BMC Cancer

Lymphoplasmacyte-rich meningioma(LPM) is a rare subtype of meningioma with a low degree of malignancy and an overall preferable prognosis. The purpose of this article is to increase the understanding of the disease, reduce misdiagnosis, and improve prognosis. A search was conducted in the PubMed database for English articles published from 1993 to 2023. The keywords were "lymphoplasmacyte-rich (all fields) and meningioma (all fields) and English (lang)" and "lymphoplasmacyte-rich meningioma (title/abstract) and English (lang)".We further analyzed the clinical manifestations, imaging manifestations, pathological features, treatment strategies, and prognosis of LPM.The possible prognostic indicators were analyzed by the log-rank test and Pearson’s chi-squared test. Fourteen reports with 95 LPM patients were included in this report, including 47 males and 48 females who were diagnosed between the ages of 9 and 79, with an average age of 45 years. The most common clinical manifestations are headache and limb movement disorders. In most cases, the tumor occurred on the convex portion of the brain. All tumors showed significant enhancement, with homogeneous enhancement being more common, and most patients showed peritumoral edema. Postoperative pathological EMA, LCA, and vimentin positivity were helpful for the final diagnosis of the patient. Log-rank tests showed a correlation between complete resection and better prognosis and recurrence. There is a lack of significant differences in the clinical symptoms and imaging manifestations of LPM compared to other diseases that need to be differentiated, and a clear diagnosis requires pathological examination. After standardized surgical treatment, the recurrence rate and mortality rate of LPM are both low. Complete surgical resection of tumors is associated with a better prognosis and lower recurrence rate.

Surgical resection remains the primary treatment for gastrointestinal (GI) malignancy including early-stage cancer. Omega-3 polyunsaturated fatty acids (n-3 PUFAs) have been reported to have beneficial clinical and immune-modulating effects in the prognosis of GI cancer patients undergoing surgery. We searched PubMed, Embase, EBSCO-Medline, Cochrane Central Register of Controlled Trials (CENTRAL), CNKI and Wanfang to identify primary research reporting the effects of n-3 PUFAs compared with isocaloric nutrition on GI cancer patients who underwent surgery up to the end of June 30, 2016. Two authors independently reviewed and selected eligible randomized controlled trials (RCTs). A total of 9 RCTs (623 participants) were included. The n-3 PUFAs regime resulted in lower levels of C-reactive protein (CRP) (P < 0.05), interleukin-6 (IL-6) (P < 0.01), and higher levels of albumin (ALB), CD3+ T cells, CD4+ T cells and CD4+/CD8+ ratio (P < 0.05) compared with the isocaloric nutrition regime. However, there was no significant difference in the level of tumor necrosis factor-α (TNF-α) between the n-3 PUFAs regime and the isocaloric nutrition regime (P = 0.17). And the level of CD8 + T cells decreased compared with the isocaloric nutrition regime (P < 0.0001). Our meta-analysis revealed that n-3 PUFAs are effective in improving the nutritional status and immune function of GI cancer patients undergoing surgery as they effectively enhance immunity and attenuate the inflammatory response.

Việc nhắm mục tiêu vi khuẩn vào khối u là một chiến lược quan trọng trong chống ung thư. Chúng tôi từng cho thấy chủng SL7838 của Salmonella typhimurium có khả năng nhắm mục tiêu và tiêu diệt các tế bào ung thư. Nghiên cứu này khám phá vai trò của việc tạo ra NO bởi vi khuẩn trong sự gây độc của SL7838 đối với tế bào ung thư. Vi khuẩn này có cơ chế tạo ra NO, nhưng cũng có khả năng phân hủy nó. Cơ chế đằng sau liệu pháp khối u của Salmonella typhimurium được điều tra thông qua các nghiên cứu in vitro và in vivo. Việc đo lường NO được thực hiện thông qua các phương pháp hóa học (in vitro) hoặc sử dụng cảm biến sinh học (in vivo). Thí nghiệm xác định độc tính của tế bào ung thư được thực hiện bằng phương pháp MTS. Sự sống sót của tế bào vi khuẩn và gánh nặng khối u được xác định bằng các kỹ thuật hình ảnh phân tử. SL7838 tạo ra nitric oxide (NO) trong các môi trường nuôi cấy kỵ khí, bên trong các tế bào ung thư bị nhiễm in vitro và trong các khối u 4T1 đã được cấy ghép vào chuột sống, được đo bằng cảm biến vi mô. Do đó, trong các điều kiện này, con đường tạo NO hoạt động tích cực hơn so với con đường phân hủy. Con đường phân hủy này bị loại bỏ trong chủng SL7842 bằng cách xóa bỏ các gen hmp- và norV, khiến SL7842 có khả năng tạo NO hiệu quả hơn SL7838. SL7842 tiêu diệt tế bào ung thư hiệu quả hơn SL7838 in vitro, và điều này phụ thuộc vào sự sẵn có của nitrat. Chủng này cũng hiệu quả hơn khoảng 100% trong việc điều trị các khối u 4T1 đã cấy ghép vào chuột so với SL7838. Khả năng tạo NO là rất quan trọng trong việc tiêu diệt tế bào ung thư bởi các chủng Salmonella.

Pancreatic cancer (PC) is a highly aggressive disease, and the lethality of this disease stems from early metastatic dissemination where surgical removal cannot provide a cure. Improvement of the therapeutic outcome and overall survival of PC patients requires to understand the fundamental processes that lead to metastasis such as the gain of cellular migration ability. One such family of proteins, which are essential players of cellular migration, is Semaphorin. Previously, we have identified one of the Semaphorin family member, Semaphorin-5A (SEMA5A) to be involved in organ-specific homing during PC metastasis. We have also demonstrated that SEMA5A has a constitutive expression in PC cell lines derived from metastatic sites in comparison with low endogenous expression in the primary tumor-derived cell line. In this study, we examined whether constitutive SEMA5A expression in metastatic PC cells regulates tumor growth and metastatic potential. We generated SEMA5A knockdown in T3M-4 and CD18/HPAF cells and assessed their phenotypes on in vitro motility, tumor growth, and metastatic progression. In contrary to our initial expectations, orthotopic injection of SEMA5A knockdown cells into nude mice resulted in a significant increase in both tumor burden and liver metastases in comparison with the Control cells. Similarly, we observed higher in vitro migratory potential with pronounced morphological changes associated with epithelial-mesenchymal transition (EMT), a decrease in the expression of epithelial marker E-cadherin (E-Cad), increase in the expression of mesenchymal markers N-cadherin (N-Cad) and Snail and the activation of the Wnt-signaling pathway in SEMA5A knockdown cells. Furthermore, re-establishing SEMA5A expression with a knockdown resistant mouse Sema5A in SEMA5A knockdown cells resulted in a reversion to the epithelial state (mesenchymal-epithelial transition; MET), as indicated by the rescue of E-Cad expression and a decrease in N-Cad and Snail expression. Collectively, our data suggest that SEMA5A expression maintains epithelial phenotype in the metastatic microenvironment.

Published findings suggest sex differences in lung cancer risk and a potential role for sex steroid hormones. Our aim was to perform a meta-analysis to investigate the effects of sex steroid hormone exposure specifically on the risk of lung cancer in women. The PubMed, MEDLINE, Web of Science, and EMBASE databases were searched. The pooled odds ratios (ORs) and 95% confidence intervals (95% CIs) for female lung cancer risk associated with sex steroid hormones were calculated overall and by study design, publication year, population, and smoking status. Sensitivity analysis, publication bias, and subgroup analysis were performed. Forty-eight studies published between 1987 and 2019 were included in the study with a total of 31,592 female lung cancer cases and 1,416,320 subjects without lung cancer. Overall, higher levels of sex steroid hormones, both endogenous (OR: 0.92, 95% CI: 0.87–0.98) and exogenous (OR: 0.86, 95% CI: 0.80–0.93), significantly decreased the risk of female lung cancer by 10% (OR: 0.90, 95% CI: 0.86–0.95). The risk of lung cancer decreased more significantly with a higher level of sex steroid hormones in non-smoking women (OR: 0.88, 95% CI: 0.78–0.99) than in smoking women (OR: 0.98, 95% CI: 0.77–1.03), especially in Asia women (OR: 0.84, 95% CI: 0.74–0.96). Our meta-analysis reveals an association between higher levels of sex steroid hormone exposure and the decreased risk of female lung cancer. Surveillance of sex steroid hormones might be used for identifying populations at high risk for lung cancer, especially among non-smoking women.

The progression of colorectal cancer (CRC) involves recurrent amplifications/mutations in the epidermal growth factor receptor (EGFR) and downstream signal transducers of the Ras pathway, KRAS and BRAF. Whether genetic events predicted to result in increased and constitutive signaling indeed lead to enhanced biological activity is often unclear and, due to technical challenges, unexplored. Here, we investigated proliferative signaling in CRC using a highly sensitive method for protein detection. The aim of the study was to determine whether multiple changes in proliferative signaling in CRC could be combined and exploited as a “complex biomarker” for diagnostic purposes. We used robotized capillary isoelectric focusing as well as conventional immunoblotting for the comprehensive analysis of epidermal growth factor receptor signaling pathways converging on extracellular regulated kinase 1/2 (ERK1/2), AKT, phospholipase Cγ1 (PLCγ1) and c-SRC in normal mucosa compared with CRC stage II and IV. Computational analyses were used to test different activity patterns for the analyzed signal transducers. Signaling pathways implicated in cell proliferation were differently dysregulated in CRC and, unexpectedly, several were downregulated in disease. Thus, levels of activated ERK1 (pERK1), but not pERK2, decreased in stage II and IV while total ERK1/2 expression remained unaffected. In addition, c-SRC expression was lower in CRC compared with normal tissues and phosphorylation on the activating residue Y418 was not detected. In contrast, PLCγ1 and AKT expression levels were elevated in disease. Immunoblotting of the different signal transducers, run in parallel to capillary isoelectric focusing, showed higher variability and lower sensitivity and resolution. Computational analyses showed that, while individual signaling changes lacked predictive power, using the combination of changes in three signaling components to create a “complex biomarker” allowed with very high accuracy, the correct diagnosis of tissues as either normal or cancerous. We present techniques that allow rapid and sensitive determination of cancer signaling that can be used to differentiate colorectal cancer from normal tissue.

This pilot trial aimed to study the feasibility and effects on quality of life (QOL) and well-being of short-term fasting (STF) during chemotherapy in patients with gynecological cancer. In an individually-randomized cross-over trial patients with gynecological cancer, 4 to 6 planned chemotherapy cycles were included. Thirty-four patients were randomized to STF in the first half of chemotherapies followed by normocaloric diet (group A;n = 18) or vice versa (group B;n = 16). Fasting started 36 h before and ended 24 h after chemotherapy (60 h-fasting period). QOL was assessed by the FACIT-measurement system. The chemotherapy-induced reduction of QOL was less than the Minimally Important Difference (MID; FACT-G = 5) with STF but greater than the MID for non-fasted periods. The mean chemotherapy-induced deterioration of total FACIT-F was 10.4 ± 5.3 for fasted and 27.0 ± 6.3 for non-fasted cycles in group A and 14.1 ± 5.6 for non-fasted and 11.0 ± 5.6 for fasted cycles in group B. There were no serious adverse effects. STF during chemotherapy is well tolerated and appears to improve QOL and fatigue during chemotherapy. Larger studies should prove the effect of STF as an adjunct to chemotherapy. This trial was registered at clinicaltrials.gov: NCT01954836 .

Prostate cancer (PCa) is the most commonly diagnosed malignancy reported to Australian cancer registries with numerous studies from individual registries summarizing diagnostic and treatment characteristics. The aim of this study was to describe annual trends in clinical and treatment characteristics, and changes in surveillance practice within a large combined cohort of men with PCa in South Australia (SA) and Victoria, Australia in 2008–2013. Common data items from clinical registries in SA and Victoria were merged to develop a cross-jurisdictional dataset consisting of 13,598 men with PCa. Frequencies were used to describe these variables using the National Comprehensive Cancer Network risk of disease progression categories in 10 year age groups. A logistic regression analysis was performed to assess the impact of a number of factors (both individually and together) on the likelihood of men receiving no active treatment within twelve months of the diagnosis (i.e. managed with active surveillance/watchful waiting). Trend analysis showed that over time: (1) men in SA and Victoria are being diagnosed at older age in 2013, 66.1 (SD = 9.7) years compared to 2009 (64.5 (SD = 9.7)); (2) diagnostic methods and characteristics have changed with time; and (3) types of the treatments have changed, with more men having no active treatment. The majority of men were diagnosed with Prostate-Specific Antigen (PSA) <10 ng/mL (66 %) and Grade Group < 4 (65 %). Nearly seventy percent received radical treatment within 12 months of diagnosis, while ~20 % had no active treatment. In 14 % of cases treatment was not recorded or had not commenced. Having no active treatment was strongly associated older age, lower PSA and lower Grade Group at diagnosis, and in 2013 it was offered more frequently (more than 3 times) than in 2009 (OR = 2.63, 95 % CI: 2.16–3.22). Findings of this study provide the first cross-jurisdictional description of PCa characteristics and management in Australia. These findings will provide benchmarking for ongoing monitoring and feedback of disease management and outcomes of PCa through the Prostate Cancer Outcomes Registry–Australia New Zealand to improve evidence-based practice.

Plasmacytoma đơn độc (SP) ở xương là một khối u tế bào plasma hiếm gặp. Hiện nay, chưa có dữ liệu kết luận trong tài liệu về liều lượng xạ trị tối ưu (RT) cho SP. Do đó, trong nghiên cứu hồi cứu lớn này, chúng tôi muốn đánh giá kết quả, các yếu tố tiên lượng và liều lượng RT tối ưu cho bệnh nhân mắc SP. Dữ liệu của 206 bệnh nhân bị SP xương mà không có bằng chứng mắc bệnh đa u tủy (MM) đã được thu thập. Chẩn đoán bệnh lý mô học đã được tiến hành cho tất cả các bệnh nhân. Phần lớn (n = 169) bệnh nhân chỉ nhận RT; 32 bệnh nhân điều trị hóa trị kết hợp với RT, và 5 bệnh nhân phẫu thuật. Thời gian theo dõi trung vị là 54 tháng (7–245). Tỷ lệ sống sót tổng thể trong 5 năm, tỷ lệ sống không bệnh (DFS) và kiểm soát tại địa phương lần lượt là 70%, 46% và 88%. Thời gian trung bình để phát triển thành MM là 21 tháng (2–135), với xác suất 5 năm là 51%. Trong các phân tích đa biến, các yếu tố thuận lợi bao gồm tuổi trẻ và kích thước khối u < 5 cm cho sống sót; tuổi trẻ cho DFS; vị trí giải phẫu (đốt sống so với các vị trí khác) cho kiểm soát tại chỗ. Tuổi lớn hơn là yếu tố tiên đoán duy nhất cho MM. Không có mối quan hệ liều-đáp ứng cho các liều 30 Gy trở lên, ngay cả đối với các khối u lớn hơn. Bệnh nhân trẻ tuổi, đặc biệt là những người có vị trí đốt sống, có kết quả tốt nhất khi điều trị bằng RT liều trung bình. Sự tiến triển thành MM vẫn là vấn đề chính. Cần có thêm các nghiên cứu tập trung vào hóa trị bổ trợ và/hoặc các tác nhân điều trị mới.