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Pancreatic cancer has been becoming the second cause of cancer death in the western world, and its disease burden has increased. Neoadjuvant therapy is one of the current research hotspots in the field of pancreatic cancer, aiming to improve the surgical rate and prognosis of pancreatic cancer. Based on the latest evidence, this review discussed neoadjuvant therapy in pancreatic cancer from the following three aspects: patient selection, protocols selection of neoadjuvant therapy, and treatment response evaluation and resectability prediction. A big controversy existed on the indications of neoadjuvant treatment, but it was agreed that any patient who is likely to achieve R0 resection due to neoadjuvant therapy should be the targeted population. A variety of chemotherapy regimens were tried for neoadjuvant therapy in pancreatic cancer, and FOLFIRINOX and Nab-Paclitaxel plus Gemcitabine are two preferred regimens at present. It was challenging to evaluate treatment response and predict resectability after neoadjuvant therapy, although imaging by CT is widely used. Based on new findings of the remarkable performance of several chemotherapy regimens with or without radiotherapy, the neoadjuvant indications of pancreatic cancer have extended in recent years. However, it is still a challenge to assess the neoadjuvant treatment response and determine the timing of surgery.

Gastric cancer (GC) is the most common gastrointestinal malignant tumor, and distant metastasis is a critical factor in the prognosis of patients with GC. Understanding the mechanism of GC metastasis will help improve patient prognosis. Studies have confirmed that urokinase-type plasminogen activator receptor (PLAUR) promotes GC metastasis; however, its relationship with anoikis resistance and associated mechanisms remains unclear. In this study, we demonstrated that PLAUR promotes the anoikis resistance and metastasis of GC cells and identified transcription Factor 7 Like 2 (TCF7L2) as an important transcriptional regulator of PLAUR. We also revealed that TCF7L2 is highly expressed in GC and promotes the anoikis resistance and metastasis of GC cells. Moreover, we found that TCF7L2 transcription activates PLAUR. Finally, we confirmed that TCF7L2 is an independent risk factor for poor prognosis of patients with GC. Our results show that TCF7L2 and PLAUR are candidate targets for developing therapeutic strategies for GC metastasis.

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The imbalance between acetylation and deacetylation of histone proteins, important for epigenetic modifications, is closely associated with various diseases, including cancer. However, knowledge regarding the modification of histones across the different types of digestive cancers is still lacking. The purpose of this research was to analyze the role of histone acetylation and deacetylation in pan-digestive cancers. We systematically characterized the molecular alterations and clinical relevance of 13 histone acetyltransferase (HAT) and 18 histone deacetylase (HDAC) genes in five types of digestive cancers, including esophageal carcinoma, gastric cancer, hepatocellular carcinoma, pancreatic cancer, and colorectal cancer. Recurrent mutations and copy number variation (CNV) were extensively found in acetylation-associated genes across pan-digestive cancers. HDAC9 and KAT6A showed widespread copy number amplification across five pan-digestive cancers, while ESCO2, EP300, and HDAC10 had prevalent copy number deletions. Accordingly, we found that HAT and HDAC genes correlated with multiple cancer hallmark-related pathways, especially the histone modification-related pathway, PRC2 complex pathway. Furthermore, the expression pattern of HAT and HDAC genes stratified patients with clinical benefit in hepatocellular carcinoma and pancreatic cancer. These results indicated that acetylation acts as a key molecular regulation of pan-digestive tumor progression.

ObjectiveAlthough photodynamic therapy (PDT) has been proven effective in various tumors, it has not been widely used as a routine treatment for colorectal cancer (CRC), and the characteristics of changes in the tumor microenvironment (TME) after PDT have not been fully elucidated. This study evaluated the efficacy of PDT in patients with advanced CRC and the changes in systemic and local immune function after PDT.MethodsPatients with stage III-IV CRC diagnosed in our hospital from November 2020 to July 2021 were retrospectively analyzed to compare the survival outcomes among each group. Subsequently, short-term efficacy, systemic and local immune function changes, and adverse reactions were assessed in CRC patients treated with PDT.ResultsA total of 52 CRC patients were enrolled in this retrospective study from November 2020 to July 2021, and the follow-up period ended in March 2022. The overall survival (OS) of the PDT group was significantly longer than that of the non-PDT group (p=0.006). The objective response rate (ORR) and disease control rate two months after PDT were 44.4% and 88.9%, respectively. Differentiation degree (p=0.020) and necrosis (p=0.039) are two crucial factors affecting the short-term efficacy of PDT. The systemic immune function of stage III patients after PDT decreased, whereas that of stage IV patients increased. Local infiltration of various immune cells such as CD3+ T cells, CD4+ T cells, CD8+ T cells, CD20+ B cells and macrophages in the tumor tissue were significantly increased. No severe adverse reactions associated with PDT were observed.ConclusionPDT is effective for CRC without significant side effects according to the available data. It alters the TME by recruiting immune cells into tumor tissues.

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