[International expert consensus on gene therapy for hereditary hearing loss: based on clinical trials].
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Journal Article↗
Biomedical subjects
B Chen
Publications and source records attributed to B Chen.
Frequency of CYP2D6*10 and *14 alleles and their influence on the metabolic activity of CYP2D6 in a healthy Chinese population.
To study the frequency of CYP2D6(*)10 and (*)14 alleles in a healthy Chinese population, and the influence of these two alleles on the metabolic activity of CYP2D6. CYP2D6(*)10 and (*)14 genotypes of 295 healthy Chinese subjects were determined using a tetra-primer method and allele-specific amplification. CYP2D6 phenotypes of 131 subjects were determined using dextramethorphan as probe drug. There were 10 subjects with a (*)14 allele, including one homozygous for (*)14. The gene frequency of (*)10 and (*)14 alleles were 55.8 and 1.8%, respectively. The metabolic ratio (MR) of dextramethorphan in 131 subjects was 0.032+/-0.106. The MR of (*)1/(*)1, (*)1/(*)10, (*)10/(*)10, (*)1/(*)14, (*)10/(*)14, and (*)14/(*)14 groups were 0.007+/-0.012, 0.009+/-0.010, 0.042+/-0.029, 0.093, 0.11, and 1.186, respectively. The MR of subjects with (*)14 allele was higher than those of (*)1/(*)1, (*)1/(*)10, or (*)10/(*)10 groups (P<0.001). The CYP2D6(*)10 and (*)14 alleles have substantial impact on the metabolic activity of CYP2D6, and the CYP2D6(*)14 allele may be the cause of the poor metabolizer phenotype in Chinese subjects.
Adult↗
Thalidomide reduces IL-18, IL-8 and TNF-alpha release from alveolar macrophages in interstitial lung disease.
Thalidomide exhibits diverse actions of anti-inflammation, immunomodulation and anti-angiogenesis. The efficacy of thalidomide treatment in sarcoidosis with lupus pernio is thought to be due to inhibition of tumour necrosis factor (TNF)-alpha. The mechanisms that underlie the properties of thalidomide are still unclear in interstitial lung disease. The current authors investigated the potential inhibitory effects of thalidomide at concentrations of 0.1, 0.01 and 0.001 mM on the production of transforming growth factor-beta, TNF-alpha, interleukin (IL)-1beta, IL-6, IL-8, IL-10, IL-12p70, IL-12p40 and IL-18 by alveolar macrophages from bronchoalveolar lavage in patients with sarcoidosis (n = 8), hypersensitivity pneumonitis (HP; n = 8) and idiopathic pulmonary fibrosis (IPF; n = 12). In sarcoidosis and HP patients, thalidomide induced a dose-dependent, partial suppression of lipopolysacchride (LPS)-stimulated TNF-alpha, IL-12p40 and IL-18 release. At the highest thalidomide concentration (0.1 mM), LPS-stimulated IL-8 production was also suppressed. In IPF patients, although spontaneous production of TNF-alpha, IL-12p40, IL-18 and IL-8 was lower than in sarcoidosis and HP patients, with LPS stimulation the cytokines were significantly elevated and also partially inhibited by thalidomide. In conclusion, thalidomide has the potential to improve the therapeutic regimens for sarcoidosis, hypersensitivity pneumonitis and idiopathic pulmonary fibrosis by reducing tumour necrosis factor-alpha, interleukin-12p40, interleukin-18 and interleukin-8 production.
Aged↗
Experimental study of bone marrow-derived mesenchymal stem cells combined with hepatocyte growth factor transplantation via noninfarct-relative artery in acute myocardial infarction.
We investigated the impact of bone marrow-derived mesenchymal stem cells (BM-MSCs) alone or in combination with hepatocyte growth factor (HGF) transplantation via noninfarct-relative artery in a swine myocardial infarction (MI) model. Donor BM-MSCs were derived in vitro from swine auto-bone marrow cultures labeled by bromodeoxyuridine (BrdU) incorporation. Host MI swine model was created by ligating the distal left anterior descending artery. After 4 weeks, age-matched male MI swines were used for the transplantation. Male MI swines were transfused via noninfarct-relative artery with vehicle (control, n=6) or BrdU-labeled BM-MSCs (5 x 10(6)) alone (MSCs, n=6) or BrdU-labeled BM-MSCs (5 x 10(6)) combined with HGF (4 x 10(9) PFU) (MSCs+HGF, n=6). To evaluate the collateral artery growth (Rentrop) and cardiac perfusion in these animals, gate cardiac perfusion imaging and coronary angiography were performed before and 4 weeks after transplantation, respectively. To assess the contribution of donor-originated cells in stimulation of cardiomyocyte regeneration and angiogenesis, immunohistochemistry for BrdU and alpha-smooth muscle actin (alpha-SMA) and quantitative image analysis were performed at 4 weeks after transplantation. The results are as follows: (1) BrdU-positive cells were detected in host myocardium in both MSCs and MSCs+HGF groups, but not in the vehicle group. Most BrdU-positive cells expressed myosin heavy chain beta. (2) alpha-SMA(-)positive arteriole densities in the infarcted border area and infarcted area were increased significantly in both transplantation groups compared with the vehicle group. (3) Gate cardiac perfusion imaging demonstrated that the cardiac perfusion was significantly improved in transplantation groups compared with the vehicle group. (4) Ejection fraction and alpha-SMA-positive arteriole densities were increased significantly in both transplantation groups compared with the vehicle group. However, there was no difference in ejection fraction and alpha-SMA-positive arteriole densities between the MSCs group and the MSCs+HGF group. Growth of collateral arteries was not detected by coronary angiography in all three groups. In conclusion, the current study indicates that BM-MSCs transplantation via noninfarct-relative artery stimulates cardiomyocyte regeneration and angiogenesis and improves cardiac function, but does not stimulate collateral artery growth. BM-MSCs transplantation combined with HGF therapy is not superior to BM-MSCs alone transplantation. BM-MSCs transplantation via noninfarct-relative artery may be an alternative for those patients who cannot be transplanted via infarct-relative artery in clinical practice.
Animals↗
Synthesis and SAR study of acridine, 2-methylquinoline and 2-phenylquinazoline analogues as anti-prion agents.
Transmissible spongiform encephalopathies (TSEs) are thought to arise from aggregation of a protease resistant protein denoted PrP(Sc), which is a misfolded isoform of the normal cellular prion protein PrP(C). Using virtual high-throughput screening we have selected structures analogous to acridine, 2-methyquinoline and 2-phenylquinazoline as potential therapeutic candidates for the treatment of TSEs. From the synthesis and screening of constructed libraries we have shown that an electron-rich aromatic ring attached through an amine linker to the position para to the ring nitrogen is beneficial to both binding to PrP(C) and the suppression of PrP(Sc) accumulation for acridine and 2-methylquinoline analogues. 2-Phenylquinazoline analogues appear to utilise a different mode of action by binding at a different location and/or pose. We report IC50s in the nanomolar range.
Acridines↗
Genetic diversity and molecular identification of mosquito species in the Anopheles maculatus group using the ITS2 region of rDNA.
The species diversity and genetic structure of mosquitoes belonging to the Anopheles maculatus group in Southeast Asia were investigated using the internal transcribed spacer 2 (ITS2) of ribosomal DNA (rDNA). A molecular phylogeny indicates the presence of at least one hitherto unrecognised species. Mosquitoes of chromosomal form K from eastern Thailand have a unique ITS2 sequence that is 3.7% divergent from the next most closely related taxon (An. sawadwongporni) in the group. In the context of negligible intraspecific variation at ITS2, this suggests that chromosomal form K is most probably a distinct species. Although An. maculatus sensu stricto from northern Thailand and southern Thailand/peninsular Malaysia differ from each other in chromosomal banding pattern and vectorial capacity, no intraspecific variation was observed in the ITS2 sequences of this species over this entire geographic area despite an extensive survey. A PCR-based identification method was developed to distinguish five species of the group (An. maculatus, An. dravidicus, An. pseudowillmori, An. sawadwongporni and chromosomal form K) to assist field-based studies in northwestern Thailand. Sequences from 187 mosquitoes (mostly An. maculatus and An. sawadwongporni) revealed no intraspecific variation in specimens from Thailand, Cambodia, mainland China, Malaysia, Taiwan and Vietnam, suggesting that this identification method will be widely applicable in Southeast Asia. The lack of detectable genetic structure also suggests that populations of these species are either connected by gene flow and/or share a recent common history.
Animals↗
Hypoxia regulates the expression of PHLDA2 in primary term human trophoblasts.
Hypoxia influences gene expression in placental trophoblasts. We sought to examine the effect of hypoxia on trophoblast expression of human PHLDA2 (also termed IPL, TSSC3 or BWR-1C), a product of an imprinted gene on human chromosome 11p15.5 whose murine ortholog plays a pivotal role in placental development. We initially confirmed that PHLDA2 was expressed in term placental villi, primarily in the trophoblast layer. Using quantitative PCR we found that the expression of PHLDA2 gradually declined during differentiation of primary term human trophoblasts. A similar expression pattern was seen for p57(Kip2) and IGF-II, both products of imprinted genes on chromosome 11p15.5. Exposure of trophoblasts to hypoxia in vitro (O(2)<or=2%) markedly reduced the expression of PHLDA2 mRNA and protein. This effect was not consistent among other chromosome 11p15.5 genes products, as the expression of p57(Kip2) decreased, but that of IGF-II increased in hypoxic trophoblasts. PHLDA2 expression in trophoblasts exposed to TGFbeta1, -beta2 or -beta3 was unchanged. We conclude that hypoxia down-regulates the expression of PHLDA2 in human term placental trophoblasts. As murine PHLDA2 limits placental growth, our results suggest that down-regulation of PHLDA2 attenuates the impact of hypoxia on placental growth.
Cells, Cultured↗
ERK activity facilitates activation of the S-phase DNA damage checkpoint by modulating ATR function.
Although Erk kinase has been recently reported to function in the DNA damage response, the mechanism governing this process is unknown. We report here that hydroxyurea (HU) activates Erk via MEK1, a process that is sensitized by a constitutively active MEK1 (MEK1Q56P) and attenuated by a dominant-negative MEK1 (MEK1K97M). While ectopic MEK1Q56P sensitized HU-induced S-phase arrest, inhibition of Erk activation via U0126, PD98059, and MEK1K97M attenuated the arrest, and thereby enhanced cells to HU-induced toxicity. Taken together, we demonstrate an important contribution of Erk to the activation of the S-phase DNA damage checkpoint. This can be attributed to Erk's regulatory role in modulating ATR function. Inhibition of Erk activation with U0126/PD98059 and MEK1K97M substantially reduced HU-induced ATR nuclear foci, leading to a dramatic reduction of gammaH2AX and its nuclear foci. Reduction of MEK1 function by a small interference RNA (siRNA) MEK1 and ectopic MEK1K97M significantly decreased HU-induced gammaH2AX. Conversely, ectopic MEK1Q56P enhanced gammaH2AX foci. Furthermore, immunofluorescent and cell fractioning experiments revealed cytosolic and nuclear localization of ATR. HU treatment caused the redistribution of ATR from the cytosol to the nucleus, a process that is inhibited by U0126. Collectively, we show that Erk kinase modulates HU-initiated DNA damage response by regulating ATR function.
3T3 Cells↗
Increased risk of chronic obstructive pulmonary diseases in coke oven workers: interaction between occupational exposure and smoking.
BACKGROUND: Coke oven workers are regularly exposed to coke oven emissions (COE) and may be at risk of developing lung diseases. There is limited evidence for the link between exposure to COE and chronic obstructive pulmonary diseases (COPD). The aim of this study was to explore the dose-response relationship between COE exposure and COPD and to assess the interaction with cigarette smoking. METHODS: Seven hundred and twelve coke oven workers and 211 controls were investigated in southern China. Benzene soluble fraction (BSF) concentrations as a surrogate of COE were measured in representative personal samples and the individual cumulative COE exposure level was quantitatively estimated. Detailed information on smoking habits and respiratory symptoms was collected and spirometric tests were performed. RESULTS: The mean BSF levels at the top of two coking plants were 743.8 and 190.5 microg/m3, respectively, which exceed the OSHA standard (150 microg/m3). After adjusting for cigarette smoking and other risk factors, there was a significant dose-dependent reduction in lung function and increased risks of chronic cough/phlegm and COPD in coke oven workers. The odds ratio for COPD was 5.80 (95% confidence interval 3.13 to 10.76) for high level cumulative COE exposure (> or =1714.0 microg/m3-years) compared with controls. The interaction between COE exposure and smoking in COPD was significant. The risk of COPD in those with the highest cumulative exposure to COE and cigarette smoking was 58-fold compared with non-smokers not exposed to COE. CONCLUSION: Long term exposure to COE increases the risk of an interaction between COPD and cigarette smoking.
Adult↗
Peroxisome proliferator-activated receptor-gamma Pro12Ala polymorphism, Helicobacter pylori infection and non-cardia gastric carcinoma in Chinese.
BACKGROUND: Peroxisome proliferator-activated receptor gamma inhibits the growth and induces apoptosis of gastric cancer cells. A common polymorphism at codon 12 of this gene (Pro12Ala) has been shown to confer protection against diabetes and colorectal cancer. AIM: To study the association between peroxisome proliferator-activated receptor gamma gene polymorphism, Helicobacter pylori infection and gastric cancer in Chinese. METHODS: One hundred and four consecutive patients with non-cardia gastric adenocarcinoma and 104 matched controls were examined. Peroxisome proliferator-activated receptor gamma Pro12Ala polymorphism was analysed by polymerase chain reaction-restriction fragment length polymorphism. RESULTS: The frequency of peroxisome proliferator-activated receptor gamma G (Ala12) allele was significantly higher among cancer patients (19.2%) than in control (8.7%; OR 2.5, 95% CI 1.1-5.8). While H. pylori infection was more prevalent in gastric cancer patients (OR 3.0; 95% CI 1.6-5.7), the combination of peroxisome proliferator-activated receptor gamma G allele and H. pylori infection further increased the risk of gastric cancer (OR 12.8, 95% CI 3.2-50.5). The presence of the Ala12 did not increase the risk of gastric cancer in H. pylori-negative subjects. CONCLUSION: Our study suggests the potential association between peroxisome proliferator-activated receptor gamma polymorphism and H. pylori infection in the development of non-cardia gastric cancer.
Adenocarcinoma↗
Influence of mizolastine on antigen-induced activation of signalling pathways in murine mast cells.
BACKGROUND: There is accumulating evidence that some antihistamines can interrupt intermediate signalling events that regulate cell function. The effect of mizolastine on both the generation and release process of many cytokines in mast cells further implies that the inhibition by mizolastine may target signalling pathways. AIM: To observe the influence of mizolastine on antigen-induced activation of signalling pathways in murine mast cells. METHODS: Western blot analysis and enzyme assay were performed. Immunoblots were prepared from whole cell lysates and probed with antibodies against Fyn, Akt, ERK, p38, phospho-Fyn, phospho-Akt, phospho-ERK and phospho-p38, respectively. RESULTS: Our study showed that signalling molecules such as IP3, Fyn, p38 and ERK were enhanced when mast cells were stimulated by antigen, and that this was not inhibited by treatment with mizolastine. Mizolastine at concentrations from 10(-9) to 10(-5) mol/L could inhibit activation of the PI3K kinase downstream signalling molecule Akt to antigen stimulation. The study also demonstrated that mizolastine exerted inhibitory ability on protein kinase C (PKC) activation in a dose-dependent manner. CONCLUSION: PKC-mediated phosphorylation of Akt can be blocked by mizolastine. There may be a PKC-independent pathway effectively activating MAPK pathways in mast cells in response to antigen induction, which cannot be affected by mizolastine.
Animals↗
Molecular variation, systematics and distribution of the Anopheles fluviatilis complex in southern Asia.
Species of the Anopheles fluviatilis James and Anopheles minimus complexes (Diptera: Culicidae) are difficult to distinguish morphologically. Members of the two complexes have been confused and, consequently, their distributions and roles in malaria transmission are uncertain. We identified numerous mosquitoes from China, Thailand, Vietnam, India, Nepal, Pakistan and Iran by single-strand conformation polymorphism (SSCP) and/or sequencing, and analysed the variation in the 28S D3 region of ribosomal DNA for members of the Minimus Subgroup and also the internal transcribed spacer region 2 (ITS2) for members of the An. fluviatilis complex. The D3 region is highly conserved between taxa and therefore could serve as a standard for molecular diagnosis of the subgroup members. D3 sequence, bionomics and malaria transmission data provide further evidence that An. fluviatilis S in India is conspecific with An. minimus C in South-east Asia. An. fluviatilis T has three ITS2 haplotypes (designated T1, T2 and Y) and its distribution in India, Nepal, Pakistan and Iran is confirmed. An. fluviatilis U is well defined on cytogenetic grounds in Uttar Pradesh, India, but is very close to An. fluviatilis T and the two species may hybridize in some regions. Variant ITS2 sequences suggest the possible existence of two additional taxa within the An. fluviatilis complex, one in Iran and another in India, provisionally designated An. fluviatilis forms V and X, respectively. The distributions of members of the An. fluviatilis and An. minimus complexes in south-central Asia are summarized.
Animals↗
Interleukin-6 release from human abdominal adipose cells is regulated by thyroid-stimulating hormone: effect of adipocyte differentiation and anatomic depot.
Adipose cells are extrathyroidal targets of thyroid-stimulating hormone (TSH). TSH stimulates interleukin-6 (IL-6) release from adipocytes. We examined TSH responsiveness as a function of stage of differentiation or adipose tissue depot in cultured adipose cells and determined the effect of TSH on extrathyroidal IL-6 production in vivo. Stromal preadipocytes, isolated from human abdominal subcutaneous or omental adipose tissue, and their differentiated counterparts were studied. IL-6 protein concentration in the medium was measured after TSH stimulation. Basal IL-6 release was greater for preadipocytes than differentiated adipocytes, whether derived from subcutaneous or omental fat depots. A depot-dependent effect (omental > subcutaneous) on basal IL-6 release was observed for preadipocytes (1.6-fold, P < 0.05); a similar trend for differentiated adipocytes was not significant (6.2-fold, P > 0.05). IL-6 responsiveness to TSH was observed upon differentiation, but only for subcutaneous adipocytes (1.9-fold over basal, P < 0.001). To determine if TSH could stimulate IL-6 release from extrathyroidal tissues in vivo, we measured serum IL-6 levels from five thyroidectomized patients who received recombinant human (rh) TSH and found that levels increased by threefold on days 3 and 4 (P < 0.05) after its administration. Our data demonstrate that stage of differentiation and fat depot origin affect basal and TSH-stimulated IL-6 release from adipose cells in culture. Furthermore, rhTSH elevates serum IL-6 response in thyroidectomized patients, indicating an extrathyroidal site of TSH action.
Abdomen↗
Developing an NLP and IR-based algorithm for analyzing gene-disease relationships.
OBJECTIVES: High-throughput techniques such as cDNA microarray, oligonucleotide arrays, and serial analysis of gene expression (SAGE) have been developed and used to automatically screen huge amounts of gene expression data. However, researchers usually spend lots of time and money on discovering gene-disease relationships by utilizing these techniques. We prototypically implemented an algorithm that can provide some kind of predicted results for biological researchers before they proceed with experiments, and it is very helpful for them to discover gene-disease relationships more efficiently. METHODS: Due to the fast development of computer technology, many information retrieval techniques have been applied to analyze huge digital biomedical databases available worldwide. Therefore we highly expect that we can apply information retrieval (IR) technique to extract useful information for the relationship of specific diseases and genes from MEDLINE articles. Furthermore, we also applied natural language processing (NLP) methods to do the semantic analysis for the relevant articles to discover the relationships between genes and diseases. RESULTS: We have extracted gene symbols from our literature collection according to disease MeSH classifications. We have also built an IR-based retrieval system, "Biomedical Literature Retrieval System (BLRS)" and applied the N-gram model to extract the relationship features which can reveal the relationship between genes and diseases. Finally, a relationship network of a specific disease has been built to represent the gene-disease relationships. CONCLUSIONS: A relationship feature is a functional word that can reveal the relationship between one single gene and a disease. By incorporating many modern IR techniques, we found that BLRS is a very powerful information discovery tool for literature searching. A relationship network which contains the information on gene symbol, relationship feature, and disease MeSH term can provide an integrated view to discover gene-disease relationships.
Algorithms↗
Telomerase activity and the subunit of telomerase in hydatidiform mole and their relationship with the development of postmolar tumor.
OBJECTIVES: To investigate the pattern of telomerase activity and the subunit of telomerase in normal placentae and GTD, and to determine the prognostic significance of telomerase activity and the subunit of telomerase in GTD. METHODS: Telomerase activity human telomerase (hTERT) and human telomerase (hTR) expression were analyzed in the initial uterine evacuation specimen of 63 hydatidiform moles (HMs), 42 normal human placental tissues, 17 malignant gestational trophoblastic tumors, primary cultures of normal villi and JAR cell lines by use of the polymerase chain reaction-based telomeric repeat amplification protocol (TRAP) assay and reverse transcription-polymerase chain reaction (RT-PCR) methods. RESULTS: Telomerase activity was 100% in primary cultures of normal villi and JAR cell lines and in less than 60-day early placental villi, while only 9.1% in greater than 60-day placental villi, 27% in HMs and 58% in malignant trophoblastic tumors. High levels of hTR could be found in all groups. hTR expression was detected in all cases of < 60-day placental villi, in 72.7% > 60-day placental villi, in 87.3% in HMs and 100% in malignant trophoblastic tumors. Telomerase activity and hTERT expression had significant differences among the groups. Telomerase activity was associated with serum hCG levels but not related to other clinical risk factors. CONCLUSIONS: Telomerase activity may be correlated with the development of trophoblastic tumors, and hTERT may be a useful diagnostic marker for detecting the existence of malignant trophoblastic cells.
Cell Line↗
Association of childhood acute lymphoblastic leukaemia with cancers in family members.
Children whose twins have had leukaemia have a higher risk of contracting acute lymphoblastic leukaemia (ALL), confirming a prenatal origin of the disease. This association was not true when considering other types of affected first-degree relatives. Children whose fathers were diagnosed with testicular cancer have a higher risk of ALL.
Adolescent↗
Clinical and cytogenetic features of 508 Chinese patients with myelodysplastic syndrome and comparison with those in Western countries.
Myelodysplastic syndrome (MDS) is a clonal hematopoietic stem cell disorder characterized by ineffective hematopoiesis and leukemia progression. Racial differences may exist on clinical pictures and the molecular events leading to MDS, which are heterogeneous. To better define the clinical and cytogenetic features in Chinese patients, a retrospective multicentric study was performed in 508 MDS cases. Compared with Western countries, Chinese patients showed younger age (median: 49 vs 65-73 years), lower percentages of RARS (2.8 vs 6.6-15.3%), and CMML (5.2 vs 11.7-30.6%). Cytogenetically, among 367 cases with evaluable data, abnormal karyotypes were found in 136 cases, including 56 numerical and 80 structural changes. Incidences of single chromosome 5 and 7 abnormalities were lower than those in Western countries (2.2 vs 17.8-42.5%). However, complex cytogenetic aberrations and chromosome translocations were frequently observed and related to poor prognosis. Both multiple chromosome deletions and translocations were detected in advanced subtypes (RAEB and RAEB-T). Analysis of 200 cases revealed a higher incidence of hepatitis-B-virus infection than that in non-MDS population (21.00 vs 9.75%). This study further confirmed: (1) different genetic/environmental backgrounds between Asian and Western MDS populations; (2) a strong predictive value of cytogenetic abnormalities on disease outcome and involvement of genomic instability in leukemia clone development.
Adolescent↗
Potent in vivo anti-tumor activity of isolated CD62L(low) lymph node cells sensitized in vivo with tumor lysate-pulsed DC-based vaccines.
BACKGROUND: DC are potent APC that can activate both CD4 and CD8 T cells in vitro and in vivo. Although the efficacy of DC-based cancer vaccines is currently being evaluated in clinical trials, the systemic immune suppression in cancer patients negatively impacts the clinical benefit of this therapeutic approach. Therefore, in this study we tested the feasibility and anti-tumor effect of adoptive immunotherapy using in vitro-activated CD62L(low) lymph node cells that were isolated from DC-vaccinated draining lymph nodes (VDLN). METHODS: DC were prepared from BM cells and loaded with tumor lysate for inoculating into naive mice. Subsequently, the VDLN were removed and CD62L(low) cells in the VDLN population isolated, expanded in vitro by 5-day culture with IL-2 and immobilized anti-CD3 stimulation, then injected into mice with established pulmonary tumors. Eighteen days after treatment, mice were killed in order to enumerate pulmonary tumor nodes. RESULTS: DC phagocytosed the tumor lysate efficiently and induced detectable T-cell responses and significant cell expansion in the draining lymph nodes. After induction of maturation by LPS treatment, DC expressed higher levels of CD40, CD86 and MHC class II molecules. When CD62L(low) VDLN cells that had been isolated and expanded in vitro were transferred into tumor-bearing mice, as few as 3 x 10(6) cells were able to cure metastatic pulmonary tumors in vivo. DISCUSSION: DC-based VDLN T cells are an important source of anti-tumor effector for adoptive immunotherapy. This study provides a novel and an effective protocol using T-cell adoptive immunotherapy for application in cancer patients; therefore, clinical trials based on this protocol may be warranted.
Animals↗