Xiaolian Tan - Academia.edu (original) (raw)

Papers by Xiaolian Tan

Research paper thumbnail of Altering the wettability of bitumen-treated glass surfaces with ionic surfactants

Fuel, 2011

The abilities of three ionic surfactants-sodium methylnaphthalene sulfonate (SMNS), sodium dodecy... more The abilities of three ionic surfactants-sodium methylnaphthalene sulfonate (SMNS), sodium dodecyl sulfate (SDS), and cetyl trimethylammonium bromide (CTAB)-to alter the wettability of bitumen-treated glass surfaces was examined. Surface wettability was characterized by contact angles, and all measurements were carried out under alkaline conditions by having sodium carbonate (Na 2 CO 3 ) dissolved in the aqueous phase. It was found that Na 2 CO 3 alone could slightly increase the hydrophilcity of bitumen-treated glass surfaces. With surfactants added to the system, it was demonstrated that SMNS and SDS (both anionic surfactants) were much more effective in enhancing the water wettability of bitumen-treated glass in comparison to CTAB (a cationic surfactant). X-ray photoelectron spectroscopy (XPS) analyses were also conducted to determine the functional groups and relative mass concentrations of various elements on the glass substrates. Based on these results, we speculate that most or all of the adsorbed hydrocarbon material could be removed from a glass substrate through synergistic effects between sodium carbonate, which provides the alkaline condition, and anionic surfactants, which likely interacted with adsorbed cationic materials. This resulted in dramatic alteration in the wettability of bitumen-treated glass surfaces-from oil-wet to water-wet.

Research paper thumbnail of Haploinsufficiency of CBFA2 causes familial thrombocytopenia with propensity to develop acute myelogenous leukaemia

Nature genetics, 1999

Familial platelet disorder with predisposition to acute myelogenous leukaemia (FPD/AML, MIM 60139... more Familial platelet disorder with predisposition to acute myelogenous leukaemia (FPD/AML, MIM 601399) is an autosomal dominant disorder characterized by qualitative and quantitative platelet defects, and propensity to develop acute myelogenous leukaemia (AML). Informative recombination events in 6 FPD/AML pedigrees with evidence of linkage to markers on chromosome 21q identified an 880-kb interval containing the disease gene. Mutational analysis of regional candidate genes showed nonsense mutations or intragenic deletion of one allele of the haematopoietic transcription factor CBFA2 (formerly AML1) that co-segregated with the disease in four FPD/AML pedigrees. We identified heterozygous CBFA2 missense mutations that co-segregated with the disease in the remaining two FPD/AML pedigrees at phylogenetically conserved amino acids R166 and R201, respectively. Analysis of bone marrow or peripheral blood cells from affected FPD/AML individuals showed a decrement in megakaryocyte colony forma...

Research paper thumbnail of Radial scars of the breast and breast carcinomas have similar alterations in expression of factors involved in vascular stroma formation

Human pathology, 2002

We recently reported that radial scars are an independent histologic risk factor for breast cance... more We recently reported that radial scars are an independent histologic risk factor for breast cancer. The reason for this association is not known. Given the importance of stromal-epithelial interactions in the pathogenesis of breast cancer, we studied radial scars for the expression of a number of factors known to be involved in the formation of vascular stroma in breast cancer. In situ hybridization was performed on formalin-fixed paraffin sections using (35)S-labeled riboprobes for collagen type 1, total fibronectin, extra domain A (ED-A)+ fibronectin, thrombospondin 1, vascular permeability factor (VPF)/vascular endothelial growth factor (VEGF), and one of its endothelial receptors, kinase insert domain-containing receptor (KDR) (vascular endothelial growth factor receptor [VEGFR-2]). Expression levels in radial scars (9 cases) were compared with those in normal breast tissue (15 cases) and infiltrating ductal breast carcinoma (4 cases). Factor VIII-related antigen immunostaining ...

Research paper thumbnail of PLAG1 Fusion Oncogenes in Lipoblastoma1

Lipoblastomas are pediatric neoplasms resulting from transformation of adipocytes. These benign t... more Lipoblastomas are pediatric neoplasms resulting from transformation of adipocytes. These benign tumors are typically composed of adipose cells in different stages of maturation within a variably myxoid matrix, and they contain clonal rearrangements of chromosome band 8q12. Because lipoblastomas resemble embryonic adipose tissue, characterization of their transforming mechanisms might reveal biological pathways in phys- iological adipogenesis. Herein, we demonstrate that

Research paper thumbnail of Enhancement of intranasal vaccination with recombinant chain A ricin vaccine (rRV) in mice by the mucosal adjuvants LTK63 and LTR72

Vaccine, 2007

Intranasal (i.n.) vaccination of mice with three doses of 40 microg of rRV stimulated low anti-ri... more Intranasal (i.n.) vaccination of mice with three doses of 40 microg of rRV stimulated low anti-ricin ELISA and neutralizing antibody responses, which were only marginally protective against aerosol-delivered 5-10 LD(50) of ricin toxin. To enhance the protection, and to reduce the lung injury of vaccinated mice that survived ricin toxin challenge, the mucosal adjuvant LTK63 or LTR72, two mutants of Escherichia coli LT enterotoxin adjuvant was administered with rRV. The safety of intranasally administered LTR63 was assessed as well. With 4, 2, or l microg of LTR63, the anti-ricin ELISA serum immunoglobulin geometric mean titer (GMT) increased up to 147-, 356-, 493-, and 17-fold for IgG, IgG1, IgG2a, and IgA, respectively. The comparable increases for GMTs of IgG and IgG1 in the presence LTR72 were up to 147-, and 617-fold, respectively. All three dose levels of LTK63 enhanced the ELISA GMTs in the lung lavage up to 192-, 22-, 4-, and 5-fold for IgG, IgG1, IgG2a, and IgA, respectively. Compared to GMT of rRV alone, the serum-neutralizing antibody GMTs for the three dose levels were enhanced up to 11-fold with LTK63. LTK63 augmented the ricin-related lymphoproliferative response of the cultured spleen lymphocytes and of the isolated CD4+ T lymphocytes. In the cultured lymphocytes, LTK63 stimulated predominantly TH1 cytokines. While only 10% of the mice that were vaccinated with rRV survived lethal challenge, in the presence of LTK63 or LTR72, the respective survival rates were augmented to 100%. Compared to the surviving mice vaccinated with rRV alone, the vaccine with LTK63 or LTR72 did not attenuate the extent of the ricin-related lung injury at a single or two time-points, respectively. Safety of LTK63 administration was indicated by the absence of histopathological changes in every organ, including the lungs and in the central nervous systems (CNS) of the mice during the entire 92 days of the study. In the nasal passages of the mice that received LTK63, a transient inflammation occurred without permanent epithelial changes. Administration of three dose levels of the adjuvant in the presence of rRV caused no additional changes. LTK63 and LTR72 both were very effective and safe mucosal adjuvants at all three dose levels employed in these studies. Both significantly enhanced the protection of a marginally effective dose of rRV against aerosol-delivered ricin challenge. LTK63 stimulated cytokines, which could be surrogate markers of efficacy, with human relevance potential. In spite of the better efficacy, rRV with LTK63, or with LTR72, failed to reduce the ricin-related lung injury. Most likely, a larger than suboptimal dose could resolve the lung injury of the vaccinated mice in the presence of a larger dose of the mucosal adjuvant.

Research paper thumbnail of Genome-Wide ORFeome Cloning and Analysis of Arabidopsis Transcription Factor Genes

Research paper thumbnail of Pharmacologic Blockade of Angiopoietin-2 Is Efficacious against Model Hemangiomas in Mice

Journal of Investigative Dermatology, 2006

Hemangioma of infancy is the most common neoplasm of childhood. While hemangiomas are classic exa... more Hemangioma of infancy is the most common neoplasm of childhood. While hemangiomas are classic examples of angiogenesis, the angiogenic factors responsible for hemangiomas are not fully understood. Previously, we demonstrated that malignant endothelial tumors arise in the setting of autocrine loops involving vascular endothelial growth factor (VEGF) and its major mitogenic receptor vascular endothelial growth factor receptor 2. Hemangiomas of infancy differ from malignant endothelial tumors in that they usually regress, or can be induced to regress by pharmacologic means, suggesting that angiogenesis in hemangiomas differs fundamentally from that of malignant endothelial tumors. Here, we demonstrate constitutive activation of the endothelial tie-2 receptor in human hemangioma of infancy and, using a murine model of hemangioma, bEnd.3 cells; we show that bEnd.3 hemangiomas produce both angiopoietin-2 (ang-2) and its receptor, tie-2, in vivo. We also demonstrate that inhibition of tie-2 signaling with a soluble tie-2 receptor decreases bEnd.3 hemangioma growth in vivo. The efficacy of tie-2 blockade suggests that either tie-2 activation or ang-2 may be required for in vivo growth. To address this issue, we used tie-2-deficient bEnd.3 hemangioma cells, which, surprisingly, were fully proficient in in vivo growth. Previous studies from our laboratory and others have implicated reactive oxygen-generating nox enzymes in the angiogenic switch, so we examined the effect of nox inhibitors on ang-2 production in vitro and on bEnd.3 tumor growth in vivo. We then inhibited ang-2 production pharmacologically using novel inhibitors of nox enzymes and found that this treatment nearly abolished bEnd.3 hemangioma growth in vivo. Signal-transduction blockade targeting ang-2 production may be useful in the treatment of human hemangiomas in vivo.

Research paper thumbnail of Orphan nuclear receptor TR3/Nur77 regulates VEGF-A-induced angiogenesis through its transcriptional activity

Journal of Experimental Medicine, 2006

angiogenesis, but the downstream steps and mechanisms by which human VEGF-A acts are incompletely... more angiogenesis, but the downstream steps and mechanisms by which human VEGF-A acts are incompletely understood. We report here that human VEGF-A exerts much of its angiogenic activity by up-regulating the expression of TR3 (mouse homologue Nur77), an immediate-early response gene and orphan nuclear receptor transcription factor previously implicated in tumor cell, lymphocyte, and neuronal growth and apoptosis. Overexpression of TR3 in human umbilical vein endothelial cells (HUVECs) resulted in VEGF-A-independent proliferation, survival, and induction of several cell cycle genes, whereas expression of antisense TR3 abrogated the response to VEGF-A in these assays and also inhibited tube formation. Nur77 was highly expressed in several types of VEGF-A-dependent pathological angiogenesis in vivo. Also, using a novel endothelial cell-selective retroviral targeting system, overexpression of Nur77 DNA potently induced angiogenesis in the absence of exogenous VEGF-A, whereas Nur77 antisense strongly inhibited VEGF-A-induced angiogenesis. B16F1 melanoma growth and angiogenesis were greatly inhibited in Nur77 −/−

Research paper thumbnail of With Propensity to Develop Acute Myelogenous Leukaemia

Familial platelet disorder with predisposition to acute myelogenous leukaemia (FPD/AML, MIM 60139... more Familial platelet disorder with predisposition to acute myelogenous leukaemia (FPD/AML, MIM 601399) is an auto- somal dominant disorder characterized by qualitative and quantitative platelet defects, and propensity to develop acute myelogenous leukaemia (AML). Informative recombination events in 6 FPD/AML pedigrees with evidence of linkage to markers on chromosome 21q identified an 880-kb interval containing the disease gene. Mutational analysis of regional candidate genes showed nonsense mutations or intragenic deletion of one allele of the haematopoietic transcription factor CBFA2 (formerly AML1) that co-segregated with the disease in four FPD/AML pedigrees. We identified heterozygous CBFA2 missense mutations that co-segregated with the disease in the remaining two FPD/AML pedigrees at phylogenetically conserved amino acids R166 and R201, respectively. Analy- sis of bone marrow or peripheral blood cells from affected FPD/AML individuals showed a decrement in megakaryocyte colony f...

Research paper thumbnail of Vascular permeability factor/vascular endothelial growth factor (VPF/VEGF) and its receptor flt-1 in microcystic meningiomas

Acta Neuropathologica, 1999

Research paper thumbnail of Role of vascular endothelial growth factor-A in recurrent respiratory papillomatosis

The Annals of otology, rhinology, and laryngology, 2005

Vascular endothelial growth factor-A (VEGF-A) is known to play an important role in the angiogeni... more Vascular endothelial growth factor-A (VEGF-A) is known to play an important role in the angiogenic response essential for tumor growth in a variety of human and experimental tumors. This study was designed to investigate whether VEGF-A may play a role in the pathogenesis of recurrent respiratory papillomatosis (RRP). A retrospective study with institutional review board approval was performed at a tertiary care medical center on 12 patients with a history of laryngeal RRP. Their ages at the time of initial diagnosis ranged from 19 to 96 months (mean, 56 months). All patients had involvement of right and left true vocal cords. All patients required multiple endoscopic procedures (range, 4 to 66; mean, 12). Normal pediatric larynx samples from 5 autopsy patients were used as controls. Formalin-fixed, paraffin-embedded sections of laryngeal squamous papillomas from the 12 patients with a diagnosis of RRP and the 5 control patients were examined by in situ hybridization for the presence...

Research paper thumbnail of Altering the wettability of bitumen-treated glass surfaces with ionic surfactants

Fuel, 2011

The abilities of three ionic surfactants-sodium methylnaphthalene sulfonate (SMNS), sodium dodecy... more The abilities of three ionic surfactants-sodium methylnaphthalene sulfonate (SMNS), sodium dodecyl sulfate (SDS), and cetyl trimethylammonium bromide (CTAB)-to alter the wettability of bitumen-treated glass surfaces was examined. Surface wettability was characterized by contact angles, and all measurements were carried out under alkaline conditions by having sodium carbonate (Na 2 CO 3 ) dissolved in the aqueous phase. It was found that Na 2 CO 3 alone could slightly increase the hydrophilcity of bitumen-treated glass surfaces. With surfactants added to the system, it was demonstrated that SMNS and SDS (both anionic surfactants) were much more effective in enhancing the water wettability of bitumen-treated glass in comparison to CTAB (a cationic surfactant). X-ray photoelectron spectroscopy (XPS) analyses were also conducted to determine the functional groups and relative mass concentrations of various elements on the glass substrates. Based on these results, we speculate that most or all of the adsorbed hydrocarbon material could be removed from a glass substrate through synergistic effects between sodium carbonate, which provides the alkaline condition, and anionic surfactants, which likely interacted with adsorbed cationic materials. This resulted in dramatic alteration in the wettability of bitumen-treated glass surfaces-from oil-wet to water-wet.

Research paper thumbnail of Haploinsufficiency of CBFA2 causes familial thrombocytopenia with propensity to develop acute myelogenous leukaemia

Nature genetics, 1999

Familial platelet disorder with predisposition to acute myelogenous leukaemia (FPD/AML, MIM 60139... more Familial platelet disorder with predisposition to acute myelogenous leukaemia (FPD/AML, MIM 601399) is an autosomal dominant disorder characterized by qualitative and quantitative platelet defects, and propensity to develop acute myelogenous leukaemia (AML). Informative recombination events in 6 FPD/AML pedigrees with evidence of linkage to markers on chromosome 21q identified an 880-kb interval containing the disease gene. Mutational analysis of regional candidate genes showed nonsense mutations or intragenic deletion of one allele of the haematopoietic transcription factor CBFA2 (formerly AML1) that co-segregated with the disease in four FPD/AML pedigrees. We identified heterozygous CBFA2 missense mutations that co-segregated with the disease in the remaining two FPD/AML pedigrees at phylogenetically conserved amino acids R166 and R201, respectively. Analysis of bone marrow or peripheral blood cells from affected FPD/AML individuals showed a decrement in megakaryocyte colony forma...

Research paper thumbnail of Radial scars of the breast and breast carcinomas have similar alterations in expression of factors involved in vascular stroma formation

Human pathology, 2002

We recently reported that radial scars are an independent histologic risk factor for breast cance... more We recently reported that radial scars are an independent histologic risk factor for breast cancer. The reason for this association is not known. Given the importance of stromal-epithelial interactions in the pathogenesis of breast cancer, we studied radial scars for the expression of a number of factors known to be involved in the formation of vascular stroma in breast cancer. In situ hybridization was performed on formalin-fixed paraffin sections using (35)S-labeled riboprobes for collagen type 1, total fibronectin, extra domain A (ED-A)+ fibronectin, thrombospondin 1, vascular permeability factor (VPF)/vascular endothelial growth factor (VEGF), and one of its endothelial receptors, kinase insert domain-containing receptor (KDR) (vascular endothelial growth factor receptor [VEGFR-2]). Expression levels in radial scars (9 cases) were compared with those in normal breast tissue (15 cases) and infiltrating ductal breast carcinoma (4 cases). Factor VIII-related antigen immunostaining ...

Research paper thumbnail of PLAG1 Fusion Oncogenes in Lipoblastoma1

Lipoblastomas are pediatric neoplasms resulting from transformation of adipocytes. These benign t... more Lipoblastomas are pediatric neoplasms resulting from transformation of adipocytes. These benign tumors are typically composed of adipose cells in different stages of maturation within a variably myxoid matrix, and they contain clonal rearrangements of chromosome band 8q12. Because lipoblastomas resemble embryonic adipose tissue, characterization of their transforming mechanisms might reveal biological pathways in phys- iological adipogenesis. Herein, we demonstrate that

Research paper thumbnail of Enhancement of intranasal vaccination with recombinant chain A ricin vaccine (rRV) in mice by the mucosal adjuvants LTK63 and LTR72

Vaccine, 2007

Intranasal (i.n.) vaccination of mice with three doses of 40 microg of rRV stimulated low anti-ri... more Intranasal (i.n.) vaccination of mice with three doses of 40 microg of rRV stimulated low anti-ricin ELISA and neutralizing antibody responses, which were only marginally protective against aerosol-delivered 5-10 LD(50) of ricin toxin. To enhance the protection, and to reduce the lung injury of vaccinated mice that survived ricin toxin challenge, the mucosal adjuvant LTK63 or LTR72, two mutants of Escherichia coli LT enterotoxin adjuvant was administered with rRV. The safety of intranasally administered LTR63 was assessed as well. With 4, 2, or l microg of LTR63, the anti-ricin ELISA serum immunoglobulin geometric mean titer (GMT) increased up to 147-, 356-, 493-, and 17-fold for IgG, IgG1, IgG2a, and IgA, respectively. The comparable increases for GMTs of IgG and IgG1 in the presence LTR72 were up to 147-, and 617-fold, respectively. All three dose levels of LTK63 enhanced the ELISA GMTs in the lung lavage up to 192-, 22-, 4-, and 5-fold for IgG, IgG1, IgG2a, and IgA, respectively. Compared to GMT of rRV alone, the serum-neutralizing antibody GMTs for the three dose levels were enhanced up to 11-fold with LTK63. LTK63 augmented the ricin-related lymphoproliferative response of the cultured spleen lymphocytes and of the isolated CD4+ T lymphocytes. In the cultured lymphocytes, LTK63 stimulated predominantly TH1 cytokines. While only 10% of the mice that were vaccinated with rRV survived lethal challenge, in the presence of LTK63 or LTR72, the respective survival rates were augmented to 100%. Compared to the surviving mice vaccinated with rRV alone, the vaccine with LTK63 or LTR72 did not attenuate the extent of the ricin-related lung injury at a single or two time-points, respectively. Safety of LTK63 administration was indicated by the absence of histopathological changes in every organ, including the lungs and in the central nervous systems (CNS) of the mice during the entire 92 days of the study. In the nasal passages of the mice that received LTK63, a transient inflammation occurred without permanent epithelial changes. Administration of three dose levels of the adjuvant in the presence of rRV caused no additional changes. LTK63 and LTR72 both were very effective and safe mucosal adjuvants at all three dose levels employed in these studies. Both significantly enhanced the protection of a marginally effective dose of rRV against aerosol-delivered ricin challenge. LTK63 stimulated cytokines, which could be surrogate markers of efficacy, with human relevance potential. In spite of the better efficacy, rRV with LTK63, or with LTR72, failed to reduce the ricin-related lung injury. Most likely, a larger than suboptimal dose could resolve the lung injury of the vaccinated mice in the presence of a larger dose of the mucosal adjuvant.

Research paper thumbnail of Genome-Wide ORFeome Cloning and Analysis of Arabidopsis Transcription Factor Genes

Research paper thumbnail of Pharmacologic Blockade of Angiopoietin-2 Is Efficacious against Model Hemangiomas in Mice

Journal of Investigative Dermatology, 2006

Hemangioma of infancy is the most common neoplasm of childhood. While hemangiomas are classic exa... more Hemangioma of infancy is the most common neoplasm of childhood. While hemangiomas are classic examples of angiogenesis, the angiogenic factors responsible for hemangiomas are not fully understood. Previously, we demonstrated that malignant endothelial tumors arise in the setting of autocrine loops involving vascular endothelial growth factor (VEGF) and its major mitogenic receptor vascular endothelial growth factor receptor 2. Hemangiomas of infancy differ from malignant endothelial tumors in that they usually regress, or can be induced to regress by pharmacologic means, suggesting that angiogenesis in hemangiomas differs fundamentally from that of malignant endothelial tumors. Here, we demonstrate constitutive activation of the endothelial tie-2 receptor in human hemangioma of infancy and, using a murine model of hemangioma, bEnd.3 cells; we show that bEnd.3 hemangiomas produce both angiopoietin-2 (ang-2) and its receptor, tie-2, in vivo. We also demonstrate that inhibition of tie-2 signaling with a soluble tie-2 receptor decreases bEnd.3 hemangioma growth in vivo. The efficacy of tie-2 blockade suggests that either tie-2 activation or ang-2 may be required for in vivo growth. To address this issue, we used tie-2-deficient bEnd.3 hemangioma cells, which, surprisingly, were fully proficient in in vivo growth. Previous studies from our laboratory and others have implicated reactive oxygen-generating nox enzymes in the angiogenic switch, so we examined the effect of nox inhibitors on ang-2 production in vitro and on bEnd.3 tumor growth in vivo. We then inhibited ang-2 production pharmacologically using novel inhibitors of nox enzymes and found that this treatment nearly abolished bEnd.3 hemangioma growth in vivo. Signal-transduction blockade targeting ang-2 production may be useful in the treatment of human hemangiomas in vivo.

Research paper thumbnail of Orphan nuclear receptor TR3/Nur77 regulates VEGF-A-induced angiogenesis through its transcriptional activity

Journal of Experimental Medicine, 2006

angiogenesis, but the downstream steps and mechanisms by which human VEGF-A acts are incompletely... more angiogenesis, but the downstream steps and mechanisms by which human VEGF-A acts are incompletely understood. We report here that human VEGF-A exerts much of its angiogenic activity by up-regulating the expression of TR3 (mouse homologue Nur77), an immediate-early response gene and orphan nuclear receptor transcription factor previously implicated in tumor cell, lymphocyte, and neuronal growth and apoptosis. Overexpression of TR3 in human umbilical vein endothelial cells (HUVECs) resulted in VEGF-A-independent proliferation, survival, and induction of several cell cycle genes, whereas expression of antisense TR3 abrogated the response to VEGF-A in these assays and also inhibited tube formation. Nur77 was highly expressed in several types of VEGF-A-dependent pathological angiogenesis in vivo. Also, using a novel endothelial cell-selective retroviral targeting system, overexpression of Nur77 DNA potently induced angiogenesis in the absence of exogenous VEGF-A, whereas Nur77 antisense strongly inhibited VEGF-A-induced angiogenesis. B16F1 melanoma growth and angiogenesis were greatly inhibited in Nur77 −/−

Research paper thumbnail of With Propensity to Develop Acute Myelogenous Leukaemia

Familial platelet disorder with predisposition to acute myelogenous leukaemia (FPD/AML, MIM 60139... more Familial platelet disorder with predisposition to acute myelogenous leukaemia (FPD/AML, MIM 601399) is an auto- somal dominant disorder characterized by qualitative and quantitative platelet defects, and propensity to develop acute myelogenous leukaemia (AML). Informative recombination events in 6 FPD/AML pedigrees with evidence of linkage to markers on chromosome 21q identified an 880-kb interval containing the disease gene. Mutational analysis of regional candidate genes showed nonsense mutations or intragenic deletion of one allele of the haematopoietic transcription factor CBFA2 (formerly AML1) that co-segregated with the disease in four FPD/AML pedigrees. We identified heterozygous CBFA2 missense mutations that co-segregated with the disease in the remaining two FPD/AML pedigrees at phylogenetically conserved amino acids R166 and R201, respectively. Analy- sis of bone marrow or peripheral blood cells from affected FPD/AML individuals showed a decrement in megakaryocyte colony f...

Research paper thumbnail of Vascular permeability factor/vascular endothelial growth factor (VPF/VEGF) and its receptor flt-1 in microcystic meningiomas

Acta Neuropathologica, 1999

Research paper thumbnail of Role of vascular endothelial growth factor-A in recurrent respiratory papillomatosis

The Annals of otology, rhinology, and laryngology, 2005

Vascular endothelial growth factor-A (VEGF-A) is known to play an important role in the angiogeni... more Vascular endothelial growth factor-A (VEGF-A) is known to play an important role in the angiogenic response essential for tumor growth in a variety of human and experimental tumors. This study was designed to investigate whether VEGF-A may play a role in the pathogenesis of recurrent respiratory papillomatosis (RRP). A retrospective study with institutional review board approval was performed at a tertiary care medical center on 12 patients with a history of laryngeal RRP. Their ages at the time of initial diagnosis ranged from 19 to 96 months (mean, 56 months). All patients had involvement of right and left true vocal cords. All patients required multiple endoscopic procedures (range, 4 to 66; mean, 12). Normal pediatric larynx samples from 5 autopsy patients were used as controls. Formalin-fixed, paraffin-embedded sections of laryngeal squamous papillomas from the 12 patients with a diagnosis of RRP and the 5 control patients were examined by in situ hybridization for the presence...