Kanker pankreas: Perbedaan antara revisi
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| accessdate = 2010-12-07 |
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| work = Department of Pharmacology and Cancer Biology, Department of Medicine, Duke University; Kelly J. Gordon, Kellye C. Kirkbride, Tam How, dan Gerard C. Blobe |
| work = Department of Pharmacology and Cancer Biology, Department of Medicine, Duke University; Kelly J. Gordon, Kellye C. Kirkbride, Tam How, dan Gerard C. Blobe |
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}}</ref> BMP-2, BMP-4 menginduksi [[metaloproteinase matriks-2|MMP-2]] dan aktivitas Panc-1, BMP-7 meningkatkan aktivitas tersebut. Pada kasus adenokarsinoma pankreatik, ekspresi BMP-2, BMPR-2 dan ALK3 mRNA menentukan daya tahan paska bedah. |
}}</ref> BMP-2, BMP-4 menginduksi [[metaloproteinase matriks-2|MMP-2]] dan aktivitas Panc-1, BMP-7 meningkatkan aktivitas tersebut. Pada kasus adenokarsinoma pankreatik, ekspresi BMP-2, BMPR-2 dan ALK3 mRNA menentukan daya tahan paska bedah. Penelitian terakhir menunjukkan peran [[asam retinoat]] untuk meredakan simtoma adenokarsinoma tersebut.<ref>{{en}}{{cite web |
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| url = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2248210 |
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| title = On the role of transforming growth factor-β in the growth inhibitory effects of retinoic acid in human pancreatic cancer cells |
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| accessdate = 2010-12-08 |
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| work = Department of Surgery and Robert H Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Department of Biomedical Sciences, Creighton University, Department of Physiology, Faculty of Medicine and Health Sciences, United Arab Emirates University; Brahmchetna Singh, Richard F Murphy, Xian-Zhong Ding, Alexandra B Roginsky, Richard H Bell, Jr, dan Thomas E Adrian |
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| quote = These results indicate that the amounts of active TGF-β2 generated by the pancreatic cancer cells treated with retinoic acid are capable of mediating its growth inhibitory effects. |
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== Lihat pula == |
== Lihat pula == |
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Revisi per 8 Desember 2010 10.32
| Kanker pankreas | |
|---|---|
 | |
| Informasi umum | |
| Spesialisasi | Onkologi, Gastroenterologi  |
Kanker pankreas adalah neoplasma yang terjadi pada kelenjar pankreas. Klasifikasi terbagi menjadi kanker endokrin dan kanker eksokrin seperti adenokarsinoma, karsinoma adenoskuamus, karsinoma SRC, karsinoma hepatoid, karsinoma koloid, karsinoma tidak terdiferensiasi, karsinoma UOGC.
Pada Panc-1, BMP-4 menginduksi EMT dan peningkatan aktivitas lesi duktular pankreatik serta adenokarsinoma duktular pankreatik.[1] BMP-2, BMP-4 menginduksi MMP-2 dan aktivitas Panc-1, BMP-7 meningkatkan aktivitas tersebut. Pada kasus adenokarsinoma pankreatik, ekspresi BMP-2, BMPR-2 dan ALK3 mRNA menentukan daya tahan paska bedah. Penelitian terakhir menunjukkan peran asam retinoat untuk meredakan simtoma adenokarsinoma tersebut.[2]
Lihat pula
Penyebab
Seperti kasus kanker pada umumnya, karsinogen tercetus oleh sinergis banyak faktor antara lain
- Kebiasaan merokok
- Kurangnya asupan sayur dan buah
- Tingginya asupan daging merah
- Gemuk
- Diabetes mellitus
- Pankreatitis kronis
- Infeksi Helicobacter pylori
- Gingivitis
Rujukan
- ^ (Inggris)"Bone morphogenetic proteins induce pancreatic cancer cell invasiveness through a Smad1-dependent mechanism that involves matrix metalloproteinase-2". Department of Pharmacology and Cancer Biology, Department of Medicine, Duke University; Kelly J. Gordon, Kellye C. Kirkbride, Tam How, dan Gerard C. Blobe. Diakses tanggal 2010-12-07.
- ^ (Inggris)"On the role of transforming growth factor-β in the growth inhibitory effects of retinoic acid in human pancreatic cancer cells". Department of Surgery and Robert H Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Department of Biomedical Sciences, Creighton University, Department of Physiology, Faculty of Medicine and Health Sciences, United Arab Emirates University; Brahmchetna Singh, Richard F Murphy, Xian-Zhong Ding, Alexandra B Roginsky, Richard H Bell, Jr, dan Thomas E Adrian. Diakses tanggal 2010-12-08.
These results indicate that the amounts of active TGF-β2 generated by the pancreatic cancer cells treated with retinoic acid are capable of mediating its growth inhibitory effects.
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