Hepatic splenosis is an uncommon condition that occurs following traumatic splenic rupture or splenectomy. The case of a 41-year-old male patient with multiple isolated liver masses indistinguishable from primary and metastatic liver tumours is reported. Following laparotomy, the liver lesions were resected and histopathology confirmed a diagnosis of hepatic splenosis. At an 18-month follow-up examination, no abnormalities in routine blood test, liver function, and liver computed tomography (CT) scanning were observed. After review of the literature, the following diagnostic criteria for hepatic splenosis are proposed: (1) a history of splenic trauma or splenectomy; (2) lesion(s) with a surrounding rim, particularly near the liver capsule identified by CT scanning; (3) findings on superparamagnetic iron oxide-enhanced magnetic resonance imaging or technetium-99m heat-damaged red cell scanning; and (4) histopathological findings (needle biopsy or surgical pathology). The following diagnostic process is also proposed: suspect diagnosis when criteria 1 and 2 are met; make diagnosis when criterion 3 is met; confirm diagnosis when criterion 4 is met. Laparotomy is recommended for either diagnosis or treatment when invasive procedures are necessary.

Cancer stem cells (CSCs) are associated with tumor progression, recurrence, and therapeutic resistance. To maintain their pool while promoting tumorigenesis, CSCs divide asymmetrically, producing a CSC and a highly proliferative, more differentiated transit‐amplifying cell. Exhausting the CSC pool has been proposed as an effective antitumor strategy; however, the mechanism underlying CSC division remains poorly understood, thereby largely limiting its clinical application. Here, through cross‐omics analysis, yin yang 2 (YY2) is identified as a novel negative regulator of CSC maintenance. It is shown that YY2 is downregulated in stem‐like tumor spheres formed by hepatocarcinoma cells and in liver cancer, in which its expression is negatively correlated with disease progression and poor prognosis. Furthermore, it is revealed that YY2 overexpression suppressed liver CSC asymmetric division, leading to depletion of the CSC pool and decreased tumor‐initiating capacity. Meanwhile, YY2 knock‐out in stem‐like tumor spheres caused enrichment in mitochondrial functions. Mechanistically, it is revealed that YY2 impaired mitochondrial fission, and consequently, liver CSC asymmetric division, by suppressing the transcription of dynamin‐related protein 1. These results unravel a novel regulatory mechanism of mitochondrial dynamic‐mediated CSCs asymmetric division and highlight the role of YY2 as a tumor suppressor and a therapeutic target in antitumor treatment.

BACKGROUND Brain metastasis from intrahepatic cholangiocarcinoma is rare. To the best of our knowledge, only a few cases have been reported. The biological behavior was complex, and treatment requires further investigation. CASE SUMMARY A 62-year-old woman complained of left limb weakness. Abdominal computed tomography showed a 5.0 cm × 5.6 cm lesion in the left lobe of the liver. Tumor markers were normal. Serological analysis indicated absence of hepatitis virus. Brain magnetic resonance imaging revealed a 1.0 cm × 1.3 cm mass in the right frontal lobe. Intrahepatic cholangiocarcinoma with brain metastasis was diagnosed by our liver cancer multidisciplinary team. After sufficient preparation, the patient underwent partial frontal lobotomy and left hemihepatectomy. Histopathological results confirmed that both the lesions were cholangiocarcinoma. Six cycles of gemcitabine combined with S1 were administered. During a 39 mo postoperative follow-up, no sign of local recurrence or distant metastasis was observed. CONCLUSION This case expands our knowledge concerning the complex and heterogeneous nature of tumor metastasis.