How is liver cancer with portal vein tumor thrombus formed? Learn about liver cancer with portal vein tumor thrombus

One of the factors that greatly affects the prognosis of liver cancer is portal vein cancer thrombosis. This complication is difficult to treat, as most of the therapeutic drugs pass through the arteries and cannot reach the veins. There are two situations in which portal vein cancer thrombosis is formed. One is direct invasion, where the cancer nodules compress the blood vessels, causing cancer cells to enter the portal vein with low pressure from the high-pressure hepatic artery; the second is secondary portal vein blood flow disorder.
The normal liver is supplied by both the portal vein and the hepatic artery. When the diseased liver is compressed by cancerous nodules and the sinusoids become narrow or the central veins are compressed and occluded, the communicating branches of the hepatic artery and portal vein open, and cancer cells enter the relatively low-pressure portal vein system along the high-pressure hepatic artery.

Portal vein cancer thrombosis is a unique phenomenon in the occurrence, development, and metastasis of primary liver cancer (hereinafter referred to as liver cancer). Portal vein cancer thrombosis not only has a high incidence, but is also a major factor affecting the prognosis of liver cancer. The portal vein is the most important blood vessel entering the liver, and portal vein cancer thrombosis can metastasize to the liver. Portal vein cancer thrombosis can easily increase the pressure of the portal vein, accelerate gastric bleeding and liver failure, and is not conducive to interventional treatment, because interventional treatment is transarterial and has no effect on cancer thrombosis in the vein.
The incidence of portal vein tumor thrombus in liver cancer is 40-70%. Liver cancer patients with portal vein tumor thrombus often lose the opportunity for radical surgery because the tumor thrombus spreads to the main trunk of the portal vein or multiple metastases in the liver. Even if there is an opportunity for surgical resection, the postoperative recurrence rate is as high as 60%. The prognosis of patients with hepatocellular carcinoma accompanied by tumor thrombus is very poor. Domestic and foreign reports have shown that if not treated, the patient's survival time is only 2.4~2.7 months; for those who receive systemic chemotherapy, the median survival time is only 3.9~9.2 months; if transcatheter hepatic arterial chemoembolization (TACE) is selectively performed on patients with portal vein main trunk tumor thrombus, the median survival time is 10~12 months; patients with operable tumor thrombus have a slightly longer survival time. However, neither TACE nor surgery is suitable for patients with cancer thrombus that has completely blocked the main trunk of the portal vein, because after the portal vein is blocked, the hepatic artery is embolized again, and the liver is completely lacking in blood supply, causing liver failure.
Mechanism of portal vein tumor thrombosis in liver cancer. For the first time, it was found that regulatory T cells in the liver cancer microenvironment, chemokines in the portal area around the cancer induced liver cancer cells to invade the portal vein in a directional manner, activated platelets enhanced the capture and adhesion of liver cancer cells, and liver cancer cell angiogenic factors induced primary tumors and portal vein tumor thrombosis angiogenesis, etc. are the key mechanisms of portal vein tumor thrombosis in liver cancer, providing a theoretical basis for the formulation of clinical treatment plans. For patients with complete obstruction of the portal vein trunk, radiotherapy should be performed first, followed by TACE; otherwise, TACE should be performed first, followed by radiotherapy. For patients with portal vein trunk and branch tumor thrombosis, after radiotherapy, the tumor thrombosis achieves CR and the portal vein blood flow is unobstructed. At this time, after the patient receives TACE, iodized oil is deposited in the residual tumor lesions in the liver. Therefore, TACE should not be performed completely before radiotherapy. Our experience is that for patients with complete obstruction of the portal vein trunk, radiotherapy should be performed first, followed by TACE; otherwise, TACE should be performed first, followed by radiotherapy. Portal vein tumor thrombosis is related to multiple mechanisms such as anatomy, hemodynamics, and biology.
In addition, hepatocellular carcinoma often invades or metastasizes to the inferior vena cava through the hepatic vein, resulting in the formation of inferior vena cava tumor thrombus. Once the tumor thrombus breaks off, fatal complications such as pulmonary infarction and cerebral infarction may occur. Some reports have shown that patients with inferior vena cava tumor thrombus can remove the tumor thrombus through extracorporeal circulation and hypothermic anesthesia.