Publications by authors named "Yohei Ando"

Background: Treating rectal cancer presents challenges due to postoperative complications and reduced quality of life (QOL). Recent evidence supports the watch-and-wait (WW) approach for patients with a clinical complete response (cCR) following preoperative treatment. In this report, we discuss a case of metastatic rectal cancer with deficient mismatch repair (dMMR) treated successfully with pembrolizumab.

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  • - The study investigates the prevalence of inherited cancer susceptibility variants in patients with pancreatic cancer and nonpancreatic periampullary cancers, emphasizing that both groups show similar rates of these variants.
  • - A total of 608 patients were analyzed, revealing that 7.7% carried significant germline variants, with 89% linked to major cancer susceptibility genes and a notable majority having a family cancer history.
  • - The findings support the recommendation for germline susceptibility testing in all patients with periampullary cancers, not just those with pancreatic cancer.
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  • The study explores how levels of the carbohydrate antigen CA19-9 and a related glycan, DUPAN-2, can aid in diagnosing pancreatic cancer, particularly highlighting differences based on genetic variants in fucosyltransferase (FUT) enzymes.
  • It involved analyzing genetic data from 938 individuals to determine how these variants affect serum levels of DUPAN-2 and CA19-9, with findings suggesting improved diagnostic sensitivity for early-stage pancreatic cancer.
  • The conclusion emphasizes the potential of combining genetic testing with tumor markers to enhance diagnostic accuracy for pancreatic cancer, showing promising results when using a combination of FUT, CA19-9, and DUPAN-2 tests.
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Article Synopsis
  • Cancer antigen 19-9 (CA19-9) is a key marker used to monitor pancreatic cancer but varies based on genetic factors from fucosyltransferase (FUT) variants, influencing its reference ranges in patients.
  • The study evaluated preoperative CA19-9 levels in 449 pancreatic cancer patients, analyzing how these levels and FUT variants correlate with survival outcomes.
  • Results indicated that higher CA19-9 levels were linked to worse outcomes in patients with higher FUT groups, while a variant-based CA19-9 test enhanced prediction of treatment response and recurrence after surgery.*
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Purpose: CA19-9 synthesis is influenced by common variants in the fucosyltransferase (FUT) enzymes FUT3 and FUT2. We developed a clinical test to detect FUT variants, and evaluated its diagnostic performance for pancreatic ductal adenocarcinoma (PDAC).

Experimental Design: A representative set of controls from the Cancer of the Pancreas Screening study was identified for each FUT functional group.

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Pancreatic ductal adenocarcinoma (PDAC) is characterized by a desmoplastic reaction caused by cancer-associated fibroblasts (CAFs), which provokes treatment resistance. CAFs are newly proposed to be heterogeneous populations with different functions within the PDAC microenvironment. The most direct sources of CAFs are resident tissue fibroblasts and mesenchymal stem cells, however, the origins and functions of CAF subtypes remain unclear.

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Background: Necroptosis is a form of programmed cell death that is accompanied by release of intracellular contents, and reportedly contributes to various diseases. Here, we investigate the significance of necroptosis in pancreatic cancer.

Methods: We used immunohistochemistry and western blot analysis to evaluate expression of the key mediators of necroptosis-receptor-interacting serine/threonine protein kinase 3 (RIP3) and mixed lineage kinase domain-like (MLKL)-in human pancreatic cancer.

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Cancer‑associated fibroblasts (CAFs) promote the progression of pancreatic ductal adenocarcinoma (PDAC) via tumor‑stromal interactions. Neutrophil extracellular traps (NETs) are extracellular DNA meshworks released from neutrophils together with proteolytic enzymes against foreign pathogens. Emerging studies suggest their contribution to liver metastasis in several types of cancer.

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Lymph node metastasis is an independent prognostic factor in pancreatic cancer. However, the mechanisms of lymph node colonization are unknown. As a mechanism of lymphatic metastasis, it has been reported for other types of cancer that spheroids from tumor cells cause circular chemorepellent‑induced defects (CCIDs) in lymphatic endothelial monolayers.

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Background: Extracellular signal-regulated kinases (ERKs) have been related to multiple cancers, including breast cancer, hepatocellular cancer, lung cancer and colorectal cancer. ERK1/2 inhibitor can suppress growth of KRAS-mutant pancreatic tumors by targeting cancer cell. However, no studies have shown the expression of ERK1/2 on pancreatic stromal and its effect on pancreatic cancer-stromal interaction.

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The pancreas is an organ prone to inflammation, fibrosis, and atrophy because of an abundance of acinar cells that produce digestive enzymes. A characteristic of pancreatic cancer is the presence of desmoplasia, inflammatory cell infiltration, and cancer-associated acinar atrophy (CAA) within the invasive front. CAA is characterized by a high frequency of small ducts and resembles acinar-to-ductal metaplasia (ADM).

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Although recent studies revealed that adipose tissue accelerates pancreatic tumor progression with excessive extracellular matrix, key players for desmoplasia in the adipose microenvironment remains unknown. Here, we investigated the roles of adipose tissue-derived stromal cells (ASCs) in desmoplastic lesions and tumor progression by in vitro and in vivo experiments. In a three-dimensional (3-D) organotypic fat invasion model using visceral fat from CAG-EGFP mice, GFP-positive fibroblastic cells infiltrated toward cancer cells.

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Stroma invasion is an important step in pancreatic cancer progression. However, how pancreatic ductal adenocarcinoma (PDAC) with ductal structure invades the surrounding stroma has not been clear. Here, we elucidated the mechanism of stromal invasion of PDAC, using organoids.

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Specific cell populations leading the local invasion of cancer are called "leading cells". However, the underlying mechanisms are unclear. Here, we identified leading cells in pancreatic cancer and determined how these cells lead and promote cancer cell invasion in the extracellular matrix (ECM).

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Background: Salinomycin has cytotoxic effects on various types of malignancy and induces autophagy. However, it has not been clarified whether autophagy induced by salinomycin treatment has a protective or cytotoxic role. We investigated whether salinomycin affects autophagy in pancreatic cancer cells and whether autophagy induced by salinomycin treatment has a protective or cytotoxic role in these cells.

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