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Liver Cancer

1. Overview
Cancer is one of the most threaten disease in the world health. WHO in its press release April 3rd 2003 claimed that top five cancers in the world are lung cancer, breast cancer, colorectal cancer, gastric cancer, and liver cancer. In November 2004 has reported that liver cancer is cancer with the fastest growth between the other kinds of cancer in United State (Kerr, 2004). Liver cancer incidence in South Asia, Southeast Asia, China, and Sub Sahara area is personally higher that liver cancer in industrial country like (Anonim, 2004). Cells in the liver will multiply to replace the damaged cells due to injury or they have been old. As with other cells formation process in the body, this process is also controlled by certain genes in the cells. Liver cancer comes from one cell undergoing change control mechanism in the cells resulting in uncontrolled cells division. Abnormal cells will form million copies, namely clone. They cannot do the normal function of liver cells and multiply continuously. These abnormal cells will produce tumor (Anonim, 2004).
Liver cancer can begin from hepatic organs (hepatocellular cancer) or also can derive from other organ, for example from colon that spread in the liver (metastatic liver cancer). Cancer that come from liver organ often called as liver cancer and include the type of cancer the fifth that have the most incidence in the world. Disease that often connect with liver cancer there are hepatitis virus and liver cirrhosis. (Bruix dan Sherman., 2005).
Benign liver tumor that often be found is hemangiomas (namely group of abnormal blood vessel that swollen), and adenomas (namely group or lump of liver tissue). Whereas liver cancer that often happens is hepatocellular carcinoma (HCC), (80% cases) that appears from its own liver cells and known as hematoma.

Cholangiocarcinoma (15% cases) derived from biliary glands in liver. Tumor klatskin is  cholangiocarcinoma that located in frontier between bile and liver. Liver cancer that seldom happen are angiocarcinoma (derived from blood vessel in liver), Lymphomas (derived from immune cells in liver), and carcinoids (derived from hormone that is made by liver cells) (Anonim, 2004).

2. Cause

The cause oflivercancerin general are hepatitis B and C virus infection, contamination, aflatoxin B1, liver cirrhosis, parasitic infection, alcohol, also heredity (Fong, 2002) . The hepatitis B and C virus infection causes the main liver cancer in the world, especially patient with antigemia and also has chronic disease hepatitis. Male patient with age more than 50 years who suffered in hepatitis B and C disease have big possibility contracting liver cancer. (Tsukuma dkk., 1993; Mor dkk., 1998) . The liver cancer symptom initially without complaint or just little complaint likes lethargic, decreased appetite, and weigh loss. Liver cancer can be known with diagnose using radiology, liver biopsy, and serology. (Bruix dan Sherman, 2005).

3. Risk Fact
Various fact risk cause liver cancer, there are:
a. The chronic hepatitis can cause changes in cancer cells that connected with the most common   of the type of liver cancer is hematoma. Usually it is caused by hepatitis B and carcinogen (chemical substance that inducting cancer) like aflatoksin.
b. Liver cirrhosis commonly caused by alcohol, hemochromatosis, Alpha 1-antitrypsin deficiency.
c. Miscellaneous irritant like polyvinyl chloride, thorotrast, and radiation.
(Anonim, 2004)

4. Stadium
Liver cancer has some growth stadium that are: (a) stadium 1, size of cancer no more than 2 cm and has no spread. In this stadium, liver cancer patient can activity and life normally, (b) stadium 2, cancer affect the blood vessel in liver or more than one tumor in liver, (c) stadium 3A, size of cancer more than 5 cm and has spread in the blood vessel near the liver, (d) stadium 3B, cancer has spread to nearby organs like gastric but not reached the lymph nodes, (e) stadium 3C, cancer in various size and has reached lymph nodes, (f) stadium 4, cancer has spread to distant organ from liver like lungs. At this stadium, liver cancer patient cannot take an activity again (Fong, 2002; Bruix dan Sherman., 2005) .

5. Cancer molecular mechanism
Enhancement or reduction of protein expression seldom happens in liver cancer case. Protein that has up-regulation like COX-2 (Qiu dkk., 2002) , cells cycle protein, growth factor, and anti-apoptosis protein (King, 2000) . The enhancement expression and or mutation in N-ras are also found in liver cancer (Adjei, 2001). Moreover also happens aneuploidi and genetic change like mutation p53 in liver cancer (Kim dan Wang, 2003).
In HCC has been known there was mutated Ras, but relative different with other cancer like colorectal cancer (Macdonald dan Ford, 1997) . Excessive ras expression can increase the number of Myc in all cases in HCC and give impression that these 2 oncogene can collaborate each other (Macdonald dan Ford, 1997) . The gene can be affect by virus infection of Hepatitis B and Hepatitis C. It give impression that that gene can be activated by specific virus (Macdonald dan Ford, 1997) .
Cancer kinetic study, find there were various kind of oncogene that play a role in carcinogenesis in the liver. The N-ras and c-myc over-expression by carcinogen compound is genetic abnormality that seldom happens in cancer (Peters dan Vousden, 1997). CYP1A2 in the liver has been known can activate pro-carcinogen compound (benzo(a)pyrene) to be reactive intermediate that interact with cellular nucleofil and eventually lead to carcinogenesis characterized by the occurred of over-expression N-Ras and c-myc (Kawajiri et al., 1993).
Also founded a high incidence in specific codon mutation point in p53 a suppressor gene  tumor, in hepatocellular that epidemiologically linked with aflatoxin [16] (Underwood, 1996). Mutation in p53 is the main cause of liver cancer in South Asia and Southeast Asia (King, 2000) .

6. Prevention

7. Treatment
The treatment that has been done until now was using chemotherapy with sitostatic medicine like 5-Fluorourasil intra-arterial, embolization, radio-immunotherapy and surgery. Patient who did not undergo therapy usually die within the duration of 3-4 months, whereas patient treated maybe can life 6-18 months if the therapy is going well (Anonim, 2001). One of the effective way to reduce liver cancer frequency is with immunization Hepatitis B. Country with good immunization Hepatitis B program shown to decrease the incidence of liver cancer with real (Anonim, 2003).

8. References

Adjei, Alex A., 2001, Review: Blocking Oncogenic Ras Signaling for Cancer Therapy, J. Nat. Canc. Inst., 93(14), 1062-1074

Anonim, 2001, Introduction to Liver Cancer, http://www.oncolink.org diakses pada tgl 7 Nopember 2004.

Anonim, 2003, Primary Liver Cancer, http://www.cancerbacup.org.uk diakses pada 20 tgl Nopember 2004.

Anonim, 2005, Liver Cancer, http:/www.cancer.org, diakses pada tanggal 11 Mei 2005.

Bruix, S dan Sherman, M., 2005. Management of Hepatocelluler Carcinoma, Hepatology, 42, 5.

Fong, Tse-Ling, 2002. Hepatocellular Carcinoma (Liver Cancer), dalam www.medicinet.com, September 2007

Kawajiri, K., Nakachi, K., Imai, K., Watanabe, J and Hayashi, S (1993) The CYP1A1 gene and cancer susceptibility. Crit Rev Oncol Hematol 14:77-87.

Kerr, M., 2004, Liver Cancer Fastest Growing Cancer in US, http//:www.nlm.nih.gov diakses pada tgl 2 Desember 2004.

Kim, J.W. dan Wang, X.W., 2003, Gene Expression Profilling of Preneoplastic Liver Desease and Liver Cancer: a new era for imptoved early detection and treatment of these deadly diseases?, Carcin, 24(3), 363-369.

King, R.J.B., 2000, Cancer Biology, 2nd Ed., Pearson Eduation Limited, London.

Macdonald, F., Ford C.H.J., 1997. Molecular Biology of Cancer. Bio Scientific Publisher, Oxford, United Kingdom.

Mor, E., Kaspa, R.T., Sheiner, P dan Schwartz, M., 1998, Treatment of Hepatocellular Carcinoma Associated with Cirrhosis in the Era of Liver Transplantation, Annals Med Rev, 129(8), 643-653.

Qiu, D., Ma, Xiong, Peng, Y., dan Chen, X., 2002, Significance of Cyclooxygenase-2 Expression in Human Primary Hepatocellular Carcinoma, J. Gastroenterol., 8(5), 815-817

Peters, Gordon., dan Vousden, K.H., 1997, Oncogenes dan Tumor Supressors, Oxford University Press, New York.

Tsukuma, H., Hiyama,T., Tanaka, S., Nakao, M., Yabuuchi, T., Kitamura, T., Nakanishi, K., Fujimoto, I., Inoue, A., yamakazi, H & Kawashima, T., 1993, Risk Factors for Hepatocellular Carcinoma among Patients with Chronic Liver Disease, The New England J of Med., 328(25), 1797-1801.

Underwood, J.C.E., 1999, Patologi Umum dan Sistematik (General and Systematic Pathology), Edisi 2, Vol.1, Editor Sarjadi, Penerbit Buku Kedokteran (EGC), Jakarta.

9.Kontributor
Fithriyatun Nisa, Ilyas Pratomo, Perdana Adi Nugroho dan Adam Hermawan