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Photothermal therapy (PTT) using a photo-absorbent in the near-infrared (NIR) region is an effective methodology for local cancer treatment. Before PTT using a NIR absorbent is executed, the operator generally determines the two parameters of fluence rate and irradiation time. However, even if the irradiation parameters are unchanged, the therapeutic effect of PTT is often different for individual tumors. Hence, we examined the therapeutic effect of PTT using a NIR absorbent (ICG lactosome) while changing two parameters (fluence rate and irradiation time) in various combinations. As a result, there was no robust correlation between those parameters and the therapeutic effect. Compared to those parameters, we found that a more reliable determinant was maintenance of the tumor temperature above 43 °C during NIR irradiation. To reconfirm the significance of the determinant, we developed a new system that can regulate the temperature at the NIR irradiation site at a constant level. By using the new system, we verified the treatment outcomes for tumors in which the NIR absorbent had accumulated. All of the tumors that had been kept at 43 °C during NIR irradiation were cured, while none of the tumors that had been kept at a temperature below 41 °C were cured. In conclusion, PTT using a NIR absorbent with thermal dosimetry is a highly reliable treatment for cancer.

Helicobacter pylori infection is a leading cause of gastric cancer, which is the second-most common cancer-related death in the world. The chronic inflammatory environment in the gastric mucosal epithelia during H. pylori infection stimulates intracellular signaling pathways, namely inflammatory signals, which may lead to the promotion and progression of cancer cells. We herein report two important signal transduction pathways, the LPS-TLR4 and CagA-MET pathways. Upon H. pylori stimulation, lipopolysaccharide (LPS) binds to toll-like receptor 4 (TLR4) mainly on macrophages and gastric epithelial cells. This induces an inflammatory response in the gastric epithelia to upregulate transcription factors, such as NF-κB, AP-1, and IRFs, all of which contribute to the initiation and progression of gastric cancer cells. Compared with other bacterial LPSs, H. pylori LPS has a unique function of inhibiting the mononuclear cell (MNC)-based production of IL-12 and IFN-γ. While this mechanism reduces the degree of inflammatory reaction of immune cells, it also promotes the survival of gastric cancer cells. The HGF/SF-MET signaling plays a major role in promoting cellular proliferation, motility, migration, survival, and angiogenesis, all of which are essential factors for cancer progression. H. pylori infection may facilitate MET downstream signaling in gastric cancer cells through its CagA protein via phosphorylation-dependent and/or phosphorylation-independent pathways. Other signaling pathways involved in H. pylori infection include EGFR, FAK, and Wnt/β-Catenin. These pathways function in the inflammatory process of gastric epithelial mucosa, as well as the progression of gastric cancer cells. Thus, H. pylori infection-mediated chronic inflammation plays an important role in the development and progression of gastric cancer.

Surgical injury can be a life‐threatening complication, not only due to the injury itself, but also due to immune responses to the injury and subsequent development of infections, which readily result in sepsis. Sepsis remains the leading cause of death in most intensive care units. Unfavorable outcomes of several high‐profile trials in the treatment of sepsis have led researchers to state that sepsis studies need a new direction. The immune response that occurs during sepsis is characterized by a cytokine‐mediated hyper‐inflammatory phase, which most patients survive, and a subsequent immunosuppressive phase. Therefore, therapies that improve host immunity might increase the survival of patients with sepsis. Many mechanisms are responsible for sepsis‐induced immunosuppression, including apoptosis of immune cells, increased regulatory T cells and expression of programmed cell death 1 on CD4+ T cells, and cellular exhaustion. Immunomodulatory molecules that were recently identified include interleukin‐7, interleukin‐15, and anti‐programmed cell death 1. Recent studies suggest that immunoadjuvant therapy is the next major advance in sepsis treatment. Sepsis‐induced immunosuppression. Immunomodulating therapy.

There is increasing evidence that postoperative infectious complications (PICs) are associated with poor prognosis after potentially curative surgery. However, the role that PICs play in tumor development remains unclear. In this article, we reviewed the literature for novel insights on the mechanisms of cancer progression associated with PICs. The Medline and EMBASE databases were searched for publications regarding the role of suppression of antitumor immunity by PIC in tumor progression and selected 916 manuscripts were selected for this review. In addition, a summary of the authors’ own experimental data from this field was set in the context of current knowledge regarding cancer progression under septic conditions. Initially, sepsis/microbial infection dramatically activates the systemic immune system with increases in pro-inflammatory mediators, which results in the development of systemic inflammatory response syndrome; however, when sepsis persists in septic patients, a shift toward an anti-inflammatory immunosuppressive state, characterized by macrophage deactivation, reduced antigen presentation, T cell anergy, and a shift in the T helper cell pattern to a predominantly TH2-type response, occurs. Thus, various cytokine reactions and the immune status dynamically change during microbial infection, including PIC. We proposed three possible mechanisms for the tumor progression associated with PIC: first, a mechanism in which microbes and/or microbial PAMPs may be directly involved in cancer growth; second, a mechanism in which factors released from immunocompetent cells during infections may affect tumor progression; and third, a mechanism in which factors suppress host tumor immunity during infections, which may result in tumor progression. A more detailed understanding by surgeons of the immunological features in cancer patients with PIC can subsequently open new avenues for improving unfavorable long-term oncological outcomes associated with PICs.

Background This study aimed to establish a simple and useful prognostic indicator for elderly esophageal cancer patients. We designed the modified geriatric nutrition risk index (mGNRI) using the inverse of C-reactive protein (CRP) instead of albumin and compared its prognostic value with those of the GNRI and other indices. Methods We included 128 patients aged > 65 years who underwent esophagectomy for esophageal cancer. We defined mGNRI as (1.489/CRP in mg/dL) + (41.7 × present/ideal body weight) and divided patients into two groups: the low-mGNRI (mGNRI < 70, n  = 50) and high-mGNRI (mGNRI ≥ 70, n  = 78) groups. We retrospectively examined the relationship between mGNRI and long-term prognosis. Results The low-mGNRI group had more advanced cancer by stage, higher rates of recurrence, and earlier recurrence than the high-mGNRI group. Univariate analysis identified the following factors as significantly associated with poor overall survival (OS): a lower American society of anesthesiologist performance status (ASA-PS), male gender, CRP-albumin ratio ≥ 0.1, CRP ≥ 1.0, low-mGNRI, tumor depth ≥ T3, Charlson comorbidity index ≥ 2, tumor size ≥ 40 mm, and age > 75 years. A low-mGNRI, ASA-PS 3, age > 75 years, and tumor depth ≥ T3 were independent unfavorable prognostic factors for OS. A low-mGNRI was an independent poor prognostic factor for relapse-free survival. We performed model selection analysis to identify the most clinically useful indices; mGNRI was the best predictive model. Conclusion mGNRI in patients with esophageal cancer correlated with early recurrence and was a useful independent prognostic factor.

BackgroundOne-lung ventilation (OLV) is the standard and widely applied ventilation approach used in video-assisted thoracoscopic surgery for esophageal cancer (VATS-e). To address the disadvantages of OLV with respect to difficulties in intubation and induction, as well as the risk of respiratory complications, two-lung ventilation (TLV) with artificial pneumothorax has been introduced for use in VATS-e. However, no studies have yet compared TLV and OLV with postoperative infection and inflammation in the prone position over time postoperatively. Here, we investigated the efficacy of TLV in patients undergoing VATS-e in the prone position.MethodsBetween April 2010 and December 2016, 119 patients underwent VATS-e under OLV or TLV with carbon dioxide insufflation. Clinical characteristics, surgical outcomes, and postoperative outcomes, including oxygenation and systemic inflammatory responses, were compared between patients who underwent OLV and those who underwent TLV.ResultsClinical characteristics other than pT stage were comparable between groups. The TLV group had shorter thoracic operation time than the OLV group. No patients underwent conversion to open thoracotomy. The PaO2/FiO2 ratios of the TLV group on postoperative day (POD) 5 and on POD7 were significantly higher than those of the OLV group. C-reactive protein levels on POD7 were lower in the TLV group than in the OLV group. There were no significant differences with respect to postoperative complications between the OLV and TLV groups. In the TLV group, the white blood cell count on POD7 was significantly lower than that in the OLV group; body temperature showed a similar trend immediately after surgery and on POD1.ConclusionsIn this study, we demonstrated that, compared with OLV, TLV in the prone position provides better oxygenation and reduced inflammation in the postoperative course. Accordingly, TLV might be more useful than OLV for ventilation during esophageal cancer surgery.

Aim Impact of several immune‐inflammatory markers on long‐term outcome has been reported in various malignancies. The aim of the present study was to evaluate through a meta‐analysis the oncological outcome of immune‐inflammatory markers, such as neutrophil to lymphocyte ratio (NLR), platelet to lymphocyte ratio (PLR), and C‐reactive protein to albumin ratio (CAR) in esophageal cancer. Methods A systematic electronic search for relevant studies was carried out in PubMed, Cochrane library, Embase, and Google scholar. Meta‐analysis was done using hazard ratio (HR) and 95% confidence interval (CI) as effect measures. A systematic review and meta‐analysis were undertaken according to the Preferred Reporting Items for Systematic Reviews and Meta‐Analyses protocol. P‐values <.01 were considered statistically significant. Results A total of 10 retrospective articles (n = 4551) were included in this study. Synthesized results showed that higher NLR and CAR were significantly associated with poor overall survival (HR 1.47, 95% CI = 1.32‐1.63, P < .00001) and HR 1.88, 95% CI = 1.28‐2.77, P < .001, respectively). On the contrary, PLR was not a prognostic factor in our analysis (HR 1.25, 95% CI = 1.01‐1.54, P < .01). Elevated NLR, PLR, and CAR were strongly associated with a higher T stage (HR 2.28, 95% CI = 1.67‐3.11; HR 1.57, 95% CI = 1.29‐1.90; HR 1.76, 95% CI = 1.16‐2.67, respectively). Begg’s funnel plots identified significant publication bias in NLR, but not in PLR and CAR. Conclusion NLR and CAR represent useful guides for the management of esophageal cancer, although publication bias should be considered. Further prospective studies are needed to confirm the results of the present study. Forest plot for the association between C‐reactive protein to albumin ratio (CAR) and overall survival of patients treated by surgery for esophageal cancer. Only three studies (n = 1033 patients) evaluated prognostic value of CAR. Cut‐off value of the included studies ranged from 0.085 to 0.5 (median, 0.22). Higher CAR was strongly associated with poorer survival versus lower CAR (HR 1.88, 95% CI = 1.28‐2.77, P = .001).

BackgroundImmunoinflammatory measures such as the neutrophil–lymphocyte ratio (NLR), the platelet–lymphocyte ratio (PLR), and the C-reactive protein (CRP)–albumin ratio (CAR) are useful prognostic measures in various malignancies. However, no study has investigated the correlation of these measures with microenvironmental inflammation. Periostin (POSTN), a small extracellular matrix protein, strongly associates with cancer microenvironmental inflammation. The current study investigated the correlation of NLR, PLR, and CAR with periostin expression in esophageal squamous cell carcinoma (ESCC).MethodsThe study retrospectively evaluated preoperative NLR, PLR, and CAR hematologically and POSTN immunohistochemically in 171 patients. The correlation of immunoinflammatory measures, POSTN expression, and survival outcomes was measured.ResultsThe study showed a significant correlation of POSTN-positive expression with poor overall survival (OS) (P < 0.0001) and recurrence-free survival (RFS) (P = 0.03). The POSTN-positive group had higher PLR (189.6 ± 8 vs. 159.3 ± 12; P = 0.04) and CAR (0.36 ± 0.06 vs. 0.14 ± 0.09; P < 0.05) than the POSTN-negative group, whereas NLR did not differ between the two groups (3.27 ± 0.19 vs. 2.65 ± 0.28; P = 0.07). The uni- and multivariate analyses showed that POSTN-positive expression (hazard ratio [HR], 1.595; 95% confidence interval [CI], 0.770–3.031; P = 0.03), CAR (HR, 1.663; 95% CI, 1.016–2.764; P = 0.03), gender (HR, 2.303; 95% CI, 1.067–6.019; P = 0.03), and tumor depth (HR, 1.957; 95% CI, 1.122–3.526; P = 0.01) were independent prognostic factors.ConclusionsBecause POSTN-positive expression strongly correlates with immunoinflammatory measures, especially PLR and CAR, it is an independent prognostic factor in ESCC.

In recent years, there has been increasing evidence that gut microbiota is associated with the onset and exacerbation of various diseases, such as gastrointestinal cancer. For instance, it is well known that local inflammation of the intestinal tract in colorectal cancer that is caused by the increased number of Fusobacterium, due to changes in the intestinal bacterial flora, is involved in carcinogenesis. In contrast, gut bacteria or their products, pathogen-associated molecular patterns, not only cause intestinal inflammation but also invade the bloodstream through dysbiosis and gut barrier dysfunction, thereby leading to systemic inflammation, namely bacterial translocation. The involvement of bacterial translocation in the carcinogenesis of gastrointestinal cancers and their prognosis is increasingly being recognized. The Toll-like receptor signaling pathways plays an important role in the carcinogenesis of such cancers. In addition, bacterial translocation influences the treatment of cancers such as surgery and chemotherapy. In this review, we outline the concept of bacterial translocation, summarize the current knowledge on the relationship between gut bacteria and gastrointestinal cancer, and provide future perspectives of this field.