Medical Oncology

Dendritic cells (DCs) are described as professional antigen-presenting cells because of their superior T-cell stimulatory capacity. For this reason, attention is being focused on using DCs for clinical applications to treat cancer patients. Although preclinical studies are promising, the majority of clinical studies with DCs have not fulfilled the expectations, yet. The field of DC biology has progressed rapidly over the past years, leading to several options for the improvement of vaccination. Among the different parameters to investigate, this review focuses on the efficiency and biological and functional consequences of different gene transfer methods into different subsets of human DCs. Another important consideration for DC-based vaccination is the elucidation of the role of maturation and apoptosis during DC differentiation.

Oncologists continue to prefer traditional low molecular weight heparins over direct oral anticoagulants (DOAC) for the treatment of venous thromboembolism (VTE) cancer-related. Recently published studies supporting the use DOACs in this patient setting confirm the safety and efficacy of the treatment, but this still does not seem to be enough. The major obstacles to their use are interaction with chemotherapeutic agents, fear of haemorrhage, poor habit of using DOACs for VTE prophylaxis. But what if the haemostasis and thrombosis laboratory reassured oncologists? In this short report we talk about this topic in order to stimulate a fruitful discussion between expert.

Rhabdomyosarcoma (RMS) is the most common soft-tissue tumor in childhood, but is extremely rare in elderly. We present a rare case of cardiac RMS, which developed 1 year after the diagnosis and management of acute lymphoblastic leukemia in a 68-year-old female. The occurrence of such phenomena is intriguing, especially in an individual without prior history of malignancy at a younger age. Through the review of the existing literature, we attempt to approach the pathogenesis and clinical manifestations of this rare clinical entity.

Vi mạch và tế bào miễn dịch là các thành phần chính của môi trường vi mô khối u (TME). Thiếu oxy đóng vai trò then chốt trong TME thông qua yếu tố tạo mạch 1-alpha (HIF-1α), dẫn đến việc tăng cường yếu tố tăng trưởng nội mô mạch máu (VEGF). VEGF, một tác nhân kích thích tạo mạch, ức chế miễn dịch khối u bằng cách ức chế sự trưởng thành của các tế bào tua, và kích thích sự phát sinh của các tế bào ức chế miễn dịch như tế bào T điều hòa, đại thực bào liên quan đến khối u, và tế bào ức chế có nguồn gốc tủy xương. HIF-1α trực tiếp kích thích các phân tử kiểm tra miễn dịch. Điều trị tập trung vào VEGF/ thụ thể VEGF (VEGFR) với tư cách là một phương pháp điều trị ung thư không chỉ có tác dụng chống tạo mạch mà còn có tác dụng hỗ trợ miễn dịch. Điều trị chống tạo mạch có khả năng biến đổi những “khối u lạnh” về mặt miễn dịch thành những “khối u nóng”. U nguyên bào thần kinh đệm (GB) là một khối u giàu mạch với sự biểu hiện VEGF cao, điều này dẫn đến sự phát triển của TME ức chế miễn dịch. Do đó, trong thập kỷ qua, nhiều liệu pháp kết hợp miễn dịch cùng với các tác nhân chống tạo mạch đã được phát triển cho nhiều khối u, bao gồm GB. Đặc biệt, liệu pháp kết hợp với một chất ức chế kiểm tra miễn dịch và liệu pháp nhắm vào VEGF/VEGFR đã được đề xuất như một chiến lược điều trị phối hợp có thể cho thấy sự thay đổi tích cực trong TME. Trong bài báo này, chúng tôi thảo luận về sự tương tác giữa các tế bào ức chế miễn dịch được tiếp xúc với VEGF trong TME thiếu oxy của GB. Các chiến lược kết hợp hiệu quả hiện tại sử dụng liệu pháp nhắm vào VEGF/VEGFR được xem xét và đề xuất như những phương pháp điều trị ung thư mới.

The aim of our study was to evaluate the effects of 5-aza-2′-deoxycytidine (5-azadC) on cell growth inhibition, cell cycle arrest, apoptosis as well as the expression levels of hMLH1 and DNMT3B in human endometrial cancer cell lines. Ishikawa, HHUA, and KLE cell lines were used. After treatment with 5-azadC, cells were measured by MTT to detect the growth inhibition. Flow cytometry analysis was used to evaluate the cell cycle distribution and apoptosis effect. The expression of hMLH1 and DNMT3B was performed by real-time PCR and Western blotting analysis. The methylation status of the hMLH1 gene was monitored by methylation-specific PCR. We confirmed that 5-azadC treatment resulted in growth inhibition, G2 arrest, and cell apoptosis in human endometrial cancer cell lines. Furthermore, the data obtained by real-time PCR and Western blotting analysis demonstrated that the expression of hMLH1 was up-regulated by 5-azadC treatment in Ishikawa cells, accompanied by down-regulation of DNMT3B expression, when 5-azadC led to cell inhibition, G2/M arrest, and apoptosis. Our results suggested that 5-azadC is a potent inhibitor of DNA methyltransferase 3B and induces apoptosis in Ishikawa cells with the up-regulation of hMLH1.

Expansion of the lung is necessary for successful pleurodesis therapy in patients with malignant pleural effusion (MPE). However, this is often impossible in multiloculated MPEs. The aim of this study was to investigate the effect of the fibrinolytic agent, streptokinase, on pleurodesis therapy used in the management of multiloculated MPE. Forty patients with multiloculated MPEs were randomly assigned to two groups: fibrinolytic and control. In the fibrinolytic group, 250,000 IU of streptokinase in 50 ml saline was applied into the pleural space at 24–36–48–60 h after opening a tube thoracostomy. In the control group, the same procedure was carried out using only 50 ml saline solution. Both groups were compared based on the following: (1) volume of pleural drainage at 24–48, 48–72, and 24–72 h, (2) chest computer tomography images before and after therapy, (3) dyspnea symptoms after therapy, and (4) recurrence rate. The mean drainage volumes for the fibrinolytic and control groups were 493 and 248 cc at 24–48 h, 446 and 198 cc at 48–72 h, and 939 and 446 cc at 24–72 h (P < 0.001). Comparison of the two groups by computer tomography revealed that 17 patients (85 %) in the fibrinolytic group had greater than 40 % improvement, whereas only 7 patients (35 %) in the control group had the same degree of improvement (P = 0.001). The dyspnea symptoms disappeared in 90 % of the patients in the fibrinolytic group and in 55 % of the patients in the control group (P = 0.03). Recurrence rate was 11 % in fibrinolytic group and 45 % in control group (P = 0.07). Streptokinase is a reliable treatment option in obtaining effective pleural drainage and increasing lung expansion in patients with multiloculated MPE.

Since the first implant of totally implantable venous access device (TIVAD), performed by Niederhuber and colleague in 1982, the systems have increasingly been used in the field of oncology. We analyzed the clinical reviews and complications of TIVAD in an effort to achieve optimal management. We retrospectively studied 442 cases with TIVAD device at our hospital and we report the results. Four hundred and forty-two TIVAD were placed in the right subclavian vein in 345 cases, the left subclavian vein in 93 cases, the right jugular vein in 2 cases, the left jugular vein in 1 case, and the right femoral vein in 1 case. The immediate complications were 28 cases in malposition of the catheter, 10 cases of arterial puncture, and 2 cases of pneumothorax. The late complications were 3 cases of pocket infection, 2 cases of catheter related to sepsis, 3 cases of catheter obstruction, 2 cases of SVC thrombosis, and 1 case of catheter fracture (pinch-off syndrome: Hinke grade 3). There were no other early or late complications. The low rate of complications in the study confirms the safety and convenience of using TIVAD in patients undergoing prolonged chemotherapy. Yet because infection, thrombosis and catheter fracture are the most common long-term complications of TIVAD, early diagnosis and management of these problems can prevent severe complications.

Serum levels of interleukin-1 beta (IL-1β), soluble interleukin 2 receptors (sIL-2R), interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor-alpha (TNF-α) were measured to predict some characteristics of febrile episodes in children with cancer and neutropenia. Forty-eight episodes of febrile neutropenia were determined in 23 pediatric cancer patients, including 35 febrile episodes without identifiable source, 7 episodes of bacteremia due to Gram-negative organisms and 4 due to Gram-positive organisms, and 2 fungal infections. Interleukin-6, sIL-2R, and IL-8 levels were significantly higher at the beginning of the febrile episodes than those of controls (p<0.001, p<0.001, and p<0.001). Interleukin-6, sIL-2R, and IL-8 levels were higher in patients with bacteremia due to Gram-negative organisms than in those with Gram-positive ones (p=0.042, p=0.006, and p=0.023, respectively). TNF-α and IL-1β levels were similar in febrile episodes and controls (p>0.05). In conclusion, sIL-2R, IL-6, and IL-8 levels may be helpful in the prediction of infection in febrile cancer patients with neutropenia and measurements of IL-1β and TNF-α were not useful for identifying the presence and the type of infection in febrile neutropenic episodes in children.