Mami Hirakawa

Gastrointestinal stromal tumor presenting with prominent calcification

We present a rare case of a gastrointestinal stromal tumor (GIST) in the stomach with prominent calcification at presentation. A 61-year-old woman visited our hospital because of epigastric discomfort. A spherical calcified lesion with a diameter of about 30 mm was incidentally shown in the left upper quadrant on an abdominal X-ray. Computed tomography demonstrated that the tumor was growing from the upper gastric body, with calcification in the peripheral ring area. A laparoscopic partial gastrectomy was performed, and the resected specimen revealed a well-circumscribed tumor with exophytic growth from the gastric muscularis propria. Microscopic examination revealed spindle-shaped tumor cells with calcification and hemorrhage. Additionally, positive immunoreactivity of the tumor to KIT and CD34 and a low mitotic index resulted in the diagnosis of very low risk GIST. There are a few case reports of heavily calcified GIST, although solitary or punctate calcification of primary GIST has been reported in several case series. Dystrophic calcification of necrotic or degenerative tissue is the supposed cause of primary calcified GISTs. In contrast, appearance of calcification after administration of imatinib mesylate, which may be one indicator of disease response, is possibly caused by a different mechanism.

Early morphological change for predicting outcome in metastatic colorectal cancer after regorafenib

Background and Objective It is unclear whether early morphological change (EMC) is a predictive marker for regorafenib in metastatic colorectal cancer (mCRC). Therefore, the present study investigated whether EMC can predict the outcome of mCRC patients receiving regorafenib. Results This study evaluated 68 patients. Among 52 patients with lung metastasis, 16 (31%) had cavity formation (CF). The median progression-free survival (PFS) and overall survival (OS) in patients with/without CF were 4.2/2.4 months (p<0.01) and 9.2/6.5 months (p=0.09), respectively. Among 45 patients with liver metastasis, 14 (31%) had active morphological response (MR). The median PFS and OS in patients with/without active MR were 5.3/2.4 months (p<0.01) and 13.6/6.9 months (p=0.02), respectively. Overall, 25 patients (37%) had EMC. The median PFS and OS in patients with/without EMC were 5.3/2.1 months (p<0.01) and 13.3/6.1 months (p<0.01), respectively. Materials and Methods This retrospective study included mCRC patients with lung and/or liver metastases receiving regorafenib. CF in lung metastasis and MR in liver metastasis were evaluated at the first post-treatment computed tomography scan. EMC was determined as CF and/or active MR. We compared PFS and OS between patients with and those without EMC. Conclusions EMC could be a useful predictive marker for regorafenib in mCRC.

Profile of trifluridine/tipiracil hydrochloride in the treatment of metastatic colorectal cancer: efficacy, safety, and place in therapy

TAS-102, with its robust survival efficacy and feasible toxicity, is one of the standard salvage-line treatments for patients with metastatic colorectal cancer (mCRC). No definitive data are available to determine which drug should be administered first during salvage-line treatment. Therefore, it is imperative that we establish the sequence of administration by considering drug toxicity profiles based on patient characteristics, such as age, performance status, comorbidities, tolerability to previous treatments, and patient preferences. The identification of predictive biomarkers in response to TAS-102 or its toxicity is urgently needed for better patient selection. Moreover, to strengthen efficacy or relieve toxicity, combinations with other agents, which could potentially emerge as standard treatment regimens, have been investigated and compared to existing active regimens for mCRC.

Identification of DNA methylation changes in esophageal cancer before/after chemoradiation therapy using a MCA-microarray and bisulfate pyrosequencing.

10550 Background: Systemic chemo- and chemoradiation therapies for esophageal squamous cell carcinoma (ESCC) patients are widely accepted. However we sometimes experience the resistance of ESCC to these therapies, and multicentric occurrence of ESCC after the successful treatment. Although there are studies, which have shown the involvements of promoter methylation of tumor suppressor genes in esophageal carcinogenesis, it remains unclear that the epigenetic changes related to treatments against ESCC. Our aim is to identify how DNA methylation status changes in tumor tissue (T) and also adjacent normal tissue (ADJ) before/after chemoradiation therapy (CRT). Methods: Tumor and adjacent normal biopsy specimens were obtained before/after treatment from 34 patients (124 samples) treated with a uniform CRT protocol. We analyzed genomewide DNA methylation of 12 non-treated test samples (T and matched ADJ: 6 each) by methylated CpG island amplification and microarray (MCAM) method (4×44K, Agilent custom array), ...