Colorectal liver metastasis(CRLM) is the major cause of death in patients diagnosed with colorectal cancer. The gold standard treatment of CRLM is surgical rese-ction. Yet, in the past, more than half of these patient...Colorectal liver metastasis(CRLM) is the major cause of death in patients diagnosed with colorectal cancer. The gold standard treatment of CRLM is surgical rese-ction. Yet, in the past, more than half of these patients were deemed unresectable due to the inadequate future liver remnant(FLR). The introduction of efficient portal vein embolization(PVE) preoperatively allowed more resections of metastasis in CRLM patients by stimulating adequate liver hypertrophy. However, several exp-erimental and clinical studies reported tumor progression after PVE which critically influences the subsequent management of these patients. The underlying path-ophysiological mechanism of tumor progression post-PVE is still not fully understood. In spite of the adverse effects of PVE, it remains a potentially curative procedure in patients who would remain otherwise unresectable because of the insufficient FLR. Currently, the challenge is to halt tumor proliferation following PVE in patients who require this technique. This could potentially be achieved by either attempting to suppress the underlying oncologic stimulus or by inhibiting tumor growth once observed after PVE, without jeopardizing liver regeneration. More research is still required to better identify patients at risk of experiencing tumor growth post-PVE.展开更多
文摘Colorectal liver metastasis(CRLM) is the major cause of death in patients diagnosed with colorectal cancer. The gold standard treatment of CRLM is surgical rese-ction. Yet, in the past, more than half of these patients were deemed unresectable due to the inadequate future liver remnant(FLR). The introduction of efficient portal vein embolization(PVE) preoperatively allowed more resections of metastasis in CRLM patients by stimulating adequate liver hypertrophy. However, several exp-erimental and clinical studies reported tumor progression after PVE which critically influences the subsequent management of these patients. The underlying path-ophysiological mechanism of tumor progression post-PVE is still not fully understood. In spite of the adverse effects of PVE, it remains a potentially curative procedure in patients who would remain otherwise unresectable because of the insufficient FLR. Currently, the challenge is to halt tumor proliferation following PVE in patients who require this technique. This could potentially be achieved by either attempting to suppress the underlying oncologic stimulus or by inhibiting tumor growth once observed after PVE, without jeopardizing liver regeneration. More research is still required to better identify patients at risk of experiencing tumor growth post-PVE.
