Use Of TGF-β1 Research Articles

Effect of simultaneous and sequential use of TGF-β1 and TGF-β3 with FGF-2 on teno/ligamentogenic differentiation of periodontal ligament stem cells

ObjectiveThe periodontal ligament is a crucial part of the periodontium, and its regeneration is challenging. This study compares the effect of simultaneous and sequential use of FGF-2 and TGF-β1 with FGF-2 and TGF-β3 on the periodontal ligament stem cells (PDLSCs) teno/ligamentogenic differentiation. DesignThis study comprises ten different groups. A control group with only PDLSCs; FGF-2 group containing PDLSCs with a medium culture supplemented with FGF-2 (50 ng/mL). In other experimental groups, different concentrations (5 ng/mL or 10 ng/mL) of TGF-β1&-β3 simultaneously or sequentially were combined with FGF-2 on the cultured PDLSCs. TGF-β was added to the medium after day 3 in the sequential groups. Methyl Thiazolyl Tetrazolium (MTT) assay on days 3, 5, and 7 and Quantitative Real-time Polymerase Chain Reaction (RT-qPCR) analysis after day 7 were conducted to investigate PLAP1, SCX, and COL3A1, RUNX2 genes. All experiments were conducted in a triplicate. The One-way and Two-way ANOVA with Tukey post hoc were utilized to analyze the results of the MTT and RT-qPCR tests, respectively. A p-value less than 0.05 is considered significant. ResultsThe proliferation of cells on days 3, 5, and 7 was not significantly different among different experimental groups (P > 0.05). A higher expression of the PLAP1, SCX, and COL3A1 have been seen in groups with sequential use of growth factors; among these groups, the group using 5 ng/mL of TGF-β3 led other groups with the most amount of significant upregulation in PLAP1(17.69 ± 1.11 fold; P < 0.0001), SCX (5.71 ± 0.38 fold; P < 0.0001), and COL1A3 (6.35 ± 0.39 fold; P < 0.0001) expression, compared to the control group. The expression of the RUNX2 decreased in all groups compared to the control group; this reduction was more in groups with sequential use of growth factors. ConclusionThe sequential use of growth factors can be more effective than simultaneous use in teno/ligamentogenic differentiation of PDLSCs. Moreover, treatment with 5 ng/mL TGF-β3 after FGF-2 was more effective than TGF-β1.

Extracellular Vesicles Secreted by TGF-β1-Treated Mesenchymal Stem Cells Promote Fracture Healing by SCD1-Regulated Transference of LRP5.

Bone fracture repair is a multiphased regenerative process requiring paracrine intervention throughout the healing process. Mesenchymal stem cells (MSCs) play a crucial role in cell-to-cell communication and the regeneration of tissue, but their transplantation is difficult to regulate. The paracrine processes that occur in MSC-derived extracellular vesicles (MSC-EVs) have been exploited for this study. The primary goal was to determine whether EVs secreted by TGF-β1-stimulated MSCs (MSCTGF-β1-EVs) exhibit greater effects on bone fracture healing than EVs secreted by PBS-treated MSCs (MSCPBS-EVs). Our research was conducted using an in vivo bone fracture model and in vitro experiments, which included assays to measure cell proliferation, migration, and angiogenesis, as well as in vivo and in vitro gain/loss of function studies. In this study, we were able to confirm that SCD1 expression and MSC-EVs can be induced by TGF-β1. After MSCTGF-β1-EVs are transplanted in mice, bone fracture repair is accelerated. MSCTGF-β1-EV administration stimulates human umbilical vein endothelial cell (HUVEC) angiogenesis, proliferation, and migration in vitro. Furthermore, we were able to demonstrate that SCD1 plays a functional role in the process of MSCTGF-β1-EV-mediated bone fracture healing and HUVEC angiogenesis, proliferation, and migration. Additionally, using a luciferase reporter assay and chromatin immunoprecipitation studies, we discovered that SREBP-1 targets the promoter of the SCD1 gene specifically. We also discovered that the EV-SCD1 protein could stimulate proliferation, angiogenesis, and migration in HUVECs through interactions with LRP5. Our findings provide evidence of a mechanism whereby MSCTGF-β1-EVs enhance bone fracture repair by regulating the expression of SCD1. The use of TGF-β1 preconditioning has the potential to maximize the therapeutic effects of MSC-EVs in the treatment of bone fractures.

Using the interplay of magnetic guidance and controlled TGF-β release from protein-based nanocapsules to stimulate chondrogenesis.

IntroductionStimulating the proliferation and differentiation of chondrocytes for the regeneration of articular cartilage is a promising strategy, but it is currently ineffective. Although both physical stimulation and growth factors play important roles in cartilage repair, their interplay remains unclear and requires further investigation. In this study, we aimed to clarify their contribution using a magnetic drug carrier that not only can deliver growth factors but also provide an external stimulation to cells in the two-dimensional environment.Materials and methodsWe developed a nanocapsule (transforming growth factor-β1 [TGF-β1]-loaded magnetic amphiphilic gelatin nanocapsules [MAGNCs]; TGF-β1@MAGNCs) composed of hexanoic-anhydride-grafted gelatin and iron oxide nanoparticles to provide a combination treatment of TGF-β1 and magnetically induced physical stimuli. With the expression of Arg-Gly-Asp peptide in the gelatin, the TGF-β1@MAGNCs have an inherent affinity for chondrogenic ATDC5 cells.ResultsIn the absence of TGF-β1, ATDC5 cells treated with a magnetic field show significantly upregulated Col2a1 expression. Moreover, TGF-β1 slowly released from biodegradable TGF-β1@ MAGNCs further improves the differentiation with increased expression of Col2a1 and Aggrecan.ConclusionOur study shows the time-dependent interplay of physical stimuli and growth factors on chondrogenic regeneration, and demonstrates the promising use of TGF-β1@MAGNCs for articular cartilage repair.

Transforming growth factor-beta1 promotes articular cartilage repair through canonical Smad and Hippo pathways in bone mesenchymal stem cells

AimsTransforming growth factor-β1 (TGF-β1) is a chondrogenic factor and has been reported to be able to enhance chondrocyte differentiation from bone marrow mesenchymal stem cells (BMSCs). Here we investigate the molecular mechanism through which TGF-β1 chronically promotes the repair of cartilage defect and inhibit chondrocyte hypertrophy. Main methodsAnimal models of full thickness cartilage defects were divided into three groups: model group, BMSCs group (treated with BMSCs/calcium alginate gel) and BMSCs+TGF-β1 group (treated with Lentivirus-TGF-β1-EGFP transduced BMSCs/calcium alginate gel). 4 and 8weeks after treatment, macroscopic observation, histopathological study and quantitative reverse transcription-polymerase chain reaction (qRT-PCR) were done to analyze phenotypes of the animals. BMSCs were transduced with Lentivirus-TGF-β1-EGFP in vitro and Western blot analysis was performed. Key findingsWe found that TGF-β1-expressiing BMSCs improved the repair of the cartilage defect. The impaired cartilage contained higher amount of GAG and type II collagen and was integrated to the surrounding normal cartilage and higher content of GAG and type II collagen. The major events include increased expression of type II collagen following Smad2/3 phosphorylation, and inhibition of cartilage hypertrophy by increasing Yes-associated protein-1 (YAP-1) and inhibiting Runx2 and Col10 after the completion of chondrogenic differentiation. SignificanceWe conclude that TGF-β1 is beneficial to chondrogenic differentiation of BMSCs via canonical Smad pathway to promote early-repairing of cartilage defect. Furthermore, TGF-β1 inhibits chondrocyte hypertrophy by decreasing hypertrophy marker gene expression via Hippo signaling. Long-term rational use of TGF-β1 may be an alternative approach in clinic for cartilage repair and regeneration.

Cerebrospinal Fluid Biomarkers as Predictors of Shunt Response in Idiopathic Normal Pressure Hydrocephalus: A Systematic Review.

The widely accepted treatment for idiopathic normal-pressure hydrocephalus (iNPH) is a cerebrospinal fluid (CSF) diversion shunt procedure, to which approximately 80% of patients will respond. The purpose of this systematic review was to identify which CSF biomarkers have been investigated in predicting shunt responsiveness in iNPH patients, and to analyze the level of evidence for each. To find all relevant articles, a comprehensive search of Medline, Embase, and PsycINFO was conducted. The literature search identified 344 unique citations, of which 13 studies satisfied the inclusion criteria and were analyzed in our review. These 13 studies reported on 37 unique biomarkers. The available studies suggest that there is evidence for the utility of CSF biomarkers in predicting shunt responsiveness in iNPH patients, though none have been shown to predict shunt response with both high sensitivity and specificity. We found that there is no available evidence for the use of Aβ38, Aβ40, Aβ43, APL1β25, APL1β27, APL1β28, sAPP, aAPPα, sAPPβ, TNF-α, MCP-1, sCD40L, sulfatide, MBP, L-PGDS, cystatin C, transthyretin, TGF-β2, or YKL-40 in predicting shunt response. There is minimal evidence for the use of TGF-β1, TBR-II, homocysteine, and interleukins (particularly IL-1β, IL-6, and IL-10). However, the available evidence suggests that these biomarkers warrant further investigation. Aβ42, tau, p-tau, NFL, and LRG have the greatest amount of evidence for their predictive value in determining shunt responsiveness in iNPH patients. Future research should be guided by, but not limited to, these biomarkers.

TGF-β1 and contact mediated suppression by CD4+CD25+CD127− T regulatory cells of patients with self-limiting hepatitis E

Background and aimLiterature on the role of Regulatory T cells (Tregs) in acute viral infections is limited. Having established that the Tregs in self-limiting hepatitis E infection are elevated and functional, this study has focused on characterizing the specificity, phenotypes and identifying the molecules or factors responsible for enhancement of Treg cells and abrogation of Treg-mediated suppression in hepatitis E. MethodsHEV rORF2p specific (a) Treg frequency, subset analysis and expression of surface and intracellular markers on Tregs and CFSE based functional analysis by flow cytometry (b) key cytokines quantification by multiplex (c) suppressive functional assay in the presence of anti-TGF-β1 or anti-IL-10 or both antibodies or Transwell insert or in combination were performed on samples from 58 acute patients (AVH-E), 45 recovered individuals from hepatitis E and 55 controls. ResultsIn AVH-E, the increased frequencies of Tregs and Teff cells were HEV rORF2p specific and Treg cells were of effector memory phenotype. Higher expressions of HEV rORF2p stimulated CTLA-4, GITR, PD1L, CD103, CD39, TLR2 and TGF-β1 molecules on Tregs of AVH-E were observed. Tregs produced TGF-β1 and inhibited the secretion of IFN-γ. Transwell insert and cytokines blocking assays indicated Tregs mediated suppression in AVH-E patients is majorly TGF-β1 mediated and partly cell-cell contact mediated. ConclusionOverall, we have identified beneficial involvement of HEV specific, functional Tregs and TGF-β1 as the regulatory molecule responsible for enhancement of Tregs in self-limiting HEV infection. Therefore, use of TGF-β1 as a possible supplement for boosting Treg response in recovery from severe hepatitis E needs evaluation.

Blood Plasma TGF- β1 Concentration in Sporadic Dilatative Pathology of Ascending Aorta: More Questions than Answers.

Transforming growth factor β1 (TGF- β1) is a cytokine that participates in a broad range of cellular regulatory processes and is associated with various diseases including aortic aneurysm. Increased TGF- β1 levels are associated with Marfan syndrome (MFS) caused by FBN1 mutations and subsequent defects in signaling system. We studied TGF- β1 levels in 62 patients with sporadic, non syndromic, dilatative pathology of ascending aorta (DPAA) and in reference group subjects (n = 212). An initial screening of 212 reference individuals identified TGF- β1 gender discrepancies and age-dependent cytokine increase in women. Patients with DPAA had increased levels of TGF- β1 in comparison to reference group subjects (median 7.7 ng/ml, range 2.1–25.3, and median 6.2 ng/ml, range 1.0–33.1, respectively). There is a significant association between TGF-β1 concentration and DPAA (OR 1.084, CI 1.027–1.144, p = 0.004) but the mechanisms of cause and effect have not been established yet. Slightly increased TGF-β1 concentrations in patients with sporadic DPAA in comparison to the reference subjects show a potential use of TGF-β1 as a biomarker for the disease. However, cytokine dependence on age, gender, and other unknown factors among individuals with no cardiovascular complains reduces its specificity for DPAA. We would also like to raise awareness regarding the choice of methods when measuring TGF-β1 levels with an emphasis on preanalytical phase and the choice of sample.

Role of ALK5/Smad2/3 and MEK1/ERK Signaling in Transforming Growth Factor Beta 1–modulated Growth, Collagen Turnover, and Differentiation of Stem Cells from Apical Papilla of Human Tooth

IntroductionTransforming growth factor β1 (TGF-β1) plays an important role in cell proliferation, matrix formation, and odontogenesis. This study investigated the effects of TGF-β1 on stem cells from apical papilla (SCAPs) and its signaling by MEK/ERK and Smad2. MethodsSCAPs were exposed to TGF-β1 with/without pretreatment and coincubation by SB431542 (an ALK5/Smad 2/3 inhibitor) or U0126 (a MEK/ERK inhibitor). Cell growth was examined by 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyl tetrazolium bromide assay or direct counting of viable cells. Collagen content was determined by using the Sircol collagen assay (Biocolor Ltd, Newtownabbey, Northern Ireland). Cell differentiation was evaluated by measuring alkaline phosphatase (ALP) activity. Smad2 and ERK1/2 phosphorylation was analyzed by Western blotting or PathScan phospho–enzyme-linked immunosorbent assay (Cell Signaling Technology Inc, Danvers, MA). ResultsTGF-β1 stimulated the growth and collagen content of cultured SCAPs. TGF-β1 stimulated ERK1/2 and Smad2 phosphorylation within 60 minutes of exposure. Pretreatment by U0126 and SB431542 effectively prevented the TGF-β1–induced cell growth and collagen content in SCAPs. TGF-β1 stimulated ALP activity at lower concentrations (0.1–1 ng/mL) but down-regulated ALP at higher concentrations (>5 ng/mL). U0126 prevented 0.5 ng/mL TGF-β1–induced ALP activity but showed little effect on 10 ng/mL TGF-β1–induced decline of ALP in SCAPs. Interestingly, SB431542 attenuated both the stimulatory and inhibitory effects on ALP by TGF-β1. ConclusionsTGF-β1 may affect the proliferation, collagen turnover, and differentiation of SCAPs via differential activation of ALK5/Smad2 and MEK/ERK signaling. These results highlight the future use of TGF-β1 and SCAP for engineering of pulpal regeneration and apexogenesis.

Clinical significance of transforming growth factor β1 in the diagnosis of the severity of acute pancreatitis

Aim. Determine the clinical-diagnostic and prognostic value of transforming growth factor s1 (TGF-s1) at different degrees of severity of acute pancreatitis (AP) on the basis of studying the characteristics of content of anti-inflammatory cytokine in serum to create a diagnostic algorithm severity and course of AP. Methods. It is analyzed the data for the study of nature of the transforming growth factor s1 (TGF-s1) content in the serum of 94 patients with AP varying severity (mild case of AP-20 patients, average case - 12, severe case -62) in the first 24-48 hours and 7-10 days of hospitalization. Results. Analysis of the data can reliably assert that the value of TGF-s1 in the first 48 hours of admission to correlate with AP severity. It is proposed the use of TGF-s1 level in clinical and diagnostic complex of diagnostic of AP severity in the first 48 hours of hospitalization. If the patient has TGF-β1≤70.0 ng / ml it is mild AP. If the level of cytokine ≥70.1 ng / ml produce differentiation between moderate and severe AP. At the level of cytokine ≥120.1 ng / ml it is severe AP and diagnosis is completed. In the case of the definition of TGF-β1 in the range of> 80.1 - <120.0 ng / ml AP degree uncertain and requires further observation and examination. Conclusions. Diagnostic thresholds of AP severity are determined. It is allowed use of TGF-β1 in a modern complex AP diagnostics. It is proven a diagnostic and prognostic significance level of anti-inflammatory cytokine TGF-s1

Transforming growth factor beta 1 augments calvarial defect healing and promotes suture regeneration.

Repair of complex cranial defects is hindered by a paucity of appropriate donor tissue. Bone morphogenetic protein 2 (BMP2) and transforming growth factor beta 1 (TGFβ1) have been shown separately to induce bone formation through physiologically distinct mechanisms and potentially improve surgical outcome for cranial defect repair by obviating the need for donor tissue. We hypothesize that a combination of BMP2 and TGFβ1 would improve calvarial defect healing by augmenting physiologic osteogenic mechanisms. Coronal suturectomies (3×15 mm) were performed in 10-day-old New Zealand White rabbits. DermaMatrix™ (3×15mm) patterned with four treatments (vehicle, 350 ng BMP2, 200 ng TGFβ1, or 350 ng BMP2+200 ng TGFβ1) was placed in suturectomy sites and rabbits were euthanized at 6 weeks of age. Two-dimensional (2D) defect healing, bone volume, and bone density were quantified by computed tomography. Regenerated bone was qualitatively assessed histologically. One-way analysis of variance revealed significant group main effects for all bone quantity measures. Analysis revealed significant differences in 2D defect healing, bone volume, and bone density between the control group and all treatment groups, but no significant differences were detected among the three growth factor treatment groups. Qualitatively, TGFβ1 treatment produced bone with morphology most similar to native bone. TGFβ1-regenerated bone contained a suture-like tissue, growing from the lateral edge of the defect margin toward the midline. Unique to the BMP2 treatment group, regenerated bone contained lacunae with chondrocytes, demonstrating the presence of endochondral ossification. Total healing in BMP2 and TGFβ1 treatment groups is not significantly different. The combination of BMP2+TGFβ1 did not significantly increase bone healing compared with treatment with BMP2 or TGFβ1 alone postoperatively at 4 weeks. We highlight the potential use of TGFβ1 to regenerate calvarial bone and cranial sutures. TGFβ1 therapy significantly augmented bony defect healing at an earlier time point when compared with control, regenerated bone along the native intramembranous ossification pathway, and (unlike BMP2 alone or in combination with TGFβ1) permitted normal suture reformation. We propose a novel method of craniofacial bone regeneration using low-dose, spatially controlled growth factor therapies to minimize potentially harmful effects while maximizing local bioavailability and regenerating native tissues.

Co-migration of colon cancer cells and CAFs induced by TGFβ₁ enhances liver metastasis.

Colorectal cancer (CRC) cells often metastatize to the liver. Cancer-associated fibroblasts (CAFs) enhance metastasis by providing cytokines that create a favorable microenvironment and by inducing co-dissemination with tumor cells. However, the mechanisms of co-metastatization remain elusive. The aim of this study is to assess the role of TGFβ1 in CRC cell-CAFs attachment and its impact on liver metastasis. CAFs were obtained after xenotransplantation of Mc38 cells into EGFP-C57BL/6 mice. Attachment experiments with CRC cells and CAFs (with or without TGFβ1 and the inhibitory peptide P17) were carried out, as well as in vivo liver metastasis assays. TGFβ1 induced adhesion of CRC cells to CAFs, whereas exposure to P17 abrogated this effect. Co-injection of Mc38 cells with CAFs intrasplenically increased liver metastasis, as compared to injection of tumor cells alone. Pretreatment of Mc38 cells with TGFβ1 enhanced the metastatic burden, in comparison to untreated Mc38 + CAFs. TGFβ1-pretreated Mc38 cells co-metastatized with CAFs to the liver in a highly efficient way. Importantly, the metastatic burden was significantly reduced (p < 0.001) when P17 was administered in mice. The number of PCNA+ and CD-31+ cells was also reduced by P17 in these animals, indicating a decrease in proliferation and angiogenesis upon TGFβ1 signaling blockade. Through microarray analysis, we identified potential TGFβ1-regulated genes that may mediate cancer cell-stroma interactions to increase metastasis. In conclusion, TGFβ1 promotes co-travelling of CRC cells and CAFs to the liver to enhance metastasis. Our results strongly support the use of TGFβ1 targeted drugs as a novel strategy to reduce liver metastasis in CRC patients.

Effect of transforming growth factor-β1 on monocyte Toll-like receptor 4 expression in septic rats.

Sepsis is a tough problem in critical ill patients. This study aimed to investigate the dynamic changes of monocyte Toll-like receptor (TLR) 4 expression in peripheral blood of septic rats and to determine the effects of transforming growth factor (TGF)-β1 on TLR4 expression. Altogether 132 clean level SD rats were randomly divided into a control group (n=12), a sepsis model group (n=60), and a TGF-β1 intervention group (n=60). In the sepsis model group and TGF-β1 intervention group, the rats were subdivided into five groups (2-hour group, 6-hour group, 12-hour group, 24-hour group, and 48-hour group), with 12 rats in each group. Cecal ligation puncture (CLP) was performed in the sepsis model group and TGF-β1 intervention group to establish models of sepsis. The rats in the sepsis model group were injected with 1 mL normal saline at the caudal vein 0.5 hour after the model establishment; the rats in the TGF-β1 intervention group were injected with 20 ng/mL or 250 g TGF-β1 0.5 hour after the model establishment. Flow cytometry was used to detect the change of monocyte TLR4 in peripheral blood, and enzyme-linked immunosorbent assay (ELISA) was used to detect the change of TNF-α level in peripheral blood. At 6-12 hours after CLP, the monocyte TLR4 in peripheral blood started to decrease, and reached the lowest level at 12 hours. Compared to the control group, the monocyte TLR4 expression at 6 and 12 hours was lowered significantly (P<0.05). Compared to the sepsis model group at 2, 24 and 48 hours after CLP, the monocyte TLR4 expression in the TGF-β1 intervention group decreased dramatically (P<0.05), but there were no differences between the two groups at 6 and 12 hours respectively. Compared to the control group, the concentration of NF-κ in liver tissue increased significantly 6 hours after CLP (P<0.05). After use of TGF-β1, the concentration of NF-κ was decreased significantly but still higher than that of the control group. Compared to the control group, the concentration of TNF-α in peripheral blood was increased significantly at 2-48 hours after CLP (P<0.05). After use of TGF-β1, TNF-α was further increased. During sepsis, TGF-β1 can decrease the monocyte TLR4 expression and NF-κ in liver tissue, but facilitate the formation of proinflammatory mediator TNF-α. This finding indicates that TGF-β1 may play a role in promoting inflammatory response during sepsis, but this regulation is not via direct regulation of monocyte TLR4 in peripheral blood.

Plasma transforming growth factor-?1 level before radiotherapy correlates with long term outcome of patients with lung carcinoma

Plasma transforming growth factor-beta1 (TGFbeta1) levels are increased in many malignancies at the time of diagnosis, including all forms of lung carcinoma. Therefore, the potential use of TGFbeta1 as a plasma marker to predict the long term outcome of lung carcinoma patients treated with radiotherapy (RT) was evaluated. Plasma samples for 59 newly diagnosed lung carcinoma patients were assayed for TGFbeta1 before RT (pre RT), at the end of RT (end RT), and during follow-up after RT. TGFbeta1 was extracted from plasma using an acid-ethanol method. An enzyme-linked immunoadsorbent assay was used to quantify the plasma TGFbeta1 levels. The normal value for this assay is < or =7.5 ng/mL. Disease status at last follow-up was without knowledge of TGFbeta1 levels. Comparisons within groups and between groups were estimated using analysis of variance and the Student t test for unpaired data, respectively. The 59 patients were divided into 2 groups according to their disease status at last follow-up: those with no evidence of disease (NED) (n = 13) and those with disease (WD) (n = 46). The median follow up was 26.8 months and 12.4 months, respectively, for the NED and WD groups. No significant differences were found in the clinical characteristics between the two groups. The plasma TGFbeta1 level before RT was significantly higher in the WD group (mean +/- standard error of the mean [SEM] = 12.5+/-1.7 ng/mL; median = 8.6 ng/mL) compared with the NED group (mean +/- SEM = 6.0+/-1.0 ng/mL; median = 6.0 ng/mL) (P = 0.037). At the time of last follow-up, WD patients had a significantly higher plasma TGFbeta1 level (mean +/- SEM = 11.6+/-1.3 ng/mL; median = 9.6 ng/mL) compared with NED patients (mean +/- SEM = 3.7+/-0.5 ng/mL; median = 3.6 ng/mL) (P = 0.002). These data demonstrate that plasma TGFbeta1 may be a useful tumor marker in patients with lung carcinoma.

Plasma transforming growth factor‐β1 level before radiotherapy correlates with long term outcome of patients with lung carcinoma

BACKGROUND Plasma transforming growth factor-β1 (TGFβ1) levels are increased in many malignancies at the time of diagnosis, including all forms of lung carcinoma. Therefore, the potential use of TGFβ1 as a plasma marker to predict the long term outcome of lung carcinoma patients treated with radiotherapy (RT) was evaluated. METHODS Plasma samples for 59 newly diagnosed lung carcinoma patients were assayed for TGFβ1 before RT (pre RT), at the end of RT (end RT), and during follow-up after RT. TGFβ1 was extracted from plasma using an acid-ethanol method. An enzyme-linked immunoadsorbent assay was used to quantify the plasma TGFβ1 levels. The normal value for this assay is ≤7.5 ng/mL. Disease status at last follow-up was without knowledge of TGFβ1 levels. Comparisons within groups and between groups were estimated using analysis of variance and the Student t test for unpaired data, respectively. RESULTS The 59 patients were divided into 2 groups according to their disease status at last follow-up: those with no evidence of disease (NED) (n = 13) and those with disease (WD) (n = 46). The median follow up was 26.8 months and 12.4 months, respectively, for the NED and WD groups. No significant differences were found in the clinical characteristics between the two groups. The plasma TGFβ1 level before RT was significantly higher in the WD group (mean ± standard error of the mean [SEM] = 12.5 ± 1.7 ng/mL; median = 8.6 ng/mL) compared with the NED group (mean ± SEM = 6.0 ± 1.0 ng/mL; median = 6.0 ng/mL) (P = 0.037). At the time of last follow-up, WD patients had a significantly higher plasma TGFβ1 level (mean ± SEM = 11.6 ± 1.3 ng/mL; median = 9.6 ng/mL) compared with NED patients (mean ± SEM = 3.7 ± 0.5 ng/mL; median = 3.6 ng/mL) (P = 0.002). CONCLUSIONS These data demonstrate that plasma TGFβ1 may be a useful tumor marker in patients with lung carcinoma. Cancer 1999;86:1712–9. © 1999 American Cancer Society.