Management of Primary Liver Cancers

The first check is whether the background liver is cirrhotic or, from vertical hepatitis B or C transmission, essentially normal; a normal liver allows extended resection with portal vein embolisation to grow the future remnant. On a cirrhotic background, the priority is ruling out disease outside the liver, then grading any portal vein invasion from VP1 (a segmental branch) to VP4 (the main portal vein). Patients with VP1 or VP2 involvement and no extrahepatic disease can still be offered transplant, upfront or after downstaging with TACE, sometimes combined with SBRT for a portal vein tumour thrombus, aiming for 12 weeks of stable disease.

Non-cirrhotic HCC is uncommon in Dr. George's own caseload, around 5 patients in every 100 he sees, but for exactly this group his unit is far more aggressive: extended resections, portal vein embolisation, and even ALPPS, a staged hepatectomy, are all options, because a normal liver can lose as much as 80 percent of its volume and still regenerate enough function from what remains.

HCC has a characteristic imaging signature, so biopsy is reserved for genuine diagnostic dilemmas. An arterially enhancing lesion with venous washout on a properly phased triphasic CT is treated as diagnostic in around 95 percent of cases; MRI is used when the CT is inconclusive. Around 40 percent of HCC patients have an elevated AFP, meaning 60 percent do not, so diagnosis relies on radiology rather than tumour markers.

No. Dr. George has operated on perihilar cholangiocarcinoma patients with bilirubin as high as 30 to 35. Surgical practice has also evolved: where extended resections once left only the left lateral section or right posterior sector achievable, his unit now more often does a left- or right-with-caudate resection with extended bile duct resection, preserving more liver parenchyma. Preoperative biliary drainage, usually percutaneous (PTBD) rather than endoscopic nasobiliary drainage, is reserved for patients with cholangitis or those planned for portal vein embolisation.

Alpha-fetoprotein is the marker primarily elevated in hepatocellular carcinoma. CA19-9 comes primarily from the biliary system and can rise somewhat in cirrhotic patients, but not to a high degree, so it remains the more specific marker for cholangiocarcinoma.

Primary liver cancers arise from two different cell types. Hepatocellular carcinoma (HCC) develops from hepatocytes and accounts for 80 to 85 percent of cases, with a particularly high burden in East Asia and North Africa. Cholangiocarcinoma develops from cholangiocytes, the cells lining the bile ducts, and accounts for the remaining 10 to 15 percent, split between intrahepatic and perihilar (Klatskin) tumours by where they arise.

Primary liver cancers originate in the liver's own hepatocytes or bile duct cells. Liver metastases, by contrast, are secondary cancers that have spread to the liver from elsewhere, commonly the colon, breast or neuroendocrine tumours, and are in practice the most frequently seen liver tumours. The distinction matters because the diagnostic and treatment pathway for primary liver cancer is entirely different.

Perihilar cholangiocarcinomas sit at the junction of the right and left hepatic ducts, the main channels through which bile drains, so they obstruct bile flow and cause jaundice early, bringing patients to diagnosis sooner. Intrahepatic tumours arise peripherally within the liver and tend to grow silently as mass forming lesions, which is why they are usually found later and carry a poorer prognosis.

HCC is staged using the Barcelona Clinic Liver Cancer (BCLC) system. Cholangiocarcinoma uses the Bismuth-Corlette classification for perihilar tumours and the AJCC system more broadly, both of which shape which patients are candidates for surgery and which need a different approach.