Patrick A Adegboyega

Louisiana State University in Shreveport, Shreveport, Louisiana, United States

Are you Patrick A Adegboyega?

Claim your profile

Publications (93)437.4 Total impact

  • Cancer Research 08/2013; 73(8 Supplement):3675-3675. DOI:10.1158/1538-7445.AM2013-3675 · 9.28 Impact Factor
  • Source
    Isaac Downs · Tak Yee Aw · Jianfeng Liu · Patrick Adegboyega · Maureen N Ajuebor
    [Show abstract] [Hide abstract]
    ABSTRACT: Acetaminophen (APAP) overdose is widely regarded as a major cause of acute liver failure in the United States. Intentional or accidental overdose of APAP in man or rodent elicits direct hepatocellular injury that is accompanied by hepatic depletion of the antioxidant, glutathione (GSH). In recent years, the innate immune response has also been shown to promote the development of APAP hepatotoxicity via indirect liver damage. In the present study, we demonstrate that Jα18(-/-) mice, which are selectively deficient in the innate immune T cell, Vα14iNKT cells, were resistant to APAP hepatotoxicity relative to WT mice as reflected by biochemical and histological liver injury markers. In parallel, improvement in the biochemical and histological parameters of liver injury in Jα18(-/-) mice was associated with a significant increase in hepatic levels of GSH, which detoxified APAP metabolites to attenuate hepatic oxidative stress, liver injury and necrosis. Notably, the protective effect of hepatic GSH during Vα14iNKT cells deficiency was demonstrated by its depletion in Jα18(-/-) mice using dl-buthionine-[S,R]-sulfoximine which exacerbated hepatic oxidative and nitrosative stress as well as liver necrosis and caused mice mortality. Extraordinarily, APAP metabolism in Jα18(-/-) mice was altered in favor of hepatic GSH conjugates and decreased glucuronide conjugates. In summary, we reveal a novel finding establishing a unique association between hepatic innate immunity and GSH levels in altering APAP metabolism to suppress liver injury and necrosis during Vα14iNKT cells deficiency in Jα18(-/-) mice.
    Biochemical and Biophysical Research Communications 10/2012; 428(2). DOI:10.1016/j.bbrc.2012.10.029 · 2.28 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The purpose of the current study was to determine whether a tropical ginger derived compound 1'-acetoxychavicol acetate (ACA), suppresses skin tumor promotion in K5.Stat3C mice. In a two-week study in which wild-type (WT) and K5.Stat3C mice were co-treated with either vehicle, ACA, galanga extract, or fluocinolone acetonide (FA) and tetradecanoyl phorbol acetate (TPA), only the galanga extract and FA suppressed TPA-induced skin hyperproliferation and wet weight. None of these agents were effective at suppressing pTyr705 Stat3 expression. However, ACA and FA showed promising inhibitory effects against skin tumorigenesis in K5.Stat3C mice. ACA also suppressed phospho-p65 NF-kappaB activation, suggesting a potential mechanism for its action.
    Journal of Experimental & Clinical Cancer Research 06/2012; 31(1):57. DOI:10.1186/1756-9966-31-57 · 4.23 Impact Factor
  • Source
    Isaac Downs · Jianfeng Liu · Tak Yee Aw · Patrick A Adegboyega · Maureen N Ajuebor
    [Show abstract] [Hide abstract]
    ABSTRACT: Uncontrolled systemic activation of the immune system is an early initiating event that leads to development of acute fulminant liver failure (FLF) in mice after treatment with agonistic Fas mAb. In this study, we demonstrate that treatment of mice with N-acetylcysteine (NAC), an ROS scavenger and glutathione (GSH) precursor, almost completely abolished Fas mAb-induced FLF through suppression of Vα14iNKT cell activation, IFN-γ signaling, apoptosis and nitrotyrosine formation in liver. In addition, enrichment of the liver with GSH due to Vα14iNKT cells deficiency, induced an anti-inflammatory response in the liver of Jα18(-/-) mice that inhibited apoptosis, nitrotyrosine formation, IFN-γ signaling and effector functions. In summary, we propose a novel and previously unrecognized pro-inflammatory and pro-apoptotic role for endogenous ROS in stimulating Th1 signaling in Vα14iNKT cells to promote the development of FLF. Therefore, our study provides critical new insights into how NAC, a ROS scavenger, regulates Th1 signaling in intrahepatic Vα14iNKT cells to impact inflammatory and pathological responses.
    PLoS ONE 06/2012; 7(6):e38051. DOI:10.1371/journal.pone.0038051 · 3.23 Impact Factor
  • Tanya Varma · Patrick Adegboyega
    [Show abstract] [Hide abstract]
    ABSTRACT: Primary cardiac synovial sarcoma is an uncommon malignant neoplasm, with only a handful of cases reported in the English literature to date. Synovial sarcomas have also been described at other unusual sites, such as the heart, pleuropulmonary region, kidney, prostate, liver, mediastinum, retroperitoneum, gastrointestinal tract, and peripheral nerve. For synovial sarcomas that arise at these unusual locations, definitive diagnosis is challenging and requires use of ancillary diagnostic procedures, such as immunohistochemistry, electron microscopy, and molecular genetic techniques, for confirmation of diagnosis. The nonrandom occurrence of t(X;18) has been found consistently in synovial sarcomas. It has also been found as a sole cytogenetic abnormality in some cases, suggesting it as a key molecular event in tumor development. This review highlights salient features of primary cardiac synovial sarcoma and the associated diagnostic challenges.
    Archives of pathology & laboratory medicine 04/2012; 136(4):454-8. DOI:10.5858/arpa.2011-0008-RS · 2.88 Impact Factor
  • Cancer Research 07/2011; 71(8 Supplement):4861-4861. DOI:10.1158/1538-7445.AM2011-4861 · 9.28 Impact Factor
  • Patrick A Adegboyega
    [Show abstract] [Hide abstract]
    ABSTRACT: A case of a 48-year-old woman with a 5 cm left vulvar mass that grew over a six month period is presented. Histopathologic examination of the excised mass was diagnostic of malignant eccrine poroma (eccrine porocarcinoma) with in-situ component. Due to the rarity of this tumor (only five vulvar cases previously reported) and its heterogeneous non-specific clinical and histologic features, the tumor often presents as a diagnostic challenge to clinicians and pathologists. The tumor may be mistaken for a metastasis in cases where the tumor cells are poorly differentiated or for a squamous cell carcinoma in cases with extensive squamous differentiation. There is a need for correct diagnosis of this rare entity - so that appropriate therapy can be instituted in a timely manner. The pertinent literature is reviewed highlighting the diagnostic histomorphologic features and the immunohistochemical profile for making the correct diagnosis of eccrine porocarcinoma.
    International journal of gynecological pathology: official journal of the International Society of Gynecological Pathologists 01/2011; 30(1):95-100. DOI:10.1097/PGP.0b013e3181ea11b1 · 1.63 Impact Factor
  • Estelle Yoo · Jaiyeola O Thomas · Patrick A Adegboyega · Timothy S Lian
    The Laryngoscope 10/2010; 120(S3):S53. DOI:10.1002/lary.21237 · 2.03 Impact Factor
  • Source
    Maureen N Ajuebor · Qingling Chen · Robert M Strieter · Patrick A Adegboyega · Tak Yee Aw
    [Show abstract] [Hide abstract]
    ABSTRACT: Replication-defective recombinant adenoviruses are the most widely studied replication-defective vectors for the potential treatment of inherited human diseases. However, broad clinical application of replication-defective adenoviruses in gene therapy is being hindered by the induction of vigorous innate and adaptive immune responses against the vector that cause deleterious effects in the liver. V(alpha)14 invariant natural killer T cells (V(alpha)14iNKT cells) are thymus-derived innate T cells at the interface between the two arms of the immune response and provide full engagement of host defense. The pathophysiological role of intrahepatic V(alpha)14iNKT cells during replication-defective adenovirus infection is not known and is the main focus of our study. Our data showed that intrahepatic V(alpha)14iNKT cells were activated in response to adenovirus infection to induce significant levels of hepatic chemokine (C-C motif) ligand 5 (CCL5) and subsequent liver toxicity. Moreover, intrahepatic CCL5 production was selectively reduced by V(alpha)14iNKT cell deficiency. In vivo studies utilizing CCL5-deficient mice or V(alpha)14iNKT cell-deficient mice demonstrated that CCL5 deficiency or V(alpha)14iNKT cell deficiency was associated with reduced liver pathology. Similar results were seen after blocking the biological effects of the CCL5 receptors. In conclusion, we have identified an important proinflammatory role for activated intrahepatic V(alpha)14iNKT cells in positively influencing hepatic CCL5 production to promote acute liver inflammation and injury. Therefore, our findings highlight the blockade of CCL5 interaction with a cognate receptor(s) as an important potential strategy to alleviate liver pathology associated with replication-defective adenovirus infection.
    Journal of Virology 09/2010; 84(17):8520-9. DOI:10.1128/JVI.00605-10 · 4.65 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Diethylene glycol (DEG) is an industrial chemical, the misuse of which has led to numerous epidemic poisonings worldwide. The mechanism of its toxicity has not been defined as to the precise relationship between the metabolism of DEG and target organ toxicity. The purpose of this study was to investigate the mechanism for the acute toxicity of DEG, and the effect of the alcohol dehydrogenase inhibitor 4-methylpyrazole (fomepizole), by determining the relationship between accumulation of DEG or its metabolites and the resulting kidney and liver toxicity. Rats were treated by oral gavage with water, 2 g/kg DEG (low dose), 10 g/kg DEG (high dose), or 10 g/kg DEG + fomepizole, and blood and urine were collected over 48 h. Rats treated with high-dose DEG had metabolic acidosis, increased BUN and creatinine, and marked kidney necrosis, noted by histopathology. A minor degree of liver damage was noted at the high dose. After low and high doses of DEG, 2-hydroxyethoxyacetic acid (HEAA) was the primary metabolite in the urine, with only minor amounts of urinary diglycolic acid (DGA). Small amounts of ethylene glycol (EG), but not oxalate or glycolate, were observed in the urine. Treatment with fomepizole blocked the formation of HEAA and DGA and the development of metabolic acidosis and the kidney and liver toxicity. These results indicate that the mechanism for the target organ toxicity results from metabolites of DEG, and not DEG itself nor formation of EG from DEG, and that fomepizole may be a useful antidote for treating DEG poisoning.
    Toxicological Sciences 09/2010; 117(1):25-35. DOI:10.1093/toxsci/kfq167 · 4.48 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: NF-kappaB is a survival signaling transcription factor complex involved in the malignant phenotype of many cancers, including squamous cell carcinomas (SCC). The citrus coumarin, auraptene (AUR), and the ethno-medicinal ginger (Alpinia galanga) phenylpropanoid, 1'-acetoxychavicol acetate (ACA), were previously shown to suppress 12-O-tetradecanoylphorbol-13-acetate (TPA) induced mouse skin tumor promotion. The goal of the present study was to determine whether AUR and ACA are effective either alone or in combination with all-trans retinoic acid (ATRA) for suppressing SCC tumor growth. We first determined the effects of orally administered ACA (100 mg/kg bw) and AUR (200 mg/kg bw) on lipopolysaccharide (LPS)-induced NF-kappaB activation in NF-kappaB-RE-luc (Oslo) luciferase reporter mice. Dietary administration of AUR and ACA +/- ATRA was next evaluated in a xenograft mouse model. Female SCID/bg mice were fed diets containing the experimental compounds, injected with 1 x 106 SRB12-p9 cells s.c., palpated and weighed twice a week for 28 days following injection. Both ACA and AUR suppressed LPS-induced NF-kappaB activation in the report mice. In the xenograft model, AUR (1000 ppm) and ACA (500 ppm) modestly suppressed tumor volume. However, in combination with ATRA at 5, 10, and 30 ppm, ACA 500 ppm significantly inhibited tumor volume by 56%, 62%, and 98%, respectively. The effect of ATRA alone was 37%, 33%, and 93% inhibition, respectively. AUR 1000 ppm and ATRA 10 ppm were not very effective when administered alone, but when combined, strongly suppressed tumor volume by 84%. Citrus AUR may synergize the tumor suppressive effects of ATRA, while ACA may prolong the inhibitory effects of ATRA. Further studies will be necessary to determine whether these combinations may be useful in the control of human SCC.
    BMC Cancer 07/2010; 10:394. DOI:10.1186/1471-2407-10-394 · 3.32 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Transitional cell carcinoma (TCC) of the bladder ranks fourth in incidence of all cancers in the developed world, yet the mechanisms of its origin and progression remain poorly understood. There are also few useful diagnostic or prognostic biomarkers for this disease. We have combined a transgenic mouse model for invasive bladder cancer (UPII-SV40Tag mice) with DNA microarray technology to determine molecular mechanisms involved in early TCC development and to identify new biomarkers for detection, diagnosis, and prognosis of TCC. We have identified genes that are differentially expressed between the bladders of UPII-SV40Tag mice and their age-matched wild-type littermates at 3, 6, 20, and 30 weeks of age. These are ages that correspond to premalignant, carcinoma in situ, and early-stage and later stage invasive TCC, respectively. Our preliminary analysis of the microarray data sets has revealed approximately 1,900 unique genes differentially expressed (> or =3-fold difference at one or more time points) between wild-type and UPII-SV40Tag urothelium during the time course of tumor development. Among these, there were a high proportion of cell cycle regulatory genes and a proliferation signaling genes that are more strongly expressed in the UPII-SV40Tag bladder urothelium. We show that several of the genes upregulated in UPII-SV40Tag urothelium, including RacGAP1, PCNA, and Hmmr, are expressed at high levels in superficial bladder TCC patient samples. These findings provide insight into the earliest events in the development of bladder TCC as well as identify several promising early-stage biomarkers.
    Cancer Prevention Research 06/2010; 3(6):776-86. DOI:10.1158/1940-6207.CAPR-09-0189 · 5.27 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Previously we reported that mice deficient in toll-like receptor 4 (TLR-4) signalling were protected from diet-induced non-alcoholic steatohepatitis (NASH). Another member of the toll-like receptor family, TLR-2, has been shown to play a role in lipid trafficking via uptake of diacylated lipoproteins. However, a role for TLR-2 in NASH has not been elucidated. The objectives of the current study were to examine the influence of dietary fat quality and TLR-2 on NASH pathogenesis. Steatohepatitis was induced in male Db, C57BL/6 and TLR-2(-/-) mice by feeding an L-amino acid-defined diet that was deficient in methionine and choline (MCDD). Mice fed the base diet supplemented with methionine and choline (control diet; CD) were used as controls. To determine the role of fat quality, MCDD was enriched with polyunsaturated corn oil (PUFA) or coconut oil that is comprised mostly of saturated fat (SAFA); the total amount of each fat was 112.9 g/kg of diet. After 8 weeks of feeding CD or MCDD, hepatic steatosis, inflammation and necrosis were evaluated in histological sections. Total RNA was extracted from frozen liver samples and mRNA expression of TNFalpha, collagen alpha1, IL-10, peroxisome proliferator-activated receptor-gamma (PPAR-gamma), TLR-4, and CD14, was analyzed via real-time PCR. Protein levels of TLR-2 were analyzed by western blot. Panlobular macrovessicular steatosis and diffuse leukocyte infiltration were noted in PUFA-fed Db mice. Histological scores demonstrated significantly less steatosis, inflammation and necrosis in SAFA-fed mice of all mouse strains. However, compared to wild type mice, hepatocellular damage was notably more severe in TLR-2(-/-) mice. Consistent with histological findings, mRNA expression of TNFalpha was elevated by approximately 3-fold in TLR-2(-/-) mice; PPAR-gamma expression was blunted in this strain compared to wild type. Expression of the matrix protein collagen alphaI was also significantly higher in TLR-2(-/-) mice, indicating a pro-fibrogenic state. Sensitivity to steatohepatitis due to dietary fat or TLR-2 deficiency correlated significantly with alterations in the expression of TLR-4 as well as the co-receptor CD-14. Our findings suggest that dietary saturated fat plays a protective role against MCDD-induced steatohepatitis, whereas TLR-2 deficiency exacerbated NASH. The mechanism underlying the response to dietary fat and TLR-2 likely involves altered signalling via the TLR-4 pathway.
    BMC Gastroenterology 05/2010; 10(1):52. DOI:10.1186/1471-230X-10-52 · 2.11 Impact Factor
  • Patrick A Adegboyega · Sarah Rodriguez · Jerry McLarty
    [Show abstract] [Hide abstract]
    ABSTRACT: Basal cell carcinoma is a very common malignant skin tumor that rarely metastasizes but is often locally aggressive. In a number of studies conducted by different investigators, Bcl2, beta-catenin, cyclin D1, hMSH2, and alpha-smooth muscle actin have been reported to have potential for predicting basal cell carcinoma aggressiveness. However, these reports were inconclusive and sometimes contradictory. We therefore studied the expression and topographic locations (tumor versus stroma) of all these gene products in a group of clinically proven aggressive basal cell carcinomas (n = 30) and randomly selected control cases of nonaggressive basal cell carcinomas (n = 33). The results were subjected to statistical analysis with Mann-Whitney test and logistic regression. The accuracy of the resulting significant discriminating criteria was further tested using the omnibus tests of model coefficients. With multivariate analysis, differential expression of Bcl-2, beta-catenin, and cyclin D1 was not significantly different between aggressive and nonaggressive tumors. hMSH2 expression was up-regulated in the aggressive tumors (P = .005). Alpha-smooth muscle actin was expressed by tumor cells in both study groups, but stromal expression of alpha-smooth muscle actin was restricted to the aggressive tumors and highly predictive of aggressive behavior (P < .001; accuracy, 87%). Logistic regression combining the expression of alpha-smooth muscle actin and hMSH2 yielded a predictive model with 97% accuracy (P < .001). These data show conclusively that aggressive basal cell carcinomas express alpha-smooth muscle actin in the stroma, whereas nonaggressive basal cell carcinomas express alpha-smooth muscle actin in the tumor cells, and that stromal expression of alpha-smooth muscle actin is an accurate, reliable, and easy to use marker of aggressiveness in basal cell carcinomas and can be used in clinical practice for surgical therapeutic decisions.
    Human pathology 04/2010; 41(8):1128-37. DOI:10.1016/j.humpath.2009.12.014 · 2.81 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Sinonasal teratocarcinosarcoma is an uncommon, aggressive, morphologically heterogenous tumor composed of cells derived from the 3 somatic layers. A histogenetic origin from a multipotential adult somatic stem cell with divergent differentiation has been favored over a germ cell origin. This assumption has been based on the lack of germ cell elements and, until recently, the absence of demonstrable amplification of 12p. We report a case that exhibited foci of yolk sac elements with papillary structures and intracytoplasmic periodic acid-Schiff-positive, diastase-resistant, α-fetoprotein-positive, hyaline globules. An expanded area of undifferentiated cells, likely precursor cells, in the basal layer of the overlying mucosal epithelium transitions into and merges with the immature epithelial, neuroepithelial, and mesenchymal components. These previously unreported histomorphological features support the hypothesis that this tumor is a teratomatous tumor arising from pluripotent embryonic stem cells in the basal layer of the sinonasal epithelium. That notion is further supported by fluorescence in situ hybridization cytogenetic analysis, which showed a distinct subpopulation of the tumor cells with an extra copy of chromosome 12p13.
    Annals of diagnostic pathology 04/2010; 15(2):135-9. DOI:10.1016/j.anndiagpath.2010.01.004 · 1.11 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: This study was undertaken to investigate epidermal growth factor receptor (EGFR) and human epidermal growth factor receptor 2 (HER-2)/neu expression in a cohort of apocrine carcinomas of the breast with emphasis on the classification of the breast tumors with apocrine morphology. In total, 55 breast carcinomas morphologically diagnosed as apocrine were evaluated for the steroid receptor expression profile characteristic of normal apocrine epithelium (androgen receptor positive/estrogen receptor (ER) negative/progesterone receptor (PR) negative), and for the expression of EGFR and Her-2/neu proteins, and the copy number ratios of the genes EGFR/CEP7 and HER-2/CEP17. On the basis of the results of steroid receptors expression, 38 (69%) cases were classified as pure apocrine carcinoma (androgen receptor positive/ER negative/PR negative), whereas 17 (31%) were re-classified as apocrine-like carcinomas because they did not have the characteristic steroid receptor expression profile. Her-2/neu overexpression was observed in 54% of the cases (57% pure apocrine carcinomas vs 47% apocrine-like carcinomas). HER-2/neu gene amplification was demonstrated in 52% of all cases (54% pure apocrine carcinomas vs 46% apocrine-like carcinomas). EGFR protein (scores 1 to 3+) was detected in 62% of all cases and was expressed in a higher proportion of pure apocrine carcinomas than in the apocrine-like carcinomas group (76 vs 29%, P=0.006). In the pure apocrine carcinoma group, Her-2/neu and EGFR protein expression were inversely correlated (P=0.006, r=−0.499). EGFR gene amplification was observed in two pure apocrine carcinomas and one apocrine-like carcinoma. Polysomy 7 was commonly present in pure apocrine carcinomas (61 vs 27% of apocrine-like carcinomas; P=0.083) and showed a weak positive correlation with EGFR protein expression (P=0.025, r=0.326). Our study showed that apocrine breast carcinomas are molecularly diverse group of carcinomas. Strictly defined pure apocrine carcinomas are either HER-2-overexpressing breast carcinomas or triple-negative breast carcinomas, whereas apocrine-like carcinomas predominantly belong to the luminal phenotype. Pure apocrine carcinomas show consistent overexpression of either EGFR or HER-2/neu, which could have significant therapeutic implications.Keywords: apocrine carcinoma; breast; HER-1/EGFR; HER-2/neu; gene amplification; polysomy
    Modern Pathology 03/2010; 23(5):644-653. DOI:10.1038/modpathol.2010.50 · 6.36 Impact Factor
  • Xiaohong I Wang · Songlin Zhang · Jaiyeola O Thomas · Patrick A Adegboyega
    [Show abstract] [Hide abstract]
    ABSTRACT: Follicular dendritic cell (FDC) sarcoma is a rare low-to-intermediate grade malignant dendritic cell neoplasm that often has an indolent clinical course. FDC sarcomas are often misdiagnosed on aspiration cytology. A 26-year-old woman presented with a solid, slowly growing, painless mass in her right neck for 3 months. Computed tomography revealed a 3.6-cm, well-defined homogenous solid mass located posterior to the mandible and submandibular glands. Fine needle aspiration cytology revealed many large, spindle to ovoid epithelioid cells in singles, small clusters, and syncytial sheets with moderate to abundant cytoplasm, indistinct cell borders, irregular nuclear membrane, fine to vesicular chromatin, and conspicuous nucleoli. The background contained many small mature lymphocytes intimately mixed with large epithelioid tumor cells. Tumor cells were strongly positive for CD21, CD35, CD23, and fascin. Diagnosis of FDC sarcoma was rendered; follow-up surgical resection and ultrastructural study confirmed the diagnosis. The cytogenetic study showed a normal female karyotype 46,XX. Although the cytomorphology of FDC sarcoma is characteristic, a preoperative diagnosis of FDC sarcoma based on fine needle aspiration cytology is very challenging, if not impossible. Immunohistochemistry is always necessary for rendering and/or confirming the diagnosis, and ultrastructural studies are helpful.
    Acta cytologica 01/2010; 54(5 Suppl):759-63. · 1.56 Impact Factor
  • Patrick A Adegboyega · Ying Pei · Jerry McLarty
    [Show abstract] [Hide abstract]
    ABSTRACT: The histopathologic diagnosis of chronic endometritis is based on the presence of plasma cells in the endometrial stroma. However, many conditions can mimic or interfere with the search for plasma cells, including the plasmacytoid stroma cells and predecidual changes of stroma cells. Eosinophils are another type of chronic inflammatory cells, which can be easily identified with routine hematoxylin and eosin stain by their characteristic eosinophilic granules. This study was conducted to investigate whether eosinophils can be used as diagnostic markers of chronic endometritis. The hematoxylin and eosin-stained glass slides of 422 consecutive endometrial biopsies were reviewed. The biopsies that have eosinophils were subjected to immunohistochemical staining with CD138, a marker for plasma cells. In all, 91 of 422 biopsies contained eosinophils with 72.5% (66/91) showing presence of plasma cells (positive staining with CD138). Of these 66 cases, only 4 cases were previously diagnosed as chronic endometritis. These results suggest the presence of eosinophils in endometrial biopsy specimen indicates a need to search for plasma cells (with immunohistochemical stain if needed) for the diagnosis of chronic endometritis.
    Human pathology 10/2009; 41(1):33-7. DOI:10.1016/j.humpath.2009.07.008 · 2.81 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Squamous cell carcinoma (SCC) of the skin is the most clinically aggressive form of nonmelanoma skin cancer. We have determined the effects of all-trans retinoic acid (ATRA), a naturally occurring chemopreventive retinoid, on signal transducer and activator of transcription 3 (Stat3) signaling during the development of skin SCC. Stat3 is a transcription factor that plays a critical role in cell proliferation and survival, and it is constitutively active in several malignant cell types. We have previously shown that Stat3 is required for the initiation, promotion, and progression of skin SCC. ATRA is a highly efficient suppressor of tumor formation in the two-stage mouse skin carcinogenesis model and we have shown that this effect correlates with the suppression of the B-Raf/Mek/Erk signaling pathway. In this study, we have determined the pattern of Stat3 phosphorylation throughout the course of the two-stage protocol, both in the presence and absence of ATRA. We have used both SENCAR mice and K5.Stat3C transgenic mice, which express the Stat3C protein, a constitutively active form of Stat3, in the skin. Using Western blotting and immunohistochemical staining with phosphospecific antibodies, we show that coadministration of ATRA suppressed the 12-O-tetradecanoylphorbol-13-acetate-induced phosphorylation of Stat3 in both models, but was only able to suppress tumor formation in the SENCAR mice. Surprisingly, ATRA actually enhanced tumor formation in 12-O-tetradecanoylphorbol-13-acetate-treated K5.Stat3C mice. We hypothesize that ATRA blocks tumor formation, at least in part, by targeting events upstream of Stat3, such as the B-Raf/Mek/Erk pathway, and that in the K5.Stat3C mice, in which Stat3 activity is constitutive, it cannot suppress tumor formation.
    Cancer Prevention Research 10/2009; 2(10):903-11. DOI:10.1158/1940-6207.CAPR-09-0041 · 5.27 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: ABSTRACT: Correction to Kleiner HE, Krishnan P, Tubbs J, Smith M, Meschonat C, Shi R, Lowery-Nordberg M, Adegboyega P, Unger M, Cardelli J et al: Tissue microarray analysis of eIF4E and its downstream effector proteins in human breast cancer. J Exp Clin Cancer Res 2009, 28:5.
    Journal of Experimental & Clinical Cancer Research 05/2009; 28(1):54. DOI:10.1186/1756-9966-28-54 · 4.23 Impact Factor

Publication Stats

2k Citations
437.40 Total Impact Points

Institutions

  • 2008–2013
    • Louisiana State University in Shreveport
      Shreveport, Louisiana, United States
  • 2007–2012
    • Louisiana State University Health Sciences Center Shreveport
      • • Department of Pathology
      • • School of Medicine
      Shreveport, Louisiana, United States
  • 1994–2010
    • University of Texas Medical Branch at Galveston
      • • Department of Pathology
      • • Department of Pediatrics
      • • Sealy Center for Cancer Cell Biology
      • • Department of Surgery
      • • Department of Internal Medicine
      Galveston, TX, United States
  • 2001–2002
    • Texas A&M University - Galveston
      Galveston, Texas, United States