In contemporary times, cancer poses the most significant threat to human life and safety. Scientists have relentlessly pursued the intricacies of carcinogenesis and explored ways to prevent and treat cancer. Carcinogenesis is a complex, multi-faceted, and multi-stage process, with numerous underlying causes, including inflammation and fibrosis. Cancer-associated fibroblasts (CAFs), however, occupy a pivotal and substantial role within the tumor microenvironment, facilitating carcinogenesis through diverse mechanisms such as creating inflammation, fostering a fibrotic tumor microenvironment, and immunosuppression. In this paper, we introduce the concept of carcinogenesis, explain its causes, describe the characteristics of CAFs and their sources, and highlight the roles and mechanisms of CAFs in promoting carcinogenesis. Ultimately, our aim is to contribute to the development of novel therapeutic strategies for cancer treatment.

Metastasis is a hallmark of advanced cancer, and the liver is a common site for secondary metastasis of many tumor cells, including colorectal, pancreatic, gastric, and prostate cancers. Macrophages in the tumor microenvironment (TME) promote tumor cell metastasis through various mechanisms, including angiogenesis and immunosuppression, and play a unique role in the development of liver metastasis. Macrophages are affected by a variety of factors. Under conditions of hypoxia and increased acidity in the TME, more factors are now found to promote the polarization of macrophages to the M2 type, including exosomes and amino acids. M2-type macrophages promote tumor cell angiogenesis through a variety of mechanisms, including the secretion of factors such as VEGF, IL-1β, and TGF-β1. M2-type macrophages are subjected to multiple regulatory mechanisms. They also interact with various cells within the tumor microenvironment to co-regulate certain conditions, including the creation of an immunosuppressive microenvironment. This interaction promotes tumor cell metastasis, drug resistance, and immune escape. Based on the advent of single-cell sequencing technology, further insights into macrophage subpopulations in the tumor microenvironment may help in exploring new therapeutic targets in the future. In this paper, we will focus on how macrophages affect the TME, how tumor cells and macrophages as well as other immune cells interact with each other, and further investigate the mechanisms involved in liver metastasis of tumor cells and their potential as therapeutic targets.

Background: How to resect the caudate lobe safely is a major challenge to current liver surgery which requires further study. Methods: Nine cases (6 hepatic cell carcinoma, 2 cavernous hemangioma and 1 intrahepatic cholangiocacinoma) were performed using the anterior transhepatic approach in the isolated complete caudate lobe resection. During the operation, we used the following techniques: the intraoperative routine use of Peng’s multifunction operative dissector (PMOD), inflow and outflow of hepatic blood control, low central venous pressure and selective use of liver hanging maneuver. Results: There were no perioperative deaths observed after the operation. The median operating time was 230 ± 43.6 minutes, the median intraoperative blood loss was 606.6 ± 266.3 ml and the median length of postoperative hospital stay was 12.6 ± 2.9 days. The incidence of complications was 22.22% (2/9). Conclusion: PMOD and “curettage and aspiration” technique can be of great help of in the dissection of vessels and parenchyma, clearly making caudate lobe resection safer, easier and faster.

Background Gastric cancer is one of the most common malignancies and is a leading cause of cancer death worldwide. Surgery is the most effective and successful method of treatment for gastric cancer, and systematic lymph node (LN) dissection is unquestionably the most effective procedure for treating LN metastases of gastric cancer. Systematic lymphadenectomy is the most important part of curative resection, but lymphadenectomy is also the most difficult procedure in gastric cancer surgery. The aim of this study is to report our three-step method for lymphadenectomy in gastric cancer. Methods In this study, the lymph node stations and groups were defined according to the 13th edition of the Japanese Classification for Gastric Carcinoma. The authors’ novel, simplified method consists of three steps: (1) the Kocher maneuver and dissection of the greater omentum together with the anterior sheet of the mesocolon, (2) dissection of the lesser omentum, and (3) lymphadenectomy following the main vessels. We primarily used Peng’s multifunctional operative dissector, which combines four different functions (cutting, separating, aspirating and coagulating). Our systematic lymphadenectomy included three steps, and the main procedure started from right to left and in the caudal to cranial direction. Results A total of 830 consecutive patients underwent our three-step-method systematic lymphadenectomy in advanced gastric cancer surgery. The mean operation time was 146 minutes, and the mean blood loss was 248 ml. The median postoperative hospital stay was 10.9 ± 4.8 days. The median number of examined LN was 31.6 (range 17 to 72) per patient, and the median number of metastatic LN was 5.6 (range 0 to 42) per patient. The overall incidence of postoperative complications was 10.6%, and the rate of hospital death was 0.9%. The overall three-year survival rate was 52.6%. Conclusions Our three-step method for lymphadenectomy is easy to perform and is a useful procedure for gastric cancer surgery.

Background: Spontaneous colonic perforation (SCP) is associated with an devastating result. The use of laparoscopy for SCP remains controversial. This study aimed to compare the postoperative outcomes of patients who received either laparoscopic or open surgery and to evaluate the efficacy of laparoscopic surgery and the risk factors affecting prognosis. Patients and Methods: A retrospective study of patients who underwent surgery for SCP from January 2005 to December 2020 was performed. Demographic data, intraoperative variables, length of stay, and surgical complications were retrieved. Results: A total of 52 patients were postoperatively diagnosed with SCP. Thirty (57.69%) procedures were performed using laparoscopic surgery (group A) and 22 (42.31%) were performed using open surgery (group B). There were no significant differences between groups A and B in terms of age, sex, chronic concomitant disease, chronic constipation, incentives, imaging findings, preoperative diagnosis, American Society of Anesthesiologists (ASA) score, Mannheim Peritonitis Index (MPI), operation time, days to resumption of liquids, site of perforation, surgical procedures, or types of perforation (P>0.05). The incidence of wound infection in group A was significantly lower than that in group B (P0.05). Significant differences were found in days to start walking and days to resumption of solids between the 2 groups (P<0.05). Group B had a longer length of hospital stay than group A (P26. Conclusions: The prognosis of SCP is poor. The operation should follow principles that are simple, rapid, and effective. If there are no contraindications, laparoscopy may be the preferred method. Hartmann procedure is a promising surgical strategy. The age, ASA score, and MPI may indicate the severity and prognosis of SCP.

Background: LINC00857 plays an oncogenic role in several cancer types. The aim of this study is to evaluate the role of LINC00857 in pancreatic ductal adenocarcinoma (PDAC) and understand its mechanism. Methods: Firstly, LINC00857 expression in PDAC was predicted using TCGA (The Cancer Genome Atlas) database followed by its determination in clinical PDAC tissues by RT-PCR (reverse transcription-polymerase chain reaction) analysis. Then, MIA PaCa-2 and PANC-1 pancreatic cancer cells were transfected with siRNAs of LINC00857, followed by CCK-8 (Cell Counting Kit-8), cell colony formation, cell apoptosis, cell scratch, and trans-well invasion assay. Besides, p-AKT(phosphorylated protein kinase B), β-catenin, Bax, and cleaved caspase3 levels were detected by western blot analysis. Finally, subcutaneous nude mouse models were created with PANC-1 cells transfected with si-LINC00857 or si-NC. Results: LINC00857 was overexpressed in PDAC and related to poor prognosis. This was validated in clinical PDAC tissues. When LINC00857 was silenced the proliferation, migration, and invasion was impaired but apoptosis of PDAC cells was induced. In addition, western blot analysis showed a correlation between LINC00857 and AKT/β-catenin. Si-LINC00857 reduced the protein level of p-AKT and β-catenin. Tumor volume and tumor weight declined in si-LINC00857 transfection group, compared to that in si-NC transfection group. Conclusions: LINC00857 knockdown suppressed proliferation, migration and invasion of PDAC cells through AKT/β-catenin signaling in part.