Hepatocellular adenoma (HCA) represents a rare benign hepatic neoplasm with potential for malignant transformation into hepatocellular carcinoma (HCC), yet the underlying mechanism remains elusive. In this study, we investigated the genomic landscape of this process to identify therapeutic strategies for blocking malignant transformation. Using micro-detection techniques, we obtained specimens of adenoma, cancerous neoplasm and adjacent normal liver from three patients undergoing hepatic resection surgery. Whole-exome sequencing (WES) was performed, and genomic interactions between HCA and HCC components within the same tumour were evaluated using somatic variant calling, copy number variation (CNV) analysis, clonality evaluation and mutational signature analysis. Our results revealed genomic heterogeneity among patient cases, yet within each sample, HCA and HCC tissues exhibited a similar mutational landscape, suggesting a high degree of homology. Using nonnegative matrix factorization and phylogenetic trees, we identified shared and distinct mutational characteristics and uncovering necessary pathways associated with HCA-HCC malignant transformation. Remarkably, we found that HCA and HCC shared a common monoclonal origin while displaying significant genetic diversity within HCA-HCC tumours, indicating fundamental genetic connections or evolutionary pathways between the two. Moreover, elevated immune therapy-related markers in these patients suggested heightened sensitivity to immune therapy, providing novel avenues for the treatment of hepatic malignancies. This study sheds light on the genetic mechanisms underlying HCA-HCC progression, offering potential targets for therapeutic intervention and highlighting the promise of immune-based therapies in managing hepatic malignancies.

METHODS: Hepatocellular adenoma (HCA) is a benign monoclonal tumour that originates from mature hepatocytes.Liver resection is recommended in case of overt malignant transformation to hepatocellular carcinoma.However, hepatobiliary surgeries are technically challenging in patients with giant HCA (GHCA) owing to the risk of catastrophic intraoperative bleeding and difficulty with its control during laparoscopic treatment. We present a technical note on the utilization of the hepatic vein as anatomical landmarks for laparoscopic removal of giant hepatic glands, without intraoperative ultrasonography and with the aid of an augmented reality navigation system during surgery.
RESULTS: This video shows aA 37-year-old man was recommended treatment for a progressively increasing HCA (from 3 to 10 cm in a year) involving the right hepatic vein (RHV), inferior vena cava (IVC) and middle hepatic vein (MHV), resulting in the invisibility of the above intrahepatic anatomic markers in CT. Laparoscopic hepatectomy was performed using the hepatic vein as anatomic markers in a treatment centre specialising in minimally invasive surgeries. The procedure involved fully mobilising the right liver, transecting the parenchyma along the demarcation line in the caudal-to-cranial direction, exposing the involved caudal MHV, isolating and transecting the involved RHV and preserving the integrity of the involved IVC.
CONCLUSIONS: Laparoscopic hepatectomy for intractable GHCA using the involved intrahepatic anatomic markers is feasible and effective. It reduces pre-operative haemorrhage and open conversion rates while maximising postoperative hepatic function.

Objective: To investigate the MRI imaging features of hepatocyte nuclear factor 1α- inactivated hepatocellular adenoma (H-HCA). Methods: Clinical data and MRI images of 19 H-HCA cases who were pathologically confirmed at Zhongshan Hospital Affiliated to Fudan University between August 2014 and July 2020 were retrospectively analyzed. Among them, there were 15 females and 4 males, aged 16-47 (32± 7) years old. Tumor number, location, shape, size, boundary, MRI plain scan signal intensity, dynamic enhancement features of each phase, presence or absence of intratumoral fat content, pseudocapsule, and others were analyzed. The differences in apparent diffusion coefficient (ADC) values between the lesion and the surrounding normal liver parenchyma were compared for statistical significance. t-test was used for statistical analysis. Results: There were a total of 24 lesions in 19 cases. 14 cases had solitary lesions, and five cases had multiple lesions. 15 and nine lesions were located in the right and left lobes of the liver, respectively. 20 lesions were round or quasi-round, and four were irregular or lobulated. The tumor\'s maximal diameter was 0.6-8.6 (3.5 ± 2.4) cm. T(1)-weighted image (WI) showed hyperintense to iso-intense signals in 20 lesions and hypointense signals in four. T(2)WI showed iso-to-slightly high signal intensity in 16 lesions, with two hyperintense and six hypointense signals. Diffusion-weighted image (DWI) revealed hyperintense to iso-intense signals. Lesions mean ADC value was (1.289 ± 0.222)×10(-3) mm(2)/s, while the adjacent normal liver parenchyma\'s mean ADC value was (1.307 ± 0.236)×10(-3) mm(2)/s, with no statistically significant difference between the two (P > 0.05). During the arterial phase, 15 of the 18 lesions that underwent dynamic contrast-enhanced scanning with gadoxetate disodium (Gd-DTPA) were mildly to moderately enhanced and three were strongly enhanced. The portal and hepatic venous phases had no continuous enhancement, while the delayed phase showed a hypointense signal. During the arterial phase, two of the six lesions scanned by gadolinium ethoxybenzyl diethylenetriamine pentaacetic acid ((Gd-EOB-DTPA) dynamic enhancement were mildly to moderately enhanced, while four were strongly enhanced. The portal and hepatic venous phases had no continuous enhancement, while the transition and hepatobiliary-specific phases showed hypointense signals. Intracellular steatosis occurred in 21 lesions, of which 19 were diffuse steatosis and 16 formed pseudocapsules in the delayed phase. Conclusion: H-HCA often occurs in young females as solitary lesions and has certain MRI features. T1WI anti-phase diffuse signal reduction and post-enhanced hypovascular withdrawal enhancement patterns can aid in accurately diagnosing the disease condition.
目的： 探讨肝细胞核因子1α失活型肝细胞腺瘤（H-HCA）的MRI影像特征。 方法： 回顾性分析复旦大学附属中山医院2014年8月至2020年7月经病理证实的19例H-HCA患者的临床资料及MRI图像，其中女性15例，男性4例，年龄16～47（32±7）岁；分析肿瘤数目、部位、形态、大小、边界，MRI平扫信号强度、动态增强各期强化特点，肿瘤内有无脂肪及其含量、假包膜等，比较病灶及其周围正常肝实质的表观扩散系数（ADC）值差异有无统计学意义。计量资料采用配对样本t检验。 结果： 19例患者共24枚病灶，14例单发，5例多发；位于肝右叶15枚、左叶9枚；20枚呈圆形及类圆形，4枚呈不规则或分叶状；肿瘤最大直径为0.6～8.6（3.5±2.4）cm。20枚病灶T(1)加权成像（WI）呈等及高信号，4枚呈低信号；16枚病灶T(2)WI呈等及稍高信号，2枚呈高信号，6枚呈低信号；弥散加权成像（DWI）均呈等及高信号；病灶的平均ADC值为（1.289±0.222）×10(-3) mm(2)/s，邻近正常肝实质平均ADC值为（1.307±0.236）×10(-3) mm(2)/s，两者差异无统计学意义(P>0.05)。行钆喷酸葡甲胺（Gd-DTPA）动态增强扫描的18枚病灶，动脉期呈轻中度强化15枚，高度强化3枚，门静脉期、肝静脉期无持续性强化，延迟期均呈低信号；行钆塞酸二钠（Gd-EOB-DTPA）动态增强扫描的6枚病灶，动脉期呈轻中度强化2枚，高度强化4枚，门静脉期、肝静脉期无持续性强化，移行期及肝胆特异期均呈低信号。21枚病灶发生细胞内脂肪变性，其中19枚弥漫性脂肪变性；16枚病灶延迟期形成假包膜。 结论： H-HCA好发于青年女性，常单发，具有一定特征性MRI特征；T(1)WI反相位弥漫性信号减低及增强后低血供退出型强化模式可有助于疾病的正确诊断。.

Hepatocellular adenomas (HCAs) are rare benign tumors of the liver that occur predominantly in women taking oral contraceptives. In children, HCAs comprise < 5% of hepatic tumors. We report a case of HCAs in a 7-year-old girl with estrogen and glucose imbalance.
A 7-year-old girl was presented to our hospital with bilateral breast enlargement for 2 months, polydipsia, polyuria, polyphagia, hyperglycemia, and significant weight gain. Computed tomography (CT) showed a 7.2 cm×6.9 cm×5.3 cm round-shaped mass in the left inner lobe of the liver, ovarian ultrasound showed multiple follicles in the ovaries bilaterally, and cranial magnetic resonance imaging (MRI) showed an enlarged superior pituitary. Hematological and biochemical results were as follows: fasting glucose was 19.7 mmol/L, estradiol was 122.9 pmol/L, follicle-stimulating hormone 10.81 IU/L, luteinizing hormone 10.99 IU/L, insulin-like growth factor 1,513 ng/mL, glutamine aminotransferase 86 U/L, and alkaline phosphatase 362 U/L. Thyroid functions, methemoglobin, fetal protein, carcinoembryonic antigen, and chorionic gonadotropin were normal. The patient had a complete surgical resection of the liver tumor, and the postoperative histopathological diagnosis was HCAs. After the surgery, insulin was injected and the glucose levels were stable. During the 36-month follow-up period, neither tumor recurrence nor significant abnormalities were detected using color Doppler ultrasound of the liver. The child\'s precocious puberty is currently under control.
HCAs are particularly rare in children with liver tumors, and risk factors for the development of HCAs in children include sex hormone imbalance, obesity, Fanconi anemia (FA), glycogen storage diseases (GSDs) type I, III, and IV, galactosemia, immunodeficiency, congenital portosystemic shunts (CPSS), cardiac hepatopathy status-post Fontan procedure, Hurler syndrome, familial adenomatous polyposis, germline HNF1A mutations, and maturity-onset diabetes of the young type 3. Most HCAs are detected during a physical examination without clinical symptoms, and some patients may present with symptoms such as abdominal pain, abdominal distension, and abdominal masse. Serum liver function tests can show increased alkaline phosphatase (ALP) and γ- glutamyl transferase (GT), whereas α-Fetoprofein (AFP) levels are normal. The definitive diagnosis relies mainly on histopathological examination. Because HCAs can rupture and bleed and become malignant. Early surgical treatment is recommended after detection.

The World Federation for Ultrasound in Medicine and Biology (WFUMB) is addressing the issue of incidental findings (IFs) with a series of publications entitled \"Incidental imaging findings-the role of ultrasound\". IFs in the liver of newborns and children are rare and much less commonly encountered than in adults; as a result, they are relatively much more frequently malignant and life-threatening, even when they are of benign histology. Conventional B-mode ultrasound is the well-established first line imaging modality for the assessment of liver pathology in pediatric patients. US technological advances, resulting in image quality improvement, contrast-enhanced ultrasound (CEUS), liver elastography and quantification tools for steatosis have expanded the use of ultrasound technology in daily practice. The following overview is intended to illustrate incidentally detected liver pathology covering all pediatric ages. It aims to aid the examiner in establishing the final diagnosis. Management of incidentally detected focal liver lesions (FLL) needs to take into account the diagnostic accuracy of each imaging modality, the patient\'s safety issues (including ionizing radiation and nephrotoxic contrast agents), the delay in diagnosis, the psychological burden on the patient and the cost for the healthcare system. Moreover, this paper should help the pediatric clinician and ultrasound practitioner to decide which pathologies need no further investigation, which ones require interval imaging and which cases require further and immediate diagnostic procedures.

Focal nodular hyperplasia (FNH) is a solid benign tumor of the liver, predominantly in young women. A correct diagnosis of FNH is essential for making appropriate clinical decisions and avoiding unnecessary liver resection. Herein, we reported that two male cases with FNH, who initially presented with persistent abdominal discomfort, were misdiagnosed with hepatocellular adenoma (HCA) and hepatocellular carcinoma (HCC) on contrast-enhanced magnetic resonance imaging and computed tomography scans, respectively. After surgery, a histological diagnosis of FNH was finally established. In this paper, we also reviewed the knowledge regarding diagnosis and differential diagnosis of FNH on imaging examinations, which are helpful for avoiding misdiagnoses and guiding clinical interventions.

To evaluate the value of a radiomics nomogram for preoperative differentiating hepatocellular adenoma (HCA) from hepatocellular carcinoma (HCC) in the noncirrhotic liver.
One hundred and thirty-one patients with HCA (n = 46) and HCC (n = 85) were divided into a training set (n = 93) and a test set (n = 38). Clinical data and CT findings were analyzed. Radiomics features were extracted from the triphasic contrast CT images. A radiomics signature was constructed with the least absolute shrinkage and selection operator algorithm and a radiomics score was calculated. Combined with the radiomics score and independent clinical factors, a radiomics nomogram was developed by multivariate logistic regression analysis. The performance of the radiomics nomogram was assessed by calibration, discrimination and clinical usefulness.
Gender, age, and enhancement pattern were the independent clinical factors. Three thousand seven hundred and sixty-eight features were extracted and reduced to 7 features as the optimal discriminators to build the radiomics signature. The radiomics nomogram (area under the curve [AUC], 0.96; 95% confidence interval [CI], 0.93-0.99) and the clinical factors model (AUC, 0.93; 95%CI, 0.88-0.99) showed better discrimination capability (p = 0.001 and 0.047) than the radiomics signature (AUC, 0.83; 95%CI, 0.74-0.92) in the training set. In the test set, the radiomics nomogram (AUC, 0.94; 95%CI, 0.87-1.00) performed better (p = 0.013) than the radiomics signature (AUC, 0.75; 95%CI, 0.59-0.91). Decision curve analysis showed the radiomics nomogram outperformed the clinical factors model and the radiomics signature in terms of clinical usefulness.
The CT-based radiomics nomogram has the potential to accurately differentiate HCA from HCC in the noncirrhotic liver.

OBJECTIVE: Mutations in hepatocyte nuclear factor 1α (HNF1α) are the cause of maturity-onset diabetes of the young type 3 (MODY3) and involved in the development of hepatocellular adenoma and abnormal lipid metabolism. Previously, we have found that the serum microRNA (miR)-122 levels in MODY3 patients were lower than those in type 2 diabetes mellitus and healthy controls. This study aimed to investigate the mechanism of decreased miR-122 levels in patients with MODY3 and whether low levels of miR-122 mediate tumorigenesis and abnormal lipid metabolism associated with HNF1α deficiency in human hepatocytes.
METHODS: The expression of miR-122 was examined by real-time PCR. Dual-luciferase reporter assay was performed to confirm the transcriptional regulation of miR-122 by HNF1α. HepG2 cells were transfected with siRNA or miRNA mimic to downregulate or upregulate the expression of HNF1α or miR-122, respectively. CCK-8 and colony formation assay were used to determine cell proliferation. Lipid accumulation was examined by Oil Red O staining and intracellular triglyceride and cholesterol quantification assays.
RESULTS: HNF1α regulated the expression of miR-122 by directly binding to its promoter. Knockdown of HNF1α in HepG2 cells reduced the expression of miR-122, increased proliferation and promoted intracellular cholesterol accumulation. Overexpression of miR-122 partially rescued the phenotypes associated with HNF1α deficiency in human hepatocytes. Mechanistically, HNF1α modulated cholesterol homeostasis via miR-122-dependent activation of sterol regulatory element-binding protein-2 (SREBP-2) and regulation of proprotein convertase subtilisin/kexin type 9 (PCSK9). Moreover, circulating miR-122 levels were associated with serum cholesterol levels.
CONCLUSIONS: Loss of HNF1α function led to hepatocyte proliferation and abnormal cholesterol metabolism by downregulating miR-122. Our findings revealed a novel mechanism that low levels of miR-122 mediate tumorigenesis and abnormal lipid metabolism associated with MODY3. MiR-122 may be a potential therapeutic target for the treatment of MODY3.

BACKGROUND: Focal nodular hyperplasia (FNH) has very low potential risk, and a tendency to spontaneously resolve. Hepatocellular adenoma (HCA) has a certain malignant tendency, and its prognosis is significantly different from FNH. Accurate identification of HCA and FNH is critical for clinical treatment.
OBJECTIVE: To analyze the value of multi-parameter ultrasound index based on logistic regression for the differential diagnosis of HCA and FNH.
METHODS: Thirty-one patients with HCA were included in the HCA group. Fifty patients with FNH were included in the FNH group. The clinical data were collected and recorded in the two groups. Conventional ultrasound, shear wave elastography, and contrast-enhanced ultrasound were performed, and the lesion location, lesion echo, Young\'s modulus (YM) value, YM ratio, and changes of time intense curve (TIC) were recorded. Multivariate logistic regression analysis was used to screen the indicators that can be used for the differential diagnosis of HCA and FNH. A ROC curve was established for the potential indicators to analyze the accuracy of the differential diagnosis of HCA and FNH. The value of the combined indicators for distinguishing HCA and FNH were explored.
RESULTS: Multivariate logistic regression analysis showed that lesion echo (P = 0.000), YM value (P = 0.000) and TIC decreasing slope (P = 0.000) were the potential indicators identifying HCA and FNH. In the ROC curve analysis, the accuracy of the YM value distinguishing HCA and FNH was the highest (AUC = 0.891), which was significantly higher than the AUC of the lesion echo and the TIC decreasing slope (P < 0.05). The accuracy of the combined diagnosis was the highest (AUC = 0.938), which was significantly higher than the AUC of the indicators diagnosing HCA individually (P < 0.05). This sensitivity was 91.23%, and the specificity was 83.33%.
CONCLUSIONS: The combination of lesion echo, YM value and TIC decreasing slope can accurately differentiate between HCA and FNH.

BACKGROUND: Hepatocellular adenoma (HCA) is very rare and has a high misdiagnosis rate through clinical and imaging examinations. We report a case of giant HCA of the left liver in a young woman that was diagnosed by medical imaging and pathology.
METHODS: A 21-year-old woman was admitted to our department for a giant hepatic tumor measuring 22 cm × 20 cm × 10 cm that completely replaced the left hepatic lobe. Her laboratory data only suggested mildly elevated liver function parameters and C-reactive protein levels. A computed tomography (CT) scan showed mixed density in the tumor. Magnetic resonance imaging (MRI) of the tumor revealed a heterogeneous hypointensity on T1-weighed MR images and heterogeneous hyperintensity on T2-weighed MR images. On dynamic contrast CT and MRI scans, the tumor presented marked enhancement and the subcapsular feeding arteries were clearly visible in the arterial phase, with persistent enhancement in the portal and delayed phases. Moreover, the tumor capsule was especially prominent on T1-weighted MR images and showed marked enhancement in the delayed phase. Based on these imaging manifestations, the tumor was initially considered to be an HCA. Subsequently, the tumor was completely resected and pathologically diagnosed as an HCA.
CONCLUSIONS: HCA is an extremely rare hepatic tumor. Preoperative misdiagnoses were common not only due to the absence of special clinical manifestations and laboratory examination findings, but also due to the clinicians\' lack of practical diagnostic experience and vigilance in identifying HCA on medical images. Our case highlights the importance of the combination of contrast-enhanced CT and MRI in the preoperative diagnosis of HCA.