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Protein Induced by Vitamin K Absence or Antagonist-II (PIVKA-II), also known as Des-γ-carboxy-prothrombin (DCP), is an abnormal form of prothrombin. Normally, the prothrombin’s 10 glutamic acid residues (Glu) in the γ-carboxyglutamic acid (Gla) domain at positions 6, 7, 14, 16, 19, 20,25, 26, 29 and 32 are γ-carboxylated to Gla by vitamin-K dependent γ- glutamyl carboxylase in the liver and then secreted into plasma. In patients with hepatocellular carcinoma (HCC), γ-carboxylation of prothrombin is impaired so that PIVKA-II is formed instead of prothrombin. PIVKA-II is considered as is an efficient biomarker specific for HCC.

Protein Induced by Vitamin K Absence or Antagonist-II (PIVKA-II), also known as Des-γ-carboxy-prothrombin (DCP), is an abnormal form of prothrombin. Normally, the prothrombin’s 10 glutamic acid residues (Glu) in the γ-carboxyglutamic acid (Gla) domain at positions 6, 7, 14, 16, 19, 20,25, 26, 29 and 32 are γ-carboxylated to Gla by vitamin-K dependent γ- glutamyl carboxylase in the liver and then secreted into plasma. In patients with hepatocellular carcinoma (HCC), γ-carboxylation of prothrombin is impaired so that PIVKA-II is formed instead of prothrombin. PIVKA-II is considered as is an efficient biomarker specific for HCC.

Protein Induced by Vitamin K Absence or Antagonist-II (PIVKA-II), also known as Des-γ-carboxy-prothrombin (DCP), is an abnormal form of prothrombin. Normally, the prothrombin’s 10 glutamic acid residues (Glu) in the γ-carboxyglutamic acid (Gla) domain at positions 6, 7, 14, 16, 19, 20,25, 26, 29 and 32 are γ-carboxylated to Gla by vitamin-K dependent γ- glutamyl carboxylase in the liver and then secreted into plasma. In patients with hepatocellular carcinoma (HCC), γ-carboxylation of prothrombin is impaired so that PIVKA-II is formed instead of prothrombin. PIVKA-II is considered as is an efficient biomarker specific for HCC.

Protein Induced by Vitamin K Absence or Antagonist-II (PIVKA-II), also known as Des-γ-carboxy-prothrombin (DCP), is an abnormal form of prothrombin. Normally, the prothrombin’s 10 glutamic acid residues (Glu) in the γ-carboxyglutamic acid (Gla) domain at positions 6, 7, 14, 16, 19, 20,25, 26, 29 and 32 are γ-carboxylated to Gla by vitamin-K dependent γ- glutamyl carboxylase in the liver and then secreted into plasma. In patients with hepatocellular carcinoma (HCC), γ-carboxylation of prothrombin is impaired so that PIVKA-II is formed instead of prothrombin. PIVKA-II is considered as is an efficient biomarker specific for HCC.

Protein Induced by Vitamin K Absence or Antagonist-II (PIVKA-II), also known as Des-γ-carboxy-prothrombin (DCP), is an abnormal form of prothrombin. Normally, the prothrombin’s 10 glutamic acid residues (Glu) in the γ-carboxyglutamic acid (Gla) domain at positions 6, 7, 14, 16, 19, 20,25, 26, 29 and 32 are γ-carboxylated to Gla by vitamin-K dependent γ- glutamyl carboxylase in the liver and then secreted into plasma. In patients with hepatocellular carcinoma (HCC), γ-carboxylation of prothrombin is impaired so that PIVKA-II is formed instead of prothrombin. PIVKA-II is considered as is an efficient biomarker specific for HCC.

Protein Induced by Vitamin K Absence or Antagonist-II (PIVKA-II), also known as Des-γ-carboxy-prothrombin (DCP), is an abnormal form of prothrombin. Normally, the prothrombin’s 10 glutamic acid residues (Glu) in the γ-carboxyglutamic acid (Gla) domain at positions 6, 7, 14, 16, 19, 20,25, 26, 29 and 32 are γ-carboxylated to Gla by vitamin-K dependent γ- glutamyl carboxylase in the liver and then secreted into plasma. In patients with hepatocellular carcinoma (HCC), γ-carboxylation of prothrombin is impaired so that PIVKA-II is formed instead of prothrombin. PIVKA-II is considered as is an efficient biomarker specific for HCC.

Protein Induced by Vitamin K Absence or Antagonist-II (PIVKA-II), also known as Des-γ-carboxy-prothrombin (DCP), is an abnormal form of prothrombin. Normally, the prothrombin’s 10 glutamic acid residues (Glu) in the γ-carboxyglutamic acid (Gla) domain at positions 6, 7, 14, 16, 19, 20,25, 26, 29 and 32 are γ-carboxylated to Gla by vitamin-K dependent γ- glutamyl carboxylase in the liver and then secreted into plasma. In patients with hepatocellular carcinoma (HCC), γ-carboxylation of prothrombin is impaired so that PIVKA-II is formed instead of prothrombin. PIVKA-II is considered as is an efficient biomarker specific for HCC.

Protein Induced by Vitamin K Absence or Antagonist-II (PIVKA-II), also known as Des-γ-carboxy-prothrombin (DCP), is an abnormal form of prothrombin. Normally, the prothrombin’s 10 glutamic acid residues (Glu) in the γ-carboxyglutamic acid (Gla) domain at positions 6, 7, 14, 16, 19, 20,25, 26, 29 and 32 are γ-carboxylated to Gla by vitamin-K dependent γ- glutamyl carboxylase in the liver and then secreted into plasma. In patients with hepatocellular carcinoma (HCC), γ-carboxylation of prothrombin is impaired so that PIVKA-II is formed instead of prothrombin. PIVKA-II is considered as is an efficient biomarker specific for HCC.

Protein Induced by Vitamin K Absence or Antagonist-II (PIVKA-II), also known as Des-γ-carboxy-prothrombin (DCP), is an abnormal form of prothrombin. Normally, the prothrombin’s 10 glutamic acid residues (Glu) in the γ-carboxyglutamic acid (Gla) domain at positions 6, 7, 14, 16, 19, 20,25, 26, 29 and 32 are γ-carboxylated to Gla by vitamin-K dependent γ- glutamyl carboxylase in the liver and then secreted into plasma. In patients with hepatocellular carcinoma (HCC), γ-carboxylation of prothrombin is impaired so that PIVKA-II is formed instead of prothrombin. PIVKA-II is considered as is an efficient biomarker specific for HCC.