Nabiha Yusuf

University of Alabama at Birmingham, Birmingham, Alabama, United States

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Publications (39)132.51 Total impact

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    ABSTRACT: UVB radiation contributes to both direct and indirect damage to the skin including the generation of free radicals and reactive oxygen species (ROS), inflammatory responses, immunosuppression, and gene mutations, which can ultimately lead to photocarcinogenesis. A plant-derived flavonoid, baicalin, has been shown to have antioxidant, anti-inflammatory, and free radical scavenging activities. Previous studies from our laboratory have shown that in murine skin, Toll like receptor-4 (TLR4) enhanced both UVB-induced DNA damage and inflammation. The aim of the current study is to investigate the efficacy of baicalin against TLR4-mediated processes in the murine keratinocyte PAM 212 cell line. Our results demonstrate that treating keratinocytes with baicalin both before and after UV radiation (100 mJ/cm(2) ) significantly inhibited the level of intracellular ROS and decreased cyclobutane pyrimidine dimers (CPDs) and 8-Oxo-2'-deoxyguanosine (8-oxo-dG)-markers of DNA damage. Furthermore, cells treated with baicalin demonstrated an inhibition of TLR4 and its downstream signaling molecules, MyD88, TRIF, TRAF6, and IRAK4. TLR4 pathway inhibition resulted in NF-κB inactivation and down-regulation of iNOS and COX-2 protein expression. Taken together, baicalin treatment effectively protected keratinocytes from UVB-induced inflammatory damage through TLR pathway modulation. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Photochemistry and Photobiology 08/2015; DOI:10.1111/php.12505 · 2.68 Impact Factor
  • Tahseen H Nasti · Daniel C Bullard · Nabiha Yusuf
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    ABSTRACT: P-selectin is an adhesion receptor that is mainly present on endothelial cells and platelets. We investigated the role of P-selectin in the regulation of different T cell subsets in the tumor microenvironment, and how that influences the growth and metastasis of mouse mammary cancer cell line 4T1 in Balb/c mice. The 4T1 cells (1 x 10(4) or 1 x 10(5)) were inoculated subcutaneously in the pre-shaved back skin of the P-selectin knockout (P-sel -/-) and wild-type (WT) mice. Mice were monitored twice weekly for the tumor growth measurements and survival studies. The tumors and the lungs were isolated for cytokine and T cell subset analysis at the end of the study. Mice lacking P-selectin had reduced tumor burden, higher survival and reduced metastasis compared to WT mice. Loss of P-selectin inhibited the infiltration of regulatory T cells and reduced pro-inflammatory cytokines, such as IL-4, IL-10, and TGFβ in the tumors. Furthermore, the CD8+ T cells and effector CD4+ T cells were functional and exhibited enhanced infiltration into the tumors of P-selectin knockout mice compared to WT mice. These results demonstrated that P-selectin is an important adhesion molecule vital for infiltration of regulatory T cells into the tumors. Thus, inhibiting P-selectin can have important therapeutic implications against breast cancer growth and metastasis. Copyright © 2015. Published by Elsevier Inc.
    Life sciences 04/2015; 131. DOI:10.1016/j.lfs.2015.02.025 · 2.30 Impact Factor
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    ABSTRACT: Heat shock proteins (HSPs) are constitutively expressed in murine skin. HSP27 is present in the epidermis, and HSP70 can be found in both the epidermis and dermis. The purpose of this study was to investigate the role of these proteins in cutaneous chemical carcinogenesis and to determine whether their effects on cell-mediated immune function were a contributing factor. In vivo inhibition of HSP27 and HSP70 produced a reduction in the T cell-mediated immune response to 7,12-dimethylbenz(a)anthracene (DMBA) and benzo(a)pyrene in C3H/HeN mice and resulted in a state of Ag-specific tolerance. When mice were pretreated with anti-HSP27 and anti-HSP70 Abs in vivo prior to subjecting them to a standard two-stage DMBA/12-O-tetradecanoylphorbol-13-acetate cutaneous carcinogenesis protocol, the percentage of mice with tumors was much greater (p < 0.05) in anti-HSP27- and HSP70-pretreated animals compared with mice pretreated with control Ab. Similar results were obtained when the data were evaluated as the cumulative number of tumors per group. Mice pretreated with HSP27 and HSP70 Abs developed more H-ras mutations and fewer DMBA-specific cytotoxic T lymphocytes. These findings indicate that in mice HSP27 and HSP70 play a key role in the induction of cell-mediated immunity to carcinogenic polyaromatic hydrocarbons. Bolstering the immune response to carcinogenic polyaromatic hydrocarbons may be an effective method for prevention of the tumors that they produce. Copyright © 2015 by The American Association of Immunologists, Inc.
    The Journal of Immunology 04/2015; DOI:10.4049/jimmunol.1402804 · 5.36 Impact Factor
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    ABSTRACT: Acquired melanocytic nevi are commonly found in sun exposed and unexposed human skin, but the potential for their transformation into invasive melanoma is not clear. Therefore, a mouse model of nevus initiation and progression was developed in C3H/HeN mice using a modified chemical carcinogenesis protocol. Nevi develop due to DNA damage initiated by dimethylbenz(a) anthracene (DMBA) followed by chronic promotion with 12-O-tetradecanoyl-phorbol-13-acetate (TPA). Dysplastic pigmented skin lesions appeared in 7-9 wk with 100% penetrance. Nests of melanocytic cells appeared in a subset of skin draining lymph nodes (dLN) by 25 wk, but not in age matched controls. Immunohistochemistry, real-time PCR, and flow cytometric analyses confirmed their melanocytic origin. Transformed cells were present in a subset of nevi and dLNs, which exhibited anchorage-independent growth, tumor development, and metastasis in nude mice. Approximately 50% of the cell lines contained H-Ras mutations and lost tumor suppressor p16(Ink4a) expression. While most studies of melanoma focus on tumor progression in transgenic mouse models where the mutations are present from birth, our model permits investigation of acquired mutations at the earliest stages of nevus initiation and promotion of nevus cell transformation. This robust nevus/melanoma model may prove useful for identifying genetic loci associated with nevus formation, novel oncogenic pathways, tumor targets for immune-prevention, screening therapeutics, and elucidating mechanisms of immune surveillance and immune evasion. © 2015 The Authors. Molecular Carcinogenesis, published by Wiley Periodicals, Inc. © 2015 The Authors. Molecular Carcinogenesis, published by Wiley Periodicals, Inc.
    Molecular Carcinogenesis 03/2015; DOI:10.1002/mc.22310 · 4.77 Impact Factor
  • Erin M. Burns · Craig A. Elmets · Nabiha Yusuf
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    ABSTRACT: Vitamin D signaling plays a key role in various important processes, including cellular proliferation, differentiation, and apoptosis, immune regulation, hormone secretion, and skeletal health. Further, vitamin D production and supplementation have been shown to exert protective effects via an unknown signaling mechanism involving the vitamin D receptor (VDR) in several diseases and cancer types, including skin cancer. With over 3.5 million new diagnoses in 2 million patients annually, skin cancer is the most common cancer type in the United States. While ultraviolet B (UVB) radiation is the main etiologic factor for non-melanoma skin cancer (NMSC), UVB also induces cutaneous vitamin D production. This paradox has been the subject of contradictory findings in the literature in regards to amount of sun exposure necessary for appropriate vitamin D production, as well as any beneficial or detrimental effects of vitamin D supplementation for disease prevention. Further clinical and epidemiological studies are necessary to elucidate the role of vitamin D in skin carcinogenesis.This article is protected by copyright. All rights reserved.
    Photochemistry and Photobiology 11/2014; 91(1). DOI:10.1111/php.12382 · 2.68 Impact Factor
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    ABSTRACT: Ultraviolet B (UVB) light is known to induce inflammation and DNA damage, which can lead to the development of non-melanoma skin cancer. Recently, the microbiome has been investigated as a potential carcinogenic mechanism as a result of inflammatory effects. Non-melanoma skin cancer is the most common cancer type in the United States and the fifth most costly cancer in the Medicare population. The high incidence rate and cost mandate new prevention and treatment options. Malaysian Tualang honey has been shown to have antioxidant and anti-inflammatory properties that may contribute to an anti-carcinogenic effect. Previously, our laboratory has demonstrated in keratinocytes that Tualang honey decreased DNA damage and inflammatory mediators following UVB exposure. The purpose of our study was to investigate the potential of Tualang honey to affect the microbiome as well as UVB-induced DNA damage and inflammation in Skh-1 hairless mice. Male and female mice received Tualang honey (0.1% v/v) in drinking water for two weeks prior to a single exposure of UVB (1 MED). Fecal samples were collected at baseline, following two weeks of honey supplementation, and after UVB exposure. DNA was isolated and samples were sequenced to examine the microbiota present. Our data demonstrate that male and female samples cluster separately. We also found differences at the phylum and species level among the different time points, suggesting that honey and/or UVB exposure may alter the murine gut microbiome. We also examined DNA damage and repair as well as inflammatory mediators in murine skin to assess the potential antioxidant and anti-inflammatory effects of Tualang honey. Our data demonstrate that Tualang honey decreases DNA damage and inflammatory mediators while increasing DNA repair mechanisms following UVB exposure. Future studies will examine the effects of Tualang honey on the microbiome and UVB-induced carcinogenesis in our murine model in order to investigate the potential of Tualang honey as a preventive treatment for non-melanoma skin cancer.
    17th Annual Research Retreat - UAB Cancer Center; 10/2014
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    ABSTRACT: Ultraviolet radiation (UVR) induces immunosuppression and is a major factor for development of skin cancer. Numerous efforts have been made to determine mechanisms for UVR induced immunosuppression and to develop strategies for prevention and treatment of UVR induced cancers. In the current study, we use IL-17 receptor (IL-17R) deficient mice to examine whether IL-17 mediated responses have a role in UVB (290-320) induced immunosuppression of contact hypersensitivity responses. Results demonstrate that IL-17 mediated responses are required for UVB induced immunosuppression of contact hypersensitivity responses. The systemic immune suppression and development of regulatory T cells are inhibited in UVB treated IL-17R deficient mice compared to wild type animals. The deficiency in IL-17R inhibits the infiltration and development of a tolerogenic myeloid cell population in UVB treated skin, which expresses CD11b and Gr-1 and produces reactive oxygen species. We speculate that the development of the tolerogenic myeloid cells is dependent on IL-17 induced chemokines and inflammatory mediators in UVB treated skin. The inhibition of the tolerogenic myeloid cells may be attributed to the suppression of regulatory T cells in UVR treated IL-17R-/- mice. The findings may be exploited to new strategies for prevention and treatment of UVR induced skin diseases and cancers.This article is protected by copyright. All rights reserved.
    Photochemistry and Photobiology 09/2014; 91(1). DOI:10.1111/php.12351 · 2.68 Impact Factor
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    Nabiha Yusuf
    Frontiers in Immunology 05/2014; 5:224. DOI:10.3389/fimmu.2014.00224
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    Erin M Burns · Nabiha Yusuf
    Frontiers in Immunology 03/2014; 5:135. DOI:10.3389/fimmu.2014.00135
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    Aimen Ismail · Nabiha Yusuf
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    ABSTRACT: Interferons (IFNs) are a family of naturally existing glycoproteins known for their antiviral activity and their ability to influence the behavior of normal and transformed cell types. Type I Interferons include IFN- α and IFN- β . Currently, IFN- α has numerous approved antitumor applications, including malignant melanoma, in which IFN- α has been shown to increase relapse free survival. Moreover, IFN- α has been successfully used in the intralesional treatment of cutaneous squamous cell carcinoma (SCC) and basal cell carcinoma (BCC). In spite of these promising clinical results; however, there exists a paucity of knowledge on the precise anti-tumor action of IFN- α / β at the cellular and molecular levels in cutaneous malignancies such as SCC, BCC, and melanoma. This review summarizes current knowledge on the extent to which Type I IFN influences proliferation, apoptosis, angiogenesis, and immune function in normal skin, cutaneous SCC, BCC, and melanoma.
    Dermatology Research and Practice 01/2014; 2014:847545. DOI:10.1155/2014/847545
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    ABSTRACT: Ultraviolet A (UVA) radiation contributes to skin photoaging. Baicalin, a plant-derived flavonoid, effectively absorbs UV rays and has been shown to have anti-oxidant and anti-inflammatory properties that may delay the photoaging process. In the current study, cultured human skin fibroblasts were incubated with 50 μg/ml baicalin 24 hours prior to 10 J/cm(2) UVA irradiation. In order to examine the efficacy of baicalin treatment in delaying UVA-induced photoaging, we investigated aging-related markers, cell cycle changes, anti-oxidant activity, telomere length, and DNA damage markers. UVA radiation caused an increased proportion of β-Gal positive cells and reduced telomere length in human skin fibroblasts. In addition, UVA radiation inhibited TGF-β1 secretion, induced G1 phase arrest, reduced SOD and GSH-Px levels, increased MDA levels, enhanced the expression of MMP-1, TIMP-1, p66, p53, and p16 mRNA, reduced c-myc mRNA expression, elevated p53 and p16 protein expression, and reduced c-myc protein expression. Baicalin treatment effectively protected human fibroblasts from these UVA radiation-induced aging responses, suggesting that the underlying mechanism involves the inhibition of oxidative damage and regulation of the expression of senescence-related genes, including those encoding for p53, p66(Shc) and p16.
    The American Journal of Chinese Medicine 01/2014; 42(3):709-27. DOI:10.1142/S0192415X14500463 · 2.63 Impact Factor
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    ABSTRACT: UVB-induced DNA damage plays a critical role in development of photoimmunosuppression. The purpose of this study was to determine whether repair of UVB-induced DNA damage is regulated by Toll-like receptor-4 (TLR4). When TLR4 gene knockout (TLR4(-/-)) and TLR4 competent (TLR4(+/+)) mice were subjected to 90 mJ/cm(2) UVB radiation locally, DNA damage in the form of CPD, were repaired more efficiently in the skin and bone marrow dendritic cells (BMDC) of TLR4(-/-) mice in comparison to TLR4(+/+) mice. Expression of DNA repair gene XPA (Xeroderma pigmentosum complementation group A) was significantly lower in skin and BMDC of TLR4(+/+) mice than TLR4(-/-) mice after UVB exposure. When cytokine levels were compared in these strains after UVB exposure, BMDC from UV-irradiated TLR4(-/-) mice produced significantly more interleukin (IL)-12 and IL-23 cytokines (P<0.05) than BMDC from TLR4(+/+) mice. Addition of anti-IL-12 and anti-IL-23 antibodies to BMDC of TLR4(-/-) mice (before UVB exposure) inhibited repair of CPD, with a concomitant decrease in XPA expression. Addition of TLR4 agonist to TLR4(+/+) BMDC cultures decreased XPA expression and inhibited CPD repair. Thus, strategies to inhibit TLR4 may allow for immunopreventive and immunotherapeutic approaches for managing UVB-induced cutaneous DNA damage and skin cancer.Journal of Investigative Dermatology accepted article preview online, 10 December 2013. doi:10.1038/jid.2013.530.
    Journal of Investigative Dermatology 12/2013; 134(6). DOI:10.1038/jid.2013.530 · 6.37 Impact Factor
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    ABSTRACT: The inflammasome is a multi-protein complex which when activated regulates caspase-1 activation and IL-1β and IL-18 secretion. NLRP3 (NACHT, LRR, and pyrin domain-containing protein 3) inflammasome is constitutively assembled and activated in human melanoma cells. We have examined the inhibitory effect of thymoquinone (2-ispropyl-5-methylbenzo-1,4-quinone), a major ingredient of black seed obtained from the plant Nigella sativa on metastatic human (A375) and mouse (B16F10) melanoma cell lines. We have assessed whether thymoquinone inhibits metastasis of melanoma cells by targeting NLRP3 subunit of inflammasomes. Using an in vitro cell migration assay, we found that thymoquinone inhibited the migration of both human and mouse melanoma cells. The inhibitory effect of thymoquinone on metastasis was also observed in vivo in B16F10 mouse melanoma model. The inhibition of migration of melanoma cells by thymoquinone was accompanied by decrease in expression of NLRP3 inflammasome resulting in decrease in proteolytic cleavage of caspase-1. Inactivation of caspase-1 by thymoquinone resulted in inhibition of IL-1β and IL-18. Treatment of mouse melanoma cells with thymoquinone also inhibited NF-κB activity. Furthermore, inhibition of reactive oxygen species (ROS) resulted in partial inactivation of NLRP3 inflammasome. Thus, thymoquinone exerts its inhibitory effect on migration of human and mouse melanoma cells by inhibition of NLRP3 inflammasome. Thus, our results indicate that thymoquinone can be a potential immunotherapeutic agent not only as an adjuvant therapy for melanoma, but also, in control and prevention of metastatic melanoma.
    Toxicology and Applied Pharmacology 04/2013; 270(1). DOI:10.1016/j.taap.2013.03.027 · 3.63 Impact Factor
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    ABSTRACT: Carbon powders can be synthesized using variety of CVD and detonation methods. Several interesting properties of carbon powder particles make them a very attractive material examined in many laboratories all over the world. However there is a lack of information discussing investigation of carbon powders directed to its application in pharmaceutical-cosmetic industry and medicine. Earlier investigation results proved that diamond powders present properties fighting free radicals. Presented work discusses the influence of carbon powder particles manufactured using MW/RF PACVD, RF PACVD and detonation methods onto hydro-lipid skin coat. Before the biological examinations physicochemical properties of carbon powders were determined. Grain size, shape and chemical composition of carbon powders were determined using the scanning electron microscopy. Surface functional groups were characterized by IR Fourier-transform spectroscopy and X-ray photoelectron spectroscopy. Structure and phase composition were investigated by means of the Raman spectroscopy. Results of allergy tests performed on laboratory mice proved that carbon powder particles synthesized using different methods do not cause allergy. In the following stage, the group of 20 patients applied the formula including carbon powder on their face skin. The influence of carbon powder onto hydro-lipid skin coat was determined by measurement of such parameters as: pH reaction, skin temperature, lipid fotometry and level of hydration. Additionally, macro pictures of places where the cream had been applied were registered. As the result of the investigation it was found that powders synthesized using various methods present different physicochemical properties which may individually affect the face skin parameters. The noticeable improvement of hydro-lipid skin coat kilter was observed.
    Journal of Nanoscience and Nanotechnology 12/2012; 12(12):9037-46. DOI:10.1166/jnn.2012.6745 · 1.34 Impact Factor
  • Cancer Research 04/2012; 72(8 Supplement):525-525. DOI:10.1158/1538-7445.AM2012-525 · 9.28 Impact Factor
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    ABSTRACT: The mechanism for inflammation associated tumor development is a central issue for tumor biology and immunology and remains to be fully elucidated. Although IL-17 is implicated in association with inflammation mediated carcinogenesis, mechanisms are largely elusive. In the current studies, we showed that IL-17 receptor-A gene deficient (IL-17R-/-) mice were resistant to chemical carcinogen-induced cutaneous carcinogenesis, a well-established inflammation associated tumor model in the skin. The deficiency in IL-17R increased the infiltration of CD8+ T cells whereas it inhibited the infiltration of CD11b+ myeloid cells and development of myeloid derived suppressor cells. Inflammation induced skin hyperplasia and production of pro-tumor inflammatory molecules were inhibited in IL-17R-/- mice. We found that pre-existing inflammation in the skin increased the susceptibility to tumor growth, which was associated with increased development of tumor specific IL-17 producing T cells. This inflammation induced susceptibility to tumor growth was abrogated in IL-17R-/- mice. Finally, neutralizing IL-17 in mice that had already developed chemical carcinogen induced skin tumors could inhibit inflammation mediated tumor progression at late stages. These results demonstrate that IL-17 mediated inflammation is an important mechanism for inflammation mediated promotion of tumor development. The study has major implications for targeting IL-17 in prevention and treatment of tumors.
    PLoS ONE 02/2012; 7(2):e32126. DOI:10.1371/journal.pone.0032126 · 3.23 Impact Factor
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    ABSTRACT: Toll-like receptors (TLRs) activate signals that are critically involved in the initiation of adaptive immune responses and many tumorigenic chemicals have been associated with activation of those pathways. To determine the role of TLR-4 (TLR4) in mammary carcinogenesis, we subjected TLR4 deficient and wild type (WT) mice to oral gavage with carcinogenic polyaromatic hydrocarbon 7,12-dimethylbenz(a)anthracene (DMBA). TLR4 deficient mice developed more tumors relative to the WT mice. T cells of TLR4 deficient mice produced elevated levels of IL-17 and lower levels of IFN-γ relative to WT mice. IL-12 secreted by CD11c(+) cells was higher in WT mice, whereas greater amounts of IL-23 were produced by CD11c(+) cells from TLR4 deficient mice. Moreover, there was higher incidence of regulatory T cells in TLR4 deficient mice than WT mice. Similarly, various markers of angiogenesis [matrix metalloproteinases (MMP)-2 and MMP-9, CD31 and vascular endothelial growth factor] were highly expressed in tumors from TLR4 deficient mice than WT mice. The results of this study indicate that TLR4 plays an important role in the prevention of DMBA induced mouse mammary tumorigenesis and efforts to divert the cell-mediated immune response may, therefore, prove to be beneficial in the prevention of mammary tumors.
    International Journal of Cancer 02/2012; 130(4):765-74. DOI:10.1002/ijc.26100 · 5.01 Impact Factor
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    ABSTRACT: Malaysian tualang honey possesses strong antioxidant and anti-inflammatory properties. Here, we evaluated the effect of tualang honey on early biomarkers of photocarcinogenesis employing PAM212 mouse keratinocyte cell line. Keratinocytes were treated with tualang honey (1.0%, v/v) before a single UVB (150 mJ cm(-2) ) irradiation. We found that the treatment of tualang honey inhibited UVB-induced DNA damage, and enhanced repair of UVB-mediated formation of cyclobutane pyrimidine dimers and 8-oxo-7,8-dihydro-2'-deoxyguanosine. Treatment of tualang honey inhibited UVB-induced nuclear translocation of NF-κB and degradation of IκBα in murine keratinocyte cell line. The treatment of tualang honey also inhibited UVB-induced inflammatory cytokines and inducible nitric oxide synthase protein expression. Furthermore, the treatment of tualang honey inhibited UVB-induced COX-2 expression and PGE2 production. Taken together, we provide evidence that the treatment of tualang honey to keratinocytes affords substantial protection from the adverse effects of UVB radiation via modulation in early biomarkers of photocarcinogenesis and provide suggestion for its photochemopreventive potential.
    Photochemistry and Photobiology 01/2012; 88(5):1198-204. DOI:10.1111/j.1751-1097.2012.01100.x · 2.68 Impact Factor
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    Debika Bhattacharya · Nabiha Yusuf
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    ABSTRACT: Breast cancer remains a major cause of death in women in the developed world. As Toll-like receptors (TLRs) are widely expressed on tumor cells and play important roles in the initiation and progression of cancer, they may thus serve as important targets and have an effective perspective on breast cancer treatment. Expression of TLRs on breast cancer cells and mononuclear inflammatory cells can promote inflammation and cell survival in the tumor microenvironment. Inflammation and cancer are related. It is well known that persistent inflammatory conditions can induce cancer formation, due to production of cytokines and chemokines, which play a crucial role in promoting angiogenesis, metastasis, and subversion of adaptive immunity. TLR signaling in tumor cells can mediate tumor cell immune escape and tumor progression, and it is regarded as one of the mechanisms for chronic inflammation in tumorigenesis and progression. This paper delineates the expression of various TLRs in promotion of inflammation and development of mammary tumors. Understanding the mechanisms through which TLRs on breast cancer cells and inflammatory cells regulate growth, survival, and metastatic progression can make them potential targets for breast cancer therapy.
    01/2012; 2012:716564. DOI:10.1155/2012/716564
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    ABSTRACT: In this study, amorphous carbonaceous nanoparticles were prepared by a simple hydrothermal process using glucose as precursor. The nearly perfect spherical particles (beads) with the dimensions in the range of 10-500 nm were obtained depending on the main process parameters (precursor concentration, temperature, and time). The particles size, surface morphology, structure, and composition have been examined by TEM, SEM, X-ray diffraction, XPS, FTIR and Raman spectroscopy. These amorphous carbonaceous nanobeads (a-CNBs) have been found nontoxic in vitro with a variety of cultured cell lines. The size-dependent effect of a-CNBs addition on cell function has been observed. For example, a-CNBs can, in some cases, substantially increase interleukin-12 (IL-12) production by bone marrow dendritic cells. It has been further demonstrated that a-CNBs can be modified with fluorescent dye molecules or loaded with anti-cancer drugs for bioimaging or therapeutic purposes, respectively. The results of these tests and the strategies for the particle preparation and functionalization for biomedical applications have been discussed.
    Journal of Nanoscience and Nanotechnology 10/2011; 11(10):8705-11. DOI:10.1166/jnn.2011.3500 · 1.34 Impact Factor

Publication Stats

509 Citations
132.51 Total Impact Points

Institutions

  • 2003–2015
    • University of Alabama at Birmingham
      • • Department of Dermatology
      • • Skin Diseases Research Center
      • • Comprehensive Cancer Center
      Birmingham, Alabama, United States
  • 2012
    • Minneapolis Veterans Affairs Hospital
      Minneapolis, Minnesota, United States