The pathogenesis of hepatocellular carcinoma (HCC) is a complex process. During the last decade, advances in genomic technologies enabled delineation of the genomic landscape of HCC, resulting in the identification of the common underlying molecular alterations. The tumor microenvironment, regulated by inflammatory cells, including cancer cells, stromal tissues, and the surrounding extracellular matrix, has been extensively studied using molecular data. The integration of molecular, immunological, histopathological, and clinical findings has provided clues to uncover predictive biomarkers to enhance responses to novel therapies. Herein, we provide an overview of the current HCC genomic landscape, previously identified gene signatures that are used routinely to predict prognosis, and an immune-specific class of HCC. Since biomarker-driven treatment is still an unmet need in HCC management, translation of these discoveries into clinical practice will lead to personalized therapies and improve patient care, especially in the era of targeted and immunotherapies.
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A 54-year old man diagnosed with advanced hepatocellular carcinoma began treatment with sorafenib. After 3 weeks of treatment, he complained of abdominal pain and nausea. Abdominal sonography showed multiple hepatic lesions only. Serum amylase and lipase levels were 35 U/L and 191 U/L, respectively. The patient was diagnosed with sorafenib-induced acute pancreatitis. After 10 days of discontinuing sorafenib he still complained of nausea and loss of appetite. Esophagogastroduodenoscopy showed a large bulging lesion, which was suspected to cause extrinsic compression on the high body of the gastric anterior wall. Computed tomography scan revealed a cystic lesion, 8.3 cm in size, in the pancreatic tail, suggesting a pancreatic pseudocyst. After the withdrawal of sorafenib, systemic chemotherapy with Adriamycin and cisplatin was administered. Four months after the discontinuation of sorafenib, the size of the pancreatic pseudocyst decreased from 8.3 cm to 3 cm. The patient's symptoms were also relieved.
Background/Aim s: The aim of the study is to investigate efficacy and safety of sorafenib
combined with transarterial chemoembolization (TACE) in Child-Pugh (CP) class-B patients
with hepatocellular carcinoma (HCC). Methods A total of 12 CP class-B patients who were initially treated with sorafenib combined
with TACE were retrospectively reviewed. At 14 days after the first TACE, patients were
continuously treated with sorafenib until unacceptable adverse events (AEs) or diseaseprogression.
Consecutive TACEs were also performed, if patients were tolerable. Results Of 12 patients, 8, 3 and 1 patients had CP-score 7, 8, and 9, respectively. The median
overall survival was 85 days. Patients underwent median 2 sessions of TACE (range 1-4) and
the median duration of sorafenib was 48days (range, 12-92 days). Three patients refused
repeated TACEs and 4 patients required delay of the consecutive TACE due to AEs of sorafenib.
Six patients required transient or permanent discontinuation of sorafenib, due to its AEs (grade
1/2 AEs, 2 patients; grade 3/4 AEs, 4 patients). High CP score (score 8/9 vs. 7) was tended to
be association with interruption of sorafenib (P=0.061) and requirement of refusal/ delay of
consecutive TACE (P=0.081). Conclusions Sorafenib combined with TACE were frequently interrupted or delayed in CP
class-B patients, mostly because of its side effects, even though there were not serious. Our
experiences suggest that combination with sorafenib and TACE might interface with each
other due to its side effects in CP class-B patients, especially patients with CP score 8/9 liver
cirrhosis.