplasma. Metformin berperan memberi efek apoptosis, autofagi, dan antiproliferasi melalui jalur p53 dengan aktivasi adenosine 5’-monophosphate (AMP)-activated protein kinase (AMPK). Review article ini bertujuan untuk mengkaji perkembangan studi terkini mengenai efek metformin pada pasien tumor otak melalui tinjauan klinisnya. Penelusuran literatur dilakukan dengan sistematis pada pangkalan data PubMed, ScienceDirect, dan SpringerLink yang diseleksi berdasarkan kriteria inklusi dan eksklusi yang ditetapkan. Manfaat klinis obat dinilai melalui Overall Survival (OS) dan Progression Free Survival (PFS) pasien tumor otak. Studi juga menunjukkan efek sinergis kombinasi metformin dengan temozolomid, tetapi tidak dengan kortikosteroid. Melalui kombinasi dengan temozolomid yang diberikan pasca radioterapi, potensi antineoplasma menghasilkan kelangsungan hidup yang lebih baik. Meskipun demikian, efikasi dan keamanan metformin perlu diuji klinis lebih lanjut pada populasi yang lebih luas.

 

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Brain tumors are a type of tumor that is very difficult to handle and causes severe mortality and morbidity. Currently, the combination of radiotherapy and chemotherapy (temozolomide and other agents), as well as corticosteroids become the primary therapy for various types of tumors, including brain tumors. However, data indicating that the combination of therapy does not provide improvement in the patient's clinical condition. This leads to the need for a new compound search or repurposing existing therapies that can improve the prognosis of brain tumor patients. Metformin, a known antidiabetic agent, has recently been examined by its potential as a antineoplastic. Metformin is responsible for the effects of apoptosis, autophagy, and antiproliferative via the p53 line with adenosine 5’-monophosphate (AMP)-activated protein kinase (AMPK) activation. This article review aims to examine the recent study developments on the effects of metformin in brain tumor patients through its clinical reviews. The literature search is systematically performed on the PubMed, ScienceDirect, and SpringerLink selected based on the defined inclusion and exclusion criteria. The clinical benefits of the drug are assessed through Overall Survival (OS) and Progression Free Survival (PFS) brain tumor patients. Studies have also demonstrated a synergistic effect of metformin combinations with temozolomide, but not with corticosteroids. Through a combination with temozolomide given post radioterapy, the potential of antineoplastic results in better survival. Nonetheless, the efficacy and safety of metformin need further clinical testing in the wider population.

 

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"buku ini membahas tentang bahaya tumor otak dan peranan pencitraan dalam otak."