UNASSIGNED: Hepatocellular carcinoma (HCC) accounts for approximately 90% of primary liver cancer and can be caused by well-known risk factors, including infection with hepatitis B and C viruses, alcohol intake, and metabolic syndrome. The overall prognosis remains poor with a median survival of 1 year for symptomatic advanced-stage cases treated with systemic therapies.
UNASSIGNED: In July 2020, a 73-year-old male patient presented at our institution with mild abdominal pain and an attack of intense cold. After a radiological workup, the diagnosis of HCC located in the caudate lobe was established. The patient underwent atypical caudate lobe resection, and pathology confirmed the diagnosis of grade 3 HCC. Postoperative MRI showed a new metastasis in the 6th liver segment 1.3 cm in diameter, and a PVT progression which now affected the whole right lobe. The patient was started on sorafenib and demonstrated a complete response which still lasts for more than two years.
UNASSIGNED: We present a rare case of a patient who demonstrated a complete response to sorafenib treatment in advanced HCC with unfavorable prognostic factors.

Lenvatinib is a tyrosine kinase inhibitor that is being used to treat neuroendocrine tumors based on the success shown in the TALENT trial. There are two documented cases of lenvatinib-induced pancreatitis in patients being treated for thyroid cancer. This report describes the first case of pancreatitis seen in a patient with a metastatic neuroendocrine tumor being treated with lenvatinib. A 68-year-old female presented with a chief complaint of epigastric abdominal pain, nausea, and vomiting. She started on lenvatinib therapy 3 months prior to presentation and discontinued the drug 1 week prior due to worsening symptoms. This patient presented with epigastric pain radiating to the back, CT imaging findings consistent with acute pancreatitis, but only a lipase of 88. Once the diagnosis of pancreatitis was made, treatment was initiated with IV fluids, holding all oral intake and pain management. The patient was discharged after she tolerated oral intake after 5 days of hospitalization. It was concluded that the pancreatitis was likely caused by lenvatinib as other etiologies of acute pancreatitis including gallstones, alcohol use, hypertriglyceridemia, and hypercalcemia were ruled out. Clinicians who are using lenvatinib to treat neuroendocrine tumors should be aware of the occurrence of pancreatitis and may consider periodic monitoring for signs and symptoms of pancreatitis. More research regarding the mechanism and development of lenvatinib-induced pancreatitis may benefit clinical decision-making in patients being considered for lenvatinib therapy. Additionally, this therapy may need to be monitored closely in patients with a history of pancreatitis.

The spectrum of TKI-related adverse events (AEs) is variable. Pleural effusion (PE) is a frequent AE attributable to dasatinib treatment, while it is only rarely associated with nilotinib. The pathogenetic mechanism leading to PE during nilotinib therapy is still unknown and its management has not yet been defined. To the best of our knowledge, only a limited number of similar case reports have already been reported in the literature so far. Here, we describe the case of a 41-year-old CML patient who developed PE during first-line nilotinib, successfully treated with steroids and nilotinib permanent discontinuation. We highlight the differences among our patient and the others, proposing therapeutic strategies to solve this rare but still possible AE, of which physicians should be aware.

Rapid tumor growth after cessation of molecularly targeted drugs, called \"disease flare,\" may occur and affect the prognosis of lung cancer. However, this phenomenon has never been reported in ROS proto-oncogene 1 (ROS1) fusion-positive lung adenocarcinoma. Herein, we report a disease flare in a patient with ROS1 fusion-positive lung adenocarcinoma. A 60-year-old female was diagnosed with stage IVA ROS1 fusion-positive lung adenocarcinoma via bronchoscopy. Although crizotinib, an ROS1 tyrosine kinase inhibitor, achieved a partial response, a mass lesion appeared in the patient\'s right kidney 12 months after starting crizotinib, which was diagnosed pathologically as crizotinib-associated renal cysts (CARCs). Given that readministration of crizotinib repeatedly induced CARC-like aseptic inflammation that appeared to be disseminated around surgical site, crizotinib treatment had to be abandoned. Around 25 days after crizotinib cessation, she was referred to the emergency department with a convulsive seizure and hemiparesis due to new, rapidly growing brain metastases. Whole-brain irradiation and administration of another ROS1 tyrosine kinase inhibitor, entrectinib, markedly ameliorated the metastases and improved hemiparesis. This has been the first report of a disease flare after crizotinib cessation due to CARCs in a patient with ROS1 fusion-positive lung adenocarcinoma. Attention should be paid to disease flare, especially in the brain, when molecularly targeted medication is stopped due to adverse events in ROS1 fusion-positive lung adenocarcinoma. Switching to drugs that penetrate the blood-brain barrier could overcome disease flare in the brain.

Metastasis from salivary gland tumors to liver is exceedingly uncommon. Reported is the first case of a mammary analog secretory carcinoma (MASC) of salivary gland origin metastasized to the liver, even after complete surgical resection. A 76 year old female, with past history of a completely extirpated right parotid gland MASC, presented 2 years after right superficial parotidectomy and right neck dissection, with back and flank pain. Subsequent abdominal and pelvic CT revealed multiple small hepatic lesions. Biopsy of the largest hepatic lesion confirmed metastatic MASC of primary parotid gland origin. Both the parotid primary and the hepatic metastases had the confirmatory ETV6 rearrangement by fluorescence in situ hybridization. Although high-grade malignancy and distant metastases of MASC of salivary gland origin to liver is rare, recognizing metastatic MASC potentially alters prognosis and determines therapeutic options.

Leptomeningeal metastases (LM) are found in approximately 3.8% of non-small cell lung cancer cases with an increased incidence in adenocarcinoma, and approximately one-third of patients will present with concomitant brain metastases. We report the case of a 50-year-old male patient with stage IV exon 19-del-EGFR mutant lung adenocarcinoma who progressed on second-generation TKI therapy with manifestation of symptomatic simultaneous diffuse brain and LM. Whole-brain radiotherapy with concurrent afatinib resulted in an almost complete regression of neurological symptoms as well as good, durable radiological response. Furthermore, treatment was well tolerated with no relevant adverse effects.