A Prospective Randomized Clinical Study of Minimally Invasive Video-assisted Thyroidectomy for Papillary Thyroid Microcarcinoma.

BACKGROUND: The purpose of this study was to observe the effectiveness of minimally invasive video-assisted thyroidectomy (MIVAT) in treating papillary thyroid microcarcinoma (PTMC). METHODS: A total of 224 patients with PTMC who met the inclusion and exclusion criteria were selected from the Department of General Surgery, Beijing Friendship Hospital, Capital Medical University, between January 2017 and December 2019. They were randomized into the MIVAT group or traditional open operation group. For both groups, we observed the number of lymph node dissections, amount of intraoperative blood loss, duration of the operation, length of the incision, and number of injuries to the recurrent laryngeal nerve. RESULTS: The average operation time (132.8±29.4 min) in the MIVAT group was significantly higher than that in the open surgery group (83.8±14.29 min) ( P =0.026). The length of incision (2.8±0.6 cm) in patients in the MIVAT group was significantly shorter than that in patients in the open group (7.4±1.1 cm) ( P =0.000). No significant differences were observed in the number of lymph node dissections ( P =0.712), the amount of intraoperative bleeding ( P =0.581), and the number of recurrent laryngeal nerve injuries ( P =0.634). The average follow-up was 5 years, and both groups had no recurrence. CONCLUSIONS: In the treatment of PTMC, MIVAT had similar outcomes as traditional open operations, although the operation time was longer. However, the length of the incision was significantly shorter and thus provided cosmetic advantages for patients.

Neoadjuvant docetaxel and capecitabine (TX) versus docetaxel and epirubicin (TE) for locally advanced or early her2-negative breast cancer: an open-label, randomized, multi-center, phase II Trial.

PURPOSE: The combination of taxanes and anthracyclines is still the mainstay of chemotherapy for early breast cancer. Capecitabine is an active drug with a favorable toxicity profile, showing strong anti-tumor activity against metastatic breast cancer. This trial assessed the efficacy and safety of the TX regimen (docetaxel and capecitabine) and compared it with the TE (docetaxel and epirubicin) regimen in locally advanced or high risk early HER2-negative breast cancer. PATIENTS AND METHODS: This randomized clinical trial was conducted at five academic centers in China. Eligible female patients were randomly assigned (1:1) to the TX (docetaxel 75 mg/m2 d1 plus capecitabine 1000 mg/m2 twice d1-14, q3w) or TE (docetaxel 75 mg/m2 d1 plus epirubicin 75 mg/m2 d1, q3w) groups for four cycles. The primary endpoint was a pathological complete response in the breast (pCR). Secondary endpoints included pCR in the breast and axilla, invasive disease-free survival (iDFS), overall survival (OS), and safety. RESULTS: Between September 1, 2012, and December 31, 2018, 113 HER2-negative patients were randomly assigned to the study groups (TX: n = 54; TE: n = 59). In the primary endpoint analysis, 14 patients in the TX group achieved a pCR, and nine patients in the TE group achieved a pCR (25.9% vs. 15.3%), with a not significant difference of 10.6% (95% CI -6.0-27.3%; P = 0.241). In a subgroup with high Ki-67 score, TX increased the pCR rate by 24.2% (95% CI 2.2-46.1%; P = 0.029). At the end of the 69-month median follow-up period, both groups had equivalent iDFS and OS rates. TX was associated with a higher incidence of hand-foot syndrome and less alopecia, with a manageable toxicity profile. CONCLUSION: The anthracycline-free TX regimen yielded comparable pCR and long-term survival rates to the TE regimen. Thus, this anthracycline-free regimen could be considered in selected patients. TRIAL REGISTRATION: ACTRN12613000206729 on 21/02/2013, retrospectively registered.

Ehm2 transcript variant 1 inhibits breast cancer progression and increases E-cadherin stability.

Ehm2/1, an Ehm2 transcript variant, regulates the cytoskeleton by binding to plasma membrane proteins. However, the role of Ehm2/1 in breast cancer development remains poorly understood. This study shows that, the expression of Ehm2/1 was decreased in breast cancer and that patients with low Ehm2/1 expression had a significantly poorer prognosis than those with high expression of Ehm2/1. Overexpression of Ehm2/1 in MCF-7 breast cancer cells inhibited cell migration and invasion. Ehm2/1 markedly increased the stability and half-life of E-cadherin. Moreover, Ehm2/1 was collocated with E-cadherin in the plasma membrane of MCF-7 cells. Furthermore, downregulation of Ehm2/1 promoted ubiquitination of E-cadherin, whereas overexpression of Ehm2/1 inhibited ubiquitination of E-cadherin. These results suggest that Ehm2/1 could suppress the migration and invasion of breast cancer cells by increasing E-cadherin stability.

Impact of changing treatment strategy based on circulating tumor cells on postoperative survival of breast cancer.

Background: We sought to explore the impact of changing treatment strategy based on circulating tumor cells (CTC) on postoperative survival of breast cancer. Methods: We retrospectively analyzed records of patients who underwent surgery for early-stage breast cancer at Beijing Friendship Hospital from January 2016 to January 2018 and regularly underwent CTC examination after surgery. During the regular examination and CTC monitoring, the patients with positive CTC results and without distant metastasis had their treatment regimen changed. Results: Of 109 patients who received CTC examination regularly after surgery, 61 (56.0%) were CTC-positive during postoperative follow-up, including 33 ER or PR-positive, and 28 ER and PR-negative patients. Of the 33 ER or PR-positive patients, 20 changed endocrine therapy drugs. Compared with those without replacement, those with changed endocrine therapy strategy had higher CTC clearance rates (90.0% vs. 53.8%, p=0.04) and significantly lower CTC-positive values (1.70 ± 1.72 vs. 0.62 ± 0.65, p = 0.04). Among the 28 patients who were CTC positive and ER and PR-negative, 11 used capecitabine. Compared with non-users, the capecitabine users had higher CTC clearance rates (100.0% vs. 52.9%, p=0.01) and more significant decrease in CTC-positive values (2.09 ± 1.14 vs. 0.82 ± 1.67, p=0.04). Disease-free survival (DFS) at 1, 3, and 5 years was significantly longer in those who changed treatment than in those who did not (respectively, 96.6% vs. 89.6%, 92.8% vs. 56.9%, 69.0% vs. 47.8%, p<0.01). By changing the treatment strategy, CTC-positive patients achieved DFS that was not significantly different from CTC-negative patients (95.0% vs. 97.7%, 77.5% vs. 82.9%, 57.6% vs. 59.9%, p=0.20). Conclusion: Timely change of treatment strategy for breast cancer patients with positive CTC results after surgery may improve CTC clearance rate and DFS.

Oncological outcome of single-port insufflation endoscopic nipple-sparing mastectomy versus open mastectomy in early breast cancer patients: a study protocol for a randomised controlled trial.

INTRODUCTION: Breast cancer is the most prevalent cancer and the leading cause of cancer-related death in women. Conventional open mastectomy (C-OM) is one of the most common procedures for breast cancer, which involves the removal of the nipple-areola complex and a large proportion of the breast skin, leading to poor cosmetic effect and restriction of upper extremity function. Single-port insufflation endoscopic nipple-sparing mastectomy (SIE-NSM) could conceal the incision along the wrinkles in the axilla, preserve all the breast skin and nipple-areola complex and provide a better cosmetic outcome and quality of life. This trial aims to investigate the oncological safety between SIE-NSM and C-OM in early breast cancer patients. METHODS AND ANALYSIS: This is a single centre, non-blinded, randomised controlled trial (RCT) and will be conducted at Beijing Friendship Hospital. Patients will be enrolled in the inpatient ward. Breast surgeons will notify patients who meet the inclusion and exclusion criteria with the instruction of this RCT. Patients will be randomly assigned to C-OM or SIE-NSM with a 3:1 allocation as per a computer-generated randomisation schedule. Patients will be followed-up for 12 months for analysing surgical outcomes. The primary outcome is the local recurrence rate at a 12-month follow-up. The secondary outcome is the distant metastasis rate, cosmetic satisfaction score and psychosocial well-being score after a 12-month follow-up. To ensure the accuracy of the cosmetic satisfaction score and psychosocial well-being score, the standard scale, Breast-Q score, will be applied. ETHICS AND DISSEMINATION: This study will be conducted according to the medical ethics committee of the Beijing Friendship Hospital and according to the principles of the Declaration of Helsinki. All patients will receive clear instruction of their disease and treatment plan. Informed consent will be obtained from all patients when they agree to comply with our research plan. The results will be disseminated at academic presentations and publications in peer-reviewed journals. The raw data will be confidentially stored in our electronic data capture database. Data will not be shared unless an appropriate data request is submitted after the trial completion and peer-review journal publication. TRIAL REGISTRATION NUMBER: NCT04461847.

PBX3-activated DLG1-AS1 can promote the proliferation, invasion, and migration of TNBC cells by sponging miR-16-5p.

DLG1-AS1 and PBX3 have been identified as acting as an oncogene in cervical cancer. However, they have not been well explored in triple-negative breast cancer (TNBC). As TNBC is one of the malignancies causing increasing death throughout the world, this study aimed to probe into the regulatory relationship between DLG1-AS1 and PBX3 in TNBC cells. In this study, real-time quantitative PCR (qRT-PCR) and western blot experiments were conducted to investigate the RNA and protein levels of genes of interest in TNBC cells. Functional experiments were implemented, such as 5-ethynyl-2'-deoxyuridine (EdU), transwell, and wound healing assays, to assess the changes in TNBC cell phenotype. Chromatin immunoprecipitation, luciferase reporter, RNA binding protein immunoprecipitation, and RNA pull-down assays were conducted to investigate the binding relationships among subject genes. The results show that DLG1-AS1 and PBX3 displayed high expression in TNBC cells, and PBX3 worked as the transcriptional activator of DLG1-AS1. Also, DLG1-AS1 served as an oncogene in TNBC cells and as a sponge for miR-16-5p to up-regulate JARID2. Meanwhile, JARID2 and PBX3 exerted oncogenic effects on TNBC cell growth. In conclusion, PBX3-activated DLG1-AS1 can promote the proliferation, invasion, and migration of TNBC cells by sponging miR-16-5p and elevating JARID2 expression.

Circular RNA RHOT1 promotes progression and inhibits ferroptosis via mir-106a-5p/STAT3 axis in breast cancer.

To explore the effect of circRHOT1 on breast cancer progression and the underlying mechanism. Significantly, our data revealed that the depletion of circRHOT1 was able to repress the proliferation and induce the apoptosis of breast cancer cells. CircRHOT1 knockdown could remarkably inhibit the invasion and migration in the breast cancer cells. Meanwhile, the depletion of circRHOT1 enhanced the erastin-induced inhibition effect on cell growth of breast cancer cells. The circRHOT1 knockdown notably increased the levels of reactive oxygen species (ROS), iron, and Fe2+ in breast cancer cells. Mechanically, circRHOT1 was able to sponge microRNA-106a-5p (miR-106a-5p) and inhibited ferroptosis by down-regulating miR-106a-5p in breast cancer cells. Besides, miR-106a-5p induced ferroptosis by targeting signal transducer and activator of transcription 3 (STAT3) in the system. Moreover, the overexpression of STAT3 and miR-106a-5p inhibitor could reverse circRHOT1 knockdown-mediated breast cancer progression. Functionally, circRHOT1 promoted the tumor growth of breast cancer in vivo. In conclusion, we discovered that circRHOT1 contributed to malignant progression and attenuated ferroptosis in breast cancer by the miR-106a-5p/STAT3 axis. Our finding provides new insights into the mechanism by which circRHOT1 promotes the development of breast cancer. CircRHOT1 and miR-106a-5p may serve as potential targets for breast cancer therapy.

Gastrointestinal motility should be emphasized after laparotomy treatment for complete small intestinal volvulus in older adults: A case report.

RATIONALE: Complete small intestinal volvulus is a rare entity in adults, unlike partial intestinal volvulus. Although prompt surgical intervention is the mainstay of treatment, attention should also be paid to recovery of intestinal function postoperatively. Ignoring this issue during the postoperative recovery process can have serious consequences. We report the case of an 82-year-old woman with complete small intestinal volvulus at the root of the superior mesenteric vessel. PATIENTS CONCERNS: The patient was admitted for acute onset (22 hours) of abdominal pain and distention. Nausea and vomiting also developed during this period. DIAGNOSES: Abdominal physical examination was suspicious for peritoneal irritation. Computed tomography scan showed anticlockwise swirl of the mesenteric vessels at the lower margin of the pancreas with distension of the entire small intestine. A complete small intestinal volvulus was diagnosed. INTERVENTIONS: Laparotomy and detorsion of the volvulus were performed after early diagnosis. OUTCOMES: The patient developed intestinal wall edema because of ischemic-reperfusion damage. She exhibited severe abdominal distention and absent intestinal motility. Two days later, she went into septic shock; she died 19 days after surgical intervention. LESSONS: Because complete small intestinal volvulus involves the entire intestine, ischemic-reperfusion intestinal damage after detorsion may be severe and can predict prognosis.

Outcomes of single-port gasless laparoscopic breast-conserving surgery for breast cancer: An observational study.

To compare the clinical efficacy and aesthetic perspectives between single-port gasless laparoscopic breast-conserving surgery (SGL-BCS) and traditional breast-conserving surgery (T-BCS) in early-stage breast cancer. A total of 70 patients who were diagnosed with stage I or stage II breast cancer participated in this study, which 35 patients underwent SGL-BCS, while others underwent T-BCS. There were no death or severe intraoperative complications, and none of the patients exhibited regional recurrence, distant metastases, or any critical complications after 2 years follow-up. SGL-BCS is feasible and safe surgery, and has advantages in terms of a single, shorter, hidden incision, high-satisficed aesthetic outcome and less intraoperative blood loss.

TXR1 and TSP1 expression varies by the molecular subtypes of breast cancer patients who received previous docetaxel-based first-line chemotherapy.

The expression of taxol resistance gene 1 and thrombospondin 1 remains unknown in human breast cancer tissues. In the current study, we sought to measure the mRNA expression levels of taxol resistance gene 1 and thrombospondin 1 in breast cancer tissue and adjacent normal tissue specimens and further analyzed their expression according to the molecular subtypes and age of breast cancer patients who had received taxane-containing regimens. Archived breast cancer and adjacent non-tumor tissue specimens were obtained at Beijing Friendship Hospital, Beijing, China. The mRNA transcript levels of taxol resistance gene 1, thrombospondin 1 and multi-drug resistance 1 were determined by quantitative RT-PCR. Taxol resistance gene 1 and multi-drug resistance 1 protein levels were measured by immunoblotting assays. Forty-nine archived breast cancer tissue specimens were included. The majority of the specimens (65.3%) were of the molecular subtype A followed by triple negative breast cancer (14.3%). The mRNA transcript levels of taxol resistance gene 1 , thrombospondin 1 and multi-drug resistance 1 in breast cancer tissues were higher than those of adjacent normal tissues. The mRNA expression of TXR1 in the HER2 subtype (4.513 ± 0.810) was the highest and in the Luminal B subtype was the lowest (3.103 ± 0.417) among the four molecular subtypes. The HER2 subtype also had the highest mRNA expression of thrombospondin 1(4.827 ± 0.927) and the Luminal B subtype had the lowest TSP1 mRNA level (3.197 ± 0.565) among the four molecular subtypes. Our study represents the first attempt in delineating taxol resistance gene 1 and thrombospondin 1 expression in breast cancer and we demonstrate that taxol resistance gene 1 and thrombospondin 1 expression may vary according to the molecular subtypes of breast cancer.

Preliminary results for treatment of early stage breast cancer with endoscopic subcutaneous mastectomy combined with endoscopic sentinel lymph node biopsy in China.

BACKGROUND AND OBJECTIVES: To evaluate efficacy and aesthetic outcome for combined endoscopic subcutaneous mastectomy (E-SM) and endoscopic sentinel lymph node biopsy (E-SLNB) in early stage breast cancer patients. METHODS: Combined E-SM+E-SLNB was compared to modified radical resection in a cohort of Chinese patients (n = 49) with stages I and II breast cancer. Patient satisfaction with the aesthetic results was assessed 1 year after surgery with a 5-item-by-4-step scoring system for evaluating cosmetic outcomes. RESULTS: All patients were alive 1 year following surgery with no locoregional recurrence or distant metastases and without any critical complications. The average length of incision was less in patients receiving E-SM+E-SLNB (4.4 vs. 19.4 cm; P < 0.001), but time in surgery was longer (131.6 vs. 99.2 min; P = 0.024). After 1 year, nearly all E-SM+E-SLNB patients rated satisfaction with their appearance as excellent or good (23/24; 95.8% vs. 19/25; 76.0%; P < 0.001), and exhibited less disturbance of sensory (P < 0.001) and motor function (P = 0.014) relative to modified radical resection. CONCLUSIONS: E-SM+E-SLNB provides significant aesthetic and functional advantages for patients with early stage breast cancer without compromising medical efficacy as assessed at 16 months postsurgery. J. Surg. Oncol. 2016;113:616-620. © 2016 Wiley Periodicals, Inc.

Vascular endothelial growth inhibitor affects the invasion, apoptosis and vascularisation in breast cancer cell line MDA-MB-231.

BACKGROUND: Breast cancer is one of the most common malignant female diseases worldwide. It is a significant threat to every woman's health. Vascular endothelial growth inhibitor (VEGI) is known to be abundant in endothelial cells. According to previous literature, overexpression of VEGI has been shown to inhibit tumor neovascularisation and progression in cellular and animal models, but there has been limited research on the significance of VEGI in the breast cancer. METHODS: In our study, cell lines MDA-MB-231 were first constructed in which VEGI mediated by lentivirus over-expressed. The effects of VEGI over-expression on MDA-MB-231 cells were investigated both in vitro and in vivo. The expression of VEGI in the MDA-MB-231 cells after infection of lentivirus was analyzed using real-time PCR and Western blotting. The effect of the biological characteristics of MDA-MB-231 cells was assessed by growth, invasion, adhesion, and migration assay with subcutaneous tumor-bearing nude mice models. Then the growth curves of the subcutaneous tumors were studied. Expressions of VEGI, CD31 and CD34 in the tumors were analyzed by immunohistochemistry and apoptosis was detected by flow cytometry and immunohistochemistry. RESULTS: Infection of MDA-MB-231 cells within the lentivirus resulted in approximately a 1 000-fold increase in the expression of VEGI. As can be seen in the invasion, adhesion and migration assay, the over-expression of VEGI can inhibit the ability of MDA-MB-231 cells during migration, adhesion and invasion. The volume of the subcutaneous tumor in the over-expression group was distinctly and significantly less than that of the control groups. Immunohistochemistry analysis of the tumor biopsies clearly showed the expression of VEGI in the over-expression group increased while CD31 and CD34 decreased significantly. In vitro and in vivo, the early apoptosis rate and the apoptosis index were increased within the VEGI over-expression group as compared with the control group. CONCLUSIONS: Taken together, recombinant lentivirus that were successfully constructed, demonstrated up-regulated VEGI gene expression in breast cancer cells. Lentivirus-mediated over-expression of VEGI weakened the ability of the breast cancer cell migration, adhesion and invasion. Over-expression of VEGI diminished the tumorigenic capacity of breast cancer cells in vivo. Up-regulation of VEGI gene expression however inhibited breast cancer MDA-MB-231 cell in the early apoptosis.

Expression of death receptor-3 in human breast cancer and its functional effects on breast cancer cells in vitro.

Death receptor-3 (DR3) plays controversial roles in cancer. Currently, DR3 is known to be a functional receptor of vascular endothelial growth inhibitor (VEGI). The role of DR3 in breast cancer remains unclear. The present study investigated DR3 expression in a clinical cohort of breast cancer patients and its role in breast cancer cells in vitro. The expression of DR3 was examined in a breast cancer cohort using quantitative PCR (Q-PCR) and immunohistochemistry (IHC) in comparison to the patients' data. In vitro function of DR3 was examined through the targeting of this molecule in MCF7 and MDA-MB-231 breast cancer cells using ribozyme transgene technology. Decreased DR3 expression was noted in breast cancer tissues compared to normal tissues and decreased expression of DR3 was generally associated with a poorer prognosis as well as a significantly shorter long-term survival (p=0.038). Targeting of DR3 in vitro in breast cancer cell lines resulted in impaired migratory rates compared to respective control cells. Collectively, these data suggest a complex role for DR3 in breast cancer development and progression.

Simultaneous determination of sunitinib and its two metabolites in plasma of Chinese patients with metastatic renal cell carcinoma by liquid chromatography-tandem mass spectrometry.

A simple and rapid liquid chromatography-tandem mass spectrometry (LC-MS/MS) method was developed and validated for the simultaneous determination of sunitinib and its two metabolites in plasma of Chinese patients with metastatic renal cell carcinoma (mRCC). After simple one-step protein precipitation with methanol-acetonitrile (1:1, v/v), all three analytes were separated on an Agilent Zorbax SB-C(18) column using a gradient mobile phase consisting of water (0.1% formic acid)-acetonitrile (0.1% formic acid) at a flow rate of 0.50 mL/min. The detection was performed in multiple reaction monitoring mode, using the transitions of m/z 399.0 → 326.2, m/z 371.0 → 283.1, m/z 343.0 → 283.1 and m/z 386.3 → 122.2 for sunitinib, M1, M2 and buspirone, respectively. The method was linear over the range of 0.10-100 ng/mL for all three analytes using only 50 µL of plasma and the lower limit of quantifications for the three analytes were all 0.10 ng/mL. The intra-day and inter-day precisions were all less than 15% and the accuracies were within the range of ±15%; recoveries were between 85.0 and 115%. The validated method was successfully applied to an explorative pharmacokinetic study of sunitinib in Chinese patients with mRCC following multi-dose oral administration.

Expression of death decoy receptor-3 (DcR3) in human breast cancer and its functional effects on breast cancer cells in vitro.

BACKGROUND: Death Decoy Receptor-3 (DcR3), otherwise known as tumour necrosis factor receptor superfamily member 6b, is suggested to be involved in the progression and immune evasion of malignant tumours. Its ligands include FASL and LIGHT (Tumour necrosis factor ligand superfamily member 14). DcR3 has been found to be amplified in certain solid tumours. However, its role in breast tumours remains unclear. In the present study, we examined the role played by DcR3 in MCF7 and MDA-MB-231 cell lines. MATERIALS AND METHODS: The expression of DcR3 was examined in MCF7 and MDA-MB-231 cell lines using immunocytochemical staining and RT-PCR. Anti-DcR3 hammerhead ribozyme transgenes were constructed and transfected into cells to create DcR3 knock-down cell sublines. The biological impact of modifying DcR3 expression in breast cancer cells was evaluated using a variety of in vitro assays, including growth, adhesion, migration and invasion models. RESULTS: MCF7 and MDA-MB-231 cells, usually expressing DcR3, were transfected with the anti-DcR3 ribozyme transgene. Stable transfectants containing the DcR3 ribozyme transgene (MCF7DcR3KO, MDA-MB-231DcR3KO) displayed a reduction of DcR3 expression at mRNA and protein levels. DcR3 knockdown in MCF7 cells was found to significantly reduce invasive capacity compared to pEF6 control cell lines (30.78 +/- 6.40 vs.151.67 +/- 17.67 P < 0.001). The rate of migration in MCF7DcR3KO was significantly lower than MCF7pEF6 (P < 0.001). In contrast, no such significant differences was seen between MDA-MB-231DcR3KO and MDA-MB-231pEF6. CONCLUSION: Suppressing DcR3 expression was found to have an inhibitory effect on cellular invasion and migration in MCF7 breast cancer cells. This suggests that the invasion and migration capacity of this breast cancer cell line may, at least partly, depend on DcR3. DcR3 may be regarded as a negative regulator for aggressiveness during the development and progression of certain types of breast cancer.

Aberrant expression and function of death receptor-3 and death decoy receptor-3 in human cancer.

Death receptor-3 (DR3) and death decoy receptor-3 (DcR3) are both members of the tumour necrosis factor receptor (TNFR) superfamily. The TNFR superfamily contains eight death domain-containing receptors, including TNFR1 (also called DR1), Fas (also called DR2), DR3, DR4, DR5, DR6, NGFR and EDAR. Upon the binding of these receptors with their corresponding ligands, the death domain recruits various proteins that mediate both the death and proliferation of cells. Receptor function is negatively regulated by decoy receptors (DcR1, DcR2, DcR3 and OPG). DR3/DcR3 are a pair of positive and negative players with which vascular endothelial growth inhibitor (VEGI) interacts. VEGI has been suggested to be a potential tumour suppressor. The inhibitory effects of VEGI on cancer are manifested in three main areas: a direct effect on cancer cells, an anti-angiogenic effect on endothelial cells, and the stimulation of dendritic cell maturation. A recent study indicated that DR3 may be a new receptor for E-selectin, which has been reported to be associated with cancer metastasis. DcR3 is a soluble receptor, highly expressed in various tumours, which lacks an apparent transmembrane segment, prevents cytokine response through ligand binding and neutralization, and is an inhibitor of apoptosis. DcR3 serves as a decoy receptor for FasL, LIGHT and VEGI. The cytokine LIGHT activates various anti-tumour functions and is expected to be a promising candidate for cancer therapy. Certain tumours may escape FasL-dependent immune-cytotoxic attack by expressing DcR3, which blocks FasL function. DR3/DcR3 play profound roles in regulating cell death and proliferation in cancer. The present review briefly discusses DR3/DcR3 and attempts to elucidate the role of these negative and positive players in cancer.