Serum Basic Fibroblast Growth Factor Research Articles

Elevated vascular endothelial growth factor levels are associated with aortopulmonary collateral vessels in patients before and after the Fontan procedure

Aortopulmonary collaterals (APCs) are frequently observed before and after the Fontan procedure. However, the mechanism of the development of APCs is unknown. We hypothesized that one or several antiangiogenic and/or angiogenic growth factors might play a role in the development of APCs. Eighty-five patients were enrolled and divided into 3 groups (Fontan group: 30 patients after the Fontan procedure, cyanotic group: 29 patients with cyanotic heart disease, and control group: 26 patients with cyanotic heart disease after biventricular repair). We measured basic fibroblast growth factor, vascular endothelial growth factor (VEGF), hepatocyte growth factor, and endostatin at catheterization. Angiographic evaluation for the presence of APCs using a 4-point scale (grade 1: absent APCs, > or = grade 2: significantly present APCs) was performed, and the relation of the serum levels of these factors to the presence of APCs was assessed. The grade of APCs significantly increased in the Fontan group, but it decreased in the control group. The serum VEGF levels were higher in the Fontan group (280 +/- 174 pg/mL) and the cyanotic group (302 +/- 245 pg/mL) than in the control group (111 +/- 91 pg/mL) (P = .0004), and they were higher in patients with APCs (383 +/- 204 pg/mL) than in those without APCs (115 +/- 65 pg/mL) (P < .0001). There was no significant difference in the serum basic fibroblast growth factor, hepatocyte growth factor, and endostatin levels between the 3 groups. Aortopulmonary collaterals increase after the Fontan procedure. Serum VEGF levels are associated with the presence of APCs. Vascular endothelial growth factor may play a role in the development of APCs in patients with cyanotic heart disease and after the Fontan procedure.

Pseudoscleroderma associated with cancer

In the period 1994-2002, we saw 71 patients with sclerotic skin changes; 66 were diagnosed with systemic sclerosis (SSc) while five (7%) were diagnosed with pseudoscleroderma associated with various malignancies. The mean duration of disease in these five patients was significantly shorter than that of patients with SSc. The incidence of positive antinuclear antibodies, Raynaud's phenomenon or oesophageal involvement in patients with pseudoscleroderma was significantly lower than that in patients with SSc. The distributions of skin sclerosis varied in each case. Serum basic fibroblast growth factor (bFGF) levels in the five patients with pseudoscleroderma were very elevated compared with levels in controls. Elevated expression of bFGF was detected on fibroblasts of affected skin and in one lung-cancer tissue sample obtained by excision.

Basic Fibroblast Growth Factor (bFGF, FGF-2) Potentiates Leukocyte Recruitment to Inflammation by Enhancing Endothelial Adhesion Molecule Expression

Basic fibroblast growth factor (bFGF, FGF-2) is a potent angiogenic factor and endothelial cell mitogen. Although bFGF levels are increased in chronically inflamed tissue, its role in inflammation is unclear. We investigated the effect of bFGF on acute dermal inflammation and the recruitment of monocytes, T cells, and neutrophils. Leukocyte recruitment to inflamed sites was quantified with radiolabeled leukocytes. Intradermal injection of bFGF in rats did not induce leukocyte recruitment or inflammation. However, the recruitment of leukocytes to inflammation induced by tumor necrosis factor-alpha, interferon-gamma, C5a, or a delayed hypersensitivity reaction was enhanced by bFGF by 55 to 132% (P < 0.05). Either acute or prolonged bFGF treatment of dermal sites had this effect. The potentiating effect of bFGF on leukocyte recruitment was also seen in joints. There was no associated modulation of vascular permeability, blood flow, or angiogenesis in the sites by bFGF. However, the expression of the endothelial cell adhesion molecules (CAMs) for leukocytes, P-selectin, E-selectin, and ICAM-1, was significantly up-regulated in the inflamed tissue by bFGF, as quantified by radiolabeled anti-CAM antibody binding in vivo. Thus, although not directly proinflammatory, bFGF synergistically potentiates inflammatory mediator-induced leukocyte recruitment, at least in part, by enhancing CAM up-regulation on endothelium.

Serial measurement of serum basic fibroblast growth factor in patients with acute cerebral infarction

Basic fibroblast growth factor (bFGF) has been reported to be involved in the pathophysiological changes following cerebral infarction. Basic fibroblast growth factor is upregulated in the brain and conduces to neuroprotection and angiogenesis in experimental brain ischemia, but the change of serum bFGF in cerebral infarction patients has not been reported. In the present study, we investigated the dynamic changes of serum bFGF in 30 patients with acute cerebral infarction and found that serum bFGF increased significantly after cerebral infarction compared with the control group ( p < 0.05). Serum bFGF peaked on day 3 (15.46 ± 5.58 pg/ml; p < 0.01) and remained significantly elevated on day 14 following cerebral infarction. In this study, it was also found that the levels of bFGF with large infarction were higher at each time point than those with moderate or small infarction ( p < 0.05). There was a positive correlation between the peak level of bFGF and improvement of clinical neurological deficits scored by Scandinavian Stroke Scale (SSS) ( r = 0.596; p < 0.05). These results suggest that the serum bFGF level increased significantly after cerebral infarction and the level of serum bFGF could be of value to estimate the infarction size and clinical prognosis.

Phase I Safety, Pharmacokinetic, and Pharmacodynamic Study of the Thrombospondin-1–Mimetic Angiogenesis Inhibitor ABT-510 in Patients With Advanced Cancer

ABT-510 is an angiogenesis inhibitor derived from thrombospondin-1, a naturally occurring inhibitor of angiogenesis. We investigated ABT-510, which was administered subcutaneously in patients with advanced solid malignancies, to assess safety, pharmacokinetics, and serum markers of angiogenesis. ABT-510 was administered subcutaneously as a continuous infusion (100 mg/24 h) and bolus injections (100, 200, and 260 mg once daily; 50 and 100 mg twice daily) in 28-day cycles. Thirty-nine patients received a total of 144 treatment cycles. Administration by continuous infusion was hampered by the onset of painful skin infiltrates at the injection site. In the bolus injection regimens, the most common toxicities observed were mild injection-site reactions and fatigue. Maximum-tolerated dose was not defined, but 260 mg was defined as the maximum clinically practical dose. ABT-510 pharmacokinetics were linear across the dosage ranges tested, and the potential therapeutic threshold (plasma concentrations > 100 ng/mL > 3 h/d) was achieved with all dose regimens. Median serum basic fibroblast growth factor (bFGF) levels decreased from 14.1 pg/mL (range, 0.5 to 77.7 pg/mL) at baseline to 3.2 pg/mL (range, 0.2 to 29.4 pg/mL) after 56 days of treatment (P = .003). No correlations with time on study or ABT-510 dose or exposure were observed for individual changes in bFGF. Stable disease lasting for six cycles or more was seen in six patients. ABT-510 demonstrated a favorable toxicity profile and linear and time-independent pharmacokinetics with biologically relevant plasma concentrations. The significant number of patients with prolonged stable disease and the convenient method of dosing merit further studies with this angiogenesis inhibitor.

Serum basic fibroblast growth factor as a marker of reflux nephropathy

Purpose The authors investigated whether serum basic fibroblast growth factor (b-FGF) can be used as a noninvasive marker of renal parenchymal damage (scarring) in cases of vesicoureteric reflux (VUR). Methods Serum levels of b-FGF were measured in 120 children with known grade III to grade V VUR and 21 controls using a standard enzyme-linked immunosorbent assay technique. Results Sixty-five children had grade III VUR, 39 had grade IV, and 16 had grade V. Renal scarring was seen in 43 children on radionuclide scanning. There were no significant differences between serum b-FGF levels for different grades of VUR without scarring and controls. However, serum b-FGF levels were significantly higher in VUR patients with renal scarring than in patients with VUR without renal scarring ( P < .001). Conclusions This report is the first to document serum b-FGF profiles in children with VUR and renal scarring. The authors recommend measuring it as a simple, noninvasive marker of renal scarring in cases of VUR.

Infliximab downregulates basic fibroblast growth factor and vascular endothelial growth factor in Crohn's disease patients.

The use of infliximab in the treatment of Crohn's disease patients with symptomatic stenosis is controversial. To explore the influence of this agent on intestinal fibrogenesis by measuring in infliximab-treated Crohn's disease patients the serum levels of basic fibroblast growth factor and vascular endothelial growth factor, two factors known to be involved in the process of intestinal wound healing and fibrosis in this condition. Serum levels of basic fibroblast growth factor and vascular endothelial growth factor were determined by enzyme-linked immunosorbent assay in 22 patients with steroid refractory or fistulizing Crohn's disease before, during (2 weeks) and after 12 weeks of treatment with infliximab, administered at week 0, 2 and 6 in a dose of 5 mg/kg. A substantial improvement in 19 of the 22 Crohn's disease patients was accompanied by a rapid and durable reduction in basic fibroblast growth factor and vascular endothelial growth factor serum levels. The action of infliximab in reducing serum basic fibroblast growth factor and vascular endothelial growth factor would seem to suggest a role of this agent in down-regulating the process of intestinal fibrogenesis in Crohn's disease.

Increased levels of serum basic fibroblast growth factor in schizophrenia

Basic fibroblast growth factor (bFGF) is a multifunctional growth factor that has been implicated in a variety of neurodevelopmental processes. The aim of the present study was to examine whether bFGF contributes to the pathophysiology of schizophrenia. Serum bFGF levels in 40 patients with schizophrenia (15 drug-naive and 25 medicated patients) and in 40 age- and sex-matched healthy normal controls were measured. Serum bFGF levels were significantly higher in the medicated patients than in the normal controls. Analysis of partial correlation coefficients showed that the increased bFGF levels might not be attributable to antipsychotic medication. Although there was no significant overall difference in bFGF levels between drug-naive patients and normal controls, the bFGF levels in these patients significantly correlated with the severity of negative symptoms. Furthermore, we found a significant negative correlation between serum bFGF levels and the age of onset in the entire patient group. Our finding of elevated bFGF levels in the serum of patients with schizophrenia, especially in earlier age-of-onset cases considered to have more neurodevelopmental insults, suggests that bFGF abnormalities may be involved in the pathophysiology of schizophrenia.

Expression of basic fibroblast growth factor is associated with poor outcome in non-Hodgkin's lymphoma.

It is now clear that angiogenesis and angiogenesis factors are important in the pathogenesis of haematological malignancies. High pretreatment levels of serum basic fibroblast growth factor have been shown to be associated with poor prognosis in patients with non-Hodgkin's lymphoma. The aim of this study was to evaluate whether non-Hodgkin's lymphoma cells express basic fibroblast growth factor and/or its receptor (fibroblast growth factor receptor-1) and whether basic fibroblast growth factor expression correlates with basic fibroblast growth factor serum levels, intratumoral microvessel density, and patient outcome. We measured basic fibroblast growth factor by enzyme-linked immunosorbent assay in sera taken from 58 patients with non-Hodgkin's lymphoma before treatment and in 19 of them also after treatment. Pathological specimens at diagnosis were evaluated by immunohistochemistry staining using polyoclonal antibody against factor-VIII-related antigen, basic fibroblast growth factor and fibroblast growth factor receptor-1 to determine the expression of the microvessel count and basic fibroblast growth factor and fibroblast growth factor receptor-1. The lymphoma specimens demonstrated positive staining for basic fibroblast growth factor (in 23%) and fibroblast growth factor receptor-1 (in 58.5%). The patients who expressed basic fibroblast growth factor had a significantly worse progression-free and overall survival than those who did not (P=0.003 and P=0.03 respectively), while patients expressing fibroblast growth factor receptor-1 were less likely to achieve complete remission than those lacking the receptor (33% vs 65% , P=0.047). There was no correlation of basic fibroblast growth factor staining with either serum basic fibroblast growth factor levels or microvessel count. Basic fibroblast growth factor serum levels did not change significantly after treatment These results suggest that non-Hodgkin's lymphoma specimens express basic fibroblast growth factor and its receptor (fibroblast growth factor receptor-1) and this expression is associated with poor patient outcome.British Journal of Cancer (2002) 86, 1770–1775. doi:10.1038/sj.bjc.6600330 www.bjcancer.com© 2002 Cancer Research UK

44 P Serum basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) in Crohn's disease patients treated with infliximab

44 P Serum basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) in Crohn's disease patients treated with infliximab

Serum basic fibroblast growth factor levels correlate with the ultrasound measurements of bowel wall thickness (BWT) in Crohn's disease (CD)

Serum basic fibroblast growth factor levels correlate with the ultrasound measurements of bowel wall thickness (BWT) in Crohn's disease (CD)

Correlation of serum basic fibroblast growth factor levels with clinicopathologic features and postoperative recurrence in hepatocellular carcinoma

Background: Basic fibroblast growth factor (bFGF) is an important positive regulator of tumor angiogenesis. This study evaluated the role of serum bFGF as a biological marker of tumor invasiveness and postresection recurrence in hepatocellular carcinoma (HCC). Methods: Concentrations of bFGF in preoperative serum samples in 88 patients undergoing resection of HCC were measured by a quantitative enzyme-linked immunosorbent assay. A single pathologist performed histopathologic examination of all tumor specimens. All patients were prospectively monitored for tumor recurrence. Results: The preoperative serum bFGF levels ranged from <0.22 to 71.2 pg/mL (median 10.8 pg/mL). There was significant correlation between high serum bFGF levels and large tumor >5 cm, presence of venous invasion or advanced pTNM stage. Patients with a serum bFGF level >10.8 pg/mL had worse disease-free survival than those with a level <10.8 pg/mL (median disease-free survival 11.2 versus 20 months, P = 0.044). Serum bFGF level >10.8 pg/mL ( P = 0.035) and tumor size >5 cm ( P = 0.004) were independent preoperative factors that predicted early recurrence after resection of HCC. Conclusions: This study supports a role of bFGF in tumor growth and invasion in HCC. A high preoperative serum bFGF level appears to be predictive of invasive tumor and early postoperative recurrence. The clinical implications of serum bFGF level in HCC warrant further investigation.

Bcl-2 expression correlates positively with serum basic fibroblast growth factor (bFGF) and negatively with cellular vascular endothelial growth factor (VEGF) in patients with chronic lymphocytic leukaemia.

A large proportion of B-chronic lymphocytic leukaemia (B-CLL) cells express the anti-apoptotic protein Bcl-2. Basic fibroblast growth factor (bFGF) has been shown to upregulate the expression of Bcl-2 in B-CLL cell lines. Vascular endothelial growth factor (VEGF) has been shown to enhance the survival of endothelial cells by upregulating the expression of Bcl-2. In the present study, we measured serum and cellular levels of bFGF and VEGF in 85 patients with CLL using a commercial quantitative sandwich enzyme immunoassay technique. Levels of Bcl-2 were also assayed concomitantly using Western blot analysis. The mean serum level of bFGF was 53.4 pg/ml (range 0-589) and that of VEGF 459.2 pg/ml (range 33-1793). The mean cellular level of bFGF was 158.3 pg/2 x 105 cells (range 0.8-841) and VEGF, 42.4 pg/2 x 105 cells (range 0-244). A high correlation was found between serum and cellular bFGF levels (P < 0.001), but not between the corresponding VEGF levels. Twenty-nine of 69 patients (42%) evaluated for Bcl-2 level, expressed it. The Bcl-2 level was positively correlated with the serum bFGF level (P = 0.007). However, surprisingly there was a negative correlation between Bcl-2 expression and intracellular VEGF level (P = 0.003). A positive correlation was also found between serum bFGF and disease follow-up time and log white blood cell count. These findings indicate that in CLL there is a correlation between angiogenesis-related factors and apoptosis-related protein expression, and elevated bFGF levels may account for the elevated Bcl-2 levels.

Antisense Inhibition of Decorin Expression in Myoblasts Decreases Cell Responsiveness to Transforming Growth Factor β and Accelerates Skeletal Muscle Differentiation

Decorin is a member of the family of the small leucine-rich proteoglycans. In addition to its function as an extracellular matrix organizer, it has the ability to activate the epidermal growth factor receptor, and it forms complexes with various isoforms of transforming growth factor beta (TGF-beta). Decorin is expressed during skeletal muscle differentiation and is up-regulated in dystrophic muscle. In this study we investigated the role of decorin in TGF-beta-dependent inhibition of myogenesis. To probe the function of decorin during myogenesis, C(2)C(12) myoblasts were stably transfected with a plasmid expressing antisense decorin mRNA. The resulting inhibition of decorin expression led to the expression of myogenin, a master transcription factor for muscle differentiation, under growth conditions and accelerated skeletal muscle differentiation as determined by the expression of creatine kinase. In contrast myogenin expression was inhibited by adenovirally induced decorin expression or by adding exogenous decorin. Reduced synthesis of decorin resulted in a 7-fold decreased sensitivity to TGF-beta-mediated inhibition of myogenin expression. In contrast, adenovirally induced decorin expression in wild type cells resulted in a 5-fold increased sensitivity to TGF-beta-mediated inhibition of myogenin expression. Transfection studies with the TGF-beta-dependent promoter of the plasminogen activator inhibitor-1 coupled with luciferase revealed that the transducing receptors for TGF-beta1 and TGF-beta2 were involved in the different responses of wild type and antisense decorin myoblasts. These results demonstrate that a reduction of decorin expression or of decorin availability results in a decreased responsiveness to TGF-beta. These findings strongly suggest a new role for decorin during skeletal muscle terminal differentiation by activating TGF-beta-dependent signaling pathways.

Impact of serum basic fibroblast growth factor on prognosis in human renal cell carcinoma

Renal cell carcinoma is often characterised by extensive vascularity and angiogenic factors may be of importance for disease progression. Using a sandwich enzyme immunoassay, basic fibroblast growth factor (bFGF) was analysed in the sera from 206 patients with renal cell carcinoma before the initiation of therapy. The median bFGF level was 3.0 pg/ml (range <1.0–70.9 pg/ml). The serum levels were significantly correlated to tumour stage and nuclear grade. Patients with tumour thrombus to the renal or the inferior caval vein had significantly higher serum bFGF levels compared with those with non-invading tumours (P=0.007). Patients with serum bFGF levels above 3.0 pg/ml had a worse prognosis, compared with those with lower levels (P=0.001). Furthermore, patients with tumours with vein invasion had a worse prognosis compared with those without invasion. After multivariate analysis, only tumour stage and grade remained as independent prognostic factors.

Release of the angiogenesis inhibitor angiostatin in patients with proliferative diabetic retinopathy: association with retinal photocoagulation.

Proliferative diabetic retinopathy is a major debilitating disease causing most cases of blindness in humans in the Western world. Photocoagulation is the established therapy of proliferative diabetic retinopathy, although the molecular mechanisms of its effects are still not known. Recently angiostatin has been characterized as a potent inhibitor of neovascularization. Apart from a possible down-regulation of angiogenic cytokines, release of angiostatin could initiate the anti-angiogenic effects of retinal photocoagulation. We investigated the regulation of angiostatin and the angiogenic cytokines vascular endothelial growth factor and basic fibroblast growth factor in vivo by comparing vitreal concentrations of 18 control patients and 34 patients with proliferative diabetic retinopathy with and without previous photocoagulation. Concentrations of basic fibroblast growth factor and angiostatin were additionally measured in serum, while vascular endothelial growth factor is known to be regulated locally in the eye. Cytokines were measured by immunological methods. Angiostatin could be detected in 2 out of 18 control patients and in 25 out of 34 diabetic patients (p < 0.00001). Most importantly, production of angiostatin in human vitreous correlated significantly with previous retinal photocoagulation (p < 0.0001) in patients with proliferative diabetic retinopathy. Only two patients (one control and one diabetic) had detectable serum concentrations of angiostatin. Additionally patients with proliferative diabetic retinopathy and with previous photocoagulation had significantly lower concentrations of vascular endothelial growth factor (0.9 +/- 0.1 ng/ml; p < 0.0001) than diabetic patients without previous photocoagulation (4.0 +/- 0.8 ng/ml). The investigation of vitreal and serum basic fibroblast growth factor concentrations yielded no significant differences between the groups. Angiostatin is not a regularly expressed angiogenesis inhibitor in human vitreous. The alterations we observed suggest that local release of angiostatin and down-regulation of vascular endothelial growth factor mediate the therapeutic effects of retinal photocoagulation in proliferative diabetic retinopathy.

A High Pretreatment Serum Basic Fibroblast Growth Factor Concentration Is an Independent Predictor of Poor Prognosis in Non-Hodgkin’s Lymphoma

Basic fibroblast growth factor (bFGF) is a secreted multifunctional cytokine and a potent stimulator of angiogenesis in vivo. Elevated bFGF concentrations have been detected in the serum and urine of cancer patients. We measured bFGF by enzyme-linked immunosorbent assay from sera taken from 160 non-Hodgkin's lymphoma (NHL) patients before treatment and stored at -20 degrees C. The patients had been observed for at least 5 years or until death. Serum bFGF concentrations (S-bFGF) ranged from undetectable to 34.7 pg/mL (median, 3.3 pg/mL). S-bFGF was detectable with a similar frequency in all subtypes of NHL. A high pretreatment S-bFGF was associated with poor overall survival. The 5-year survival rate of the patients within the highest quartile of S-bFGF concentrations (S-bFGF = 5.5 pg/mL) was only 39%, in contrast to a 60% survival rate of the patients with lower S-bFGF (P =.019). A high S-bFGF (within the highest quartile) was associated with poor outcome also in large-cell diffuse and immunoblastic lymphomas (5-year survival rates of 28% v 56%, respectively; P =.027), which was the largest histologic subgroup (n = 66) within the series. In multivariate analyses, S-bFGF was an independent prognostic factor, both when the highest quartile was used as a cut-off value (P =.0079) and when S-bFGF and the other parameters were entered into the model as continuous variables (P =.024). In the multivariate analyses, S-bFGF had a noticeably stronger prognostic value than serum lactate dehydrogenase and the number of extranodal tumor sites, both of which are currently included as components in the International Prognostic Index.

Expression of basic fibroblast growth factor and its receptor in angiosarcoma

Angiosarcoma, a rare aggressive malignant tumor thought to be of vascular origin with high potential for metastasis, frequently occurs on the scalp of elderly people. Recent findings have shown that overexpression of basic fibroblast growth factor and its receptor is associated with neoplasia, which suggests that basic fibroblast growth factor promotes tumor vascularization and subsequent growth. In this study, we examined the immunohistologic localization of basic fibroblast growth factor and its receptor in angiosarcoma. Our results suggest that basic fibroblast growth factor synthesized in the tumor endothelial cells plays an important role in the growth and progression in angiosarcoma and that serum basic fibroblast growth factor levels are elevated in patients with nodular type angiosarcoma. (J Am Acad Dermatol 1999;41:127-9.)

Vascular endothelial growth factor platelet counts, and prognosis in renal cancer

Angiogenesis, is essential for tumour growth beyond 1–2 mm in diameter. In malignant tumours such as renal-cell cancer (RCC), high microvessel counts, an indirect measure of angiogenesis, are associated with a poor prognosis. 1 Yoshino S Kato M Odaka K Prognostic significance of microvessel count in low stage renal cell carcinoma. Int J Urol. 1995; 2: 156-160 Crossref PubMed Scopus (98) Google Scholar Vascular endothelial growth factor (VEGF) is a homodimeric cytokine encoded on chromosome 6p21·3. Due to alternative exon splicing, four different forms of VEGF have been identified, of 121, 165, 189, and 206 aminoacids. VEGF is a potent stimulator of angiogenesis both in vitro and in vivo. 2 Takahashi A Sasaki H Kim SJ et al. Markedly increased amounts of messenger RNAs for vascular endothelial growth factor and placental growth factor in renal cell carcinoma associated with angiogenesis. Cancer Res. 1994; 54: 4333-4337 Google Scholar , 3 Banks RE Forbes MA Kinsey SE et al. Release of the angiogenic cytokine vascular endothelial growth factor (VEGF) from platelets: significance for VEGF measurements and cancer biology. Br J Cancer. 1998; 77: 956-964 Crossref PubMed Scopus (515) Google Scholar In RCC, overexpression of VEGF is associated with tumour angiogenesis. 3 Banks RE Forbes MA Kinsey SE et al. Release of the angiogenic cytokine vascular endothelial growth factor (VEGF) from platelets: significance for VEGF measurements and cancer biology. Br J Cancer. 1998; 77: 956-964 Crossref PubMed Scopus (515) Google Scholar In patients with cancer a positive correlation between serum VEGF levels and disease progression has been shown. 4 Dirix LY Vermeulen PB Hubens G et al. Serum basic fibroblast growth factor and vascular endothelial growth factor and tumour growth kinetics in advanced colorectal cancer. Ann Oncol. 1996; 7: 843-848 Crossref PubMed Scopus (136) Google Scholar

Serum and Urine basic Fibroblast Growth Factor (bFGF) in Cervical Cancer Patients

Serum and Urine basic Fibroblast Growth Factor (bFGF) in Cervical Cancer Patients