Patrick A Adegboyega

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

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Publications (96)461.99 Total impact

  • No preview · Article · Aug 2013 · Cancer Research
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    ABSTRACT: Background: Helicobacter species are best known for their roles in the pathology of gastritis; however, sev-eral Helicobacter species also colonize the intestine, and less is known about effects of Helicobacter on the development of intestinal inflammation. To evaluate contributions of Helicobacter in inflammatory bowel disease, we investigated whether and how pre-existing intestinal colonization would affect disease severity and biomarkers of inflammation in experimental IBD. Materials and Methods: Mice were infected with H. muridarum 2 weeks prior to induction of colitis medi-ated by 3% dextran sulfate (DSS). Disease activity in-dex, stool blood and consistency, colon length, mye-loperoxidase, histopathology, blood and lymphatic vessels, and numbers of dilated mucosal crypts were measured in control, DSS-only, H. muridarum-infec-ted, and H. muridarum-infected + DSS mice. Results: Prior to DSS challenge, H. muridarum-infected mice showed little distal gut injury by several indices of colon inflammation with decreased blood vessel den-sity in the submucosa, and lower lymphatic density in the mucosa and submucosa. However, after DSS coli-tis, H. muridarum-infected mice exhibited significant-ly greater disease. Weight change, stool bleeding, di-arrhea, and angiogenesis were all increased in H. mu-ridarum-infected mice in DSS colitis compared to DSS controls. Conclusions: Our data show that Helicoba-cter colonization of the intestine, unlike that of the stomach, lowers basal gut inflammatory scores, but increases disease activity and inflammation in an acute colitis model. Intestinal Helicobacter infection may therefore represent a significant sub-clinical factor which predisposes the gut to inflammatory injury.
    Full-text · Article · Jul 2013 · Open Journal of Gastroenterology
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    Isaac Downs · Tak Yee Aw · Jianfeng Liu · Patrick Adegboyega · Maureen N Ajuebor
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    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.
    Full-text · Article · Oct 2012 · Biochemical and Biophysical Research Communications
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    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.
    Full-text · Article · Jun 2012 · Journal of Experimental & Clinical Cancer Research
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    Isaac Downs · Jianfeng Liu · Tak Yee Aw · Patrick A Adegboyega · Maureen N Ajuebor
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    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.
    Full-text · Article · Jun 2012 · PLoS ONE
  • Tanya Varma · Patrick Adegboyega
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    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.
    No preview · Article · Apr 2012 · Archives of pathology & laboratory medicine

  • No preview · Article · Jul 2011 · Cancer Research
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    ABSTRACT: Helicobacter pylori persistently colonizes humans, causing gastritis, ulcers, and gastric cancer. Adherence to the gastric epithelium has been shown to enhance inflammation, yet only a few H. pylori adhesins have been paired with targets in host tissue. The alpAB locus has been reported to encode adhesins involved in adherence to human gastric tissue. We report that abrogation of H. pylori AlpA and AlpB reduces binding of H. pylori to laminin while expression of plasmid-borne alpA or alpB confers laminin-binding ability to Escherichia coli. An H. pylori strain lacking only AlpB is also deficient in laminin binding. Thus, we conclude that both AlpA and AlpB contribute to H. pylori laminin binding. Contrary to expectations, the H. pylori SS1 mutant deficient in AlpA and AlpB causes more severe inflammation than the isogenic wild-type strain in gerbils. Identification of laminin as the target of AlpA and AlpB will facilitate future investigations of host-pathogen interactions occurring during H. pylori infection.
    Full-text · Article · May 2011 · Infection and immunity
  • Patrick A Adegboyega
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    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.
    No preview · Article · Jan 2011 · International journal of gynecological pathology: official journal of the International Society of Gynecological Pathologists
  • Estelle Yoo · Jaiyeola O Thomas · Patrick A Adegboyega · Timothy S Lian
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    ABSTRACT: Title: Follicular Dendritic Cell Sarcoma: A Differential in Neck Mass Objectives: This study describes clinicopathologic features of the follicular dendritic cell sarcoma (FDCS), discusses the importance of including FDCS in the evaluation of neck masses, and addresses the controversy in therapeutic management of FDCS. Study Design: Retrospective case report Methods: Retrospective chart review of a patient with histopathologic diagnosis of follicular dendritic cell sarcoma on a surgical specimen at a tertiary care hospital with a follow-up duration of 12 months. Results: The patient is a 27 year old Caucasian woman with a 5 cm right neck mass that has been gradually enlarging for 7 months without compressive symptoms. The immunohistochemical evaluation of the fine needle aspirate of this mass demonstrated strongly positive follicular dendritic markers, CD21 and CD35, with positive results for vimentin. Flow cytometry was negative for lymphoma. Histologic features in surgical specimen demonstrated large spindle cells with prominent meningioma-like whorls intermingled in a background of small lymphocytes with effacement of the lymph node by the tumor cells. The patient was treated with primary surgical resection with disease free margins. She refused further adjuvant radiation therapy considering life-long morbidity resulting from irradiation. Conclusions: Follicular dendritic cell sarcoma can mimic clinical presentation of various neoplastic lesions in the head and neck. Immunohistochemical staining positive for CD21, CD35, vimentin, negative result on the flow cytometry, along with a histologic evidence of follicular dendritic cell proliferation lead to a diagnosis of FDCS. The controversy in treatment method of surgery alone versus surgery with adjuvant therapy requires further investigation in the future. Copyright © 2010 The American Laryngological, Rhinological, and Otological Society, Inc.
    No preview · Article · Oct 2010 · The Laryngoscope
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    Maureen N Ajuebor · Qingling Chen · Robert M Strieter · Patrick A Adegboyega · Tak Yee Aw
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    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. Vα14 invariant natural killer T cells (Vα14iNKT 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 Vα14iNKT cells during replication-defective adenovirus infection is not known and is the main focus of our study. Our data showed that intrahepatic Vα14iNKT 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 Vα14iNKT cell deficiency. In vivo studies utilizing CCL5-deficient mice or Vα14iNKT cell-deficient mice demonstrated that CCL5 deficiency or Vα14iNKT 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 Vα14iNKT 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.
    Full-text · Article · Sep 2010 · Journal of Virology
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    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.
    No preview · Article · Sep 2010 · Toxicological Sciences
  • Xiaohong I Wang · Songlin Zhang · Jaiyeola O Thomas · Patrick A Adegboyega
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    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.
    No preview · Article · Sep 2010 · Acta cytologica
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    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.
    Full-text · Article · Jul 2010 · BMC Cancer
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    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.
    Full-text · Article · Jun 2010 · Cancer Prevention Research
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    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.
    Full-text · Article · May 2010 · BMC Gastroenterology
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    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.
    No preview · Article · Apr 2010 · Annals of diagnostic pathology
  • Patrick A Adegboyega · Sarah Rodriguez · Jerry McLarty
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    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.
    No preview · Article · Apr 2010 · Human pathology
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    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
    Full-text · Article · Mar 2010 · Modern Pathology
  • Patrick A Adegboyega · Ying Pei · Jerry McLarty
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    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.
    No preview · Article · Oct 2009 · Human pathology

Publication Stats

2k Citations
461.99 Total Impact Points


  • 2008-2013
    • Louisiana State University in Shreveport
      Shreveport, Louisiana, United States
  • 2007-2010
    • Louisiana State University Health Sciences Center Shreveport
      • • Department of Pathology
      • • School of Medicine
      Shreveport, Louisiana, United States
  • 1995-2010
    • University of Texas Medical Branch at Galveston
      • • Department of Pathology
      • • Department of Pediatrics
      • • Department of Internal Medicine
      Galveston, TX, United States
  • 2001-2008
    • Texas A&M University - Galveston
      Galveston, Texas, United States
  • 2002
    • University of Kentucky
      • Department of Plant Pathology
      Lexington, Kentucky, United States
  • 1996
    • University of Miami
      كورال غيبلز، فلوريدا, Florida, United States