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Title: Potential mechanism of phytochemical-induced apoptosis in human prostate cancer cells: Genistein and beta-lapachone.
Creator: Saddler, Shawnette Simone, Florida Atlantic University, Kumi-Diaka, James
Abstract/Description: The present study was undertaken to determine the chemotherapeutic potential of genistein and beta-lapachone and possible mechanisms of action in prostate cancer in vitro. The bioassays used included: MTT and LDH chemosensitivity-cytotoxicity assays, NQO1 detection, annexin V-FITC, TUNEL and the caspase protease (CPP32) apoptotic detection assays. The results showed that: (i) PC3 cells are sensitive to single and combination treatments in a dose and time dependent manner; (ii) there was...
Show moreThe present study was undertaken to determine the chemotherapeutic potential of genistein and beta-lapachone and possible mechanisms of action in prostate cancer in vitro. The bioassays used included: MTT and LDH chemosensitivity-cytotoxicity assays, NQO1 detection, annexin V-FITC, TUNEL and the caspase protease (CPP32) apoptotic detection assays. The results showed that: (i) PC3 cells are sensitive to single and combination treatments in a dose and time dependent manner; (ii) there was treatment-induced dual death pathways (apoptosis and necrosis) with increasing toxicity (necrosis) at higher concentrations in single and combination treatments; (iii) combination treatment was more growth inhibitory than single treatments; (iv) the NQO1 enzyme substantially enhances the toxicity of beta-lapachone but not genistein, while genistein exerted its apoptotic inducing effects via the caspase 3 pathway. The overall results indicate that combination treatments with beta-lapachone and genistein are more efficacious in killing PC3 human prostate cancer cells than treatment with either agent alone.
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Date Issued: 2003
PURL: http://purl.flvc.org/fcla/dt/13042
Subject Headings: Prostate--Cancer--Cytopathology, Apoptosis, Prostate--Cancer--Molecular aspects
Format: Document (PDF)

Title: A Study on Reversing the Immunosuppressive Phenotype of Tumor Associated Macrophages.
Creator: Liddle, Genevieve M., Hartmann, James X., Florida Atlantic University, Charles E. Schmidt College of Science, Department of Biological Sciences
Abstract/Description: Extracellular stimuli may influence the M1/M2 phenotypic polarization of macrophages. We examined M1/M2 biomarkers, phagocytic activity, and tumoricidal activity in RAW 264.7 mouse macrophages. Macrophages were treated with conditioned media (CM) from 4T1 breast cancer cells, curcumin, 22-oxacalcitriol, LPS, or a combination of the previously listed. Arginase activity, a M2 phenotypic biomarker, was upregulated by the treatment of macrophages with conditioned media. Curcumin, 22-...
Show moreExtracellular stimuli may influence the M1/M2 phenotypic polarization of macrophages. We examined M1/M2 biomarkers, phagocytic activity, and tumoricidal activity in RAW 264.7 mouse macrophages. Macrophages were treated with conditioned media (CM) from 4T1 breast cancer cells, curcumin, 22-oxacalcitriol, LPS, or a combination of the previously listed. Arginase activity, a M2 phenotypic biomarker, was upregulated by the treatment of macrophages with conditioned media. Curcumin, 22- oxacalcitriol, and LPS partially inhibited RAW 264.7 arginase activity in the presence of 4T1 breast cancer media. 22-oxacalcitriol increased the phagocytic ability of RAW 264.7 macrophages in the presence of M2 polarizing substances produced by the 4T1 breast cancer cells. Also, LPS increased RAW 264.7 phagocytic ability in the presence of 4T1 breast cancer CM. This study looked at the potential substances that would possibly reverse the M2 tumor promoting macrophage phenotype seen in the breast cancer tumor environment.
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Date Issued: 2017
PURL: http://purl.flvc.org/fau/fd/FA00004867
Subject Headings: Macrophages., Breast--Cancer--Treatment., Tumors--Immunological aspects., Cancer--Immunological aspects., Biological response modifiers., Cancer--Molecular aspects.
Format: Document (PDF)

Title: Anticancer activity of two dietary phytochemicals: Genistein and beta-lapachone.
Creator: Merchant, Kendra T., Florida Atlantic University, Kumi-Diaka, James
Abstract/Description: Phytochemicals are biologically active secondary plant metabolites that have been shown to exhibit anti-cancer activity. The dietary phytochemicals genistein isoflavone and beta-lapachone, were investigated to determine their effect on the growth of human prostate adenocarcinoma cells in vitro. The cells were exposed to varying concentrations of both phytochemicals in single and combination treatments for specified time periods and their effect was determined using post-treatment cell...
Show morePhytochemicals are biologically active secondary plant metabolites that have been shown to exhibit anti-cancer activity. The dietary phytochemicals genistein isoflavone and beta-lapachone, were investigated to determine their effect on the growth of human prostate adenocarcinoma cells in vitro. The cells were exposed to varying concentrations of both phytochemicals in single and combination treatments for specified time periods and their effect was determined using post-treatment cell viability, treatment-induced apoptosis and cell signaling assays. The overall results revealed that both phytochemicals inhibited cell growth and proliferation and induced apoptosis in a dose-dependent manner for both single and combination treatments. However, combination treatments were not significantly more effective than single treatment with either drug. Both phytochemicals could therefore offer therapeutic efficacy in human prostate adenocarcinoma.
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Date Issued: 2005
PURL: http://purl.flvc.org/fcla/dt/13250
Subject Headings: Phytochemicals--Physiological effect, Prostate--Cancer--Molecular aspects, Apoptosis--Molecular aspects, Prostate--Cancer--Treatment
Format: Document (PDF)

Title: Initial evaluation of organotin monomers and polymers as potential anticancer agents.
Creator: Doucette, Randy D., Florida Atlantic University, Louda, Deborah W.
Abstract/Description: A large number of metal-containing compounds show significant activity against cancer cells and incorporating a metal into a polymer offers several possible advantages. Compounds of the type R2SnCl2 (R = methyl, ethyl, propyl, butyl, t-butyl, octyl and phenyl) were tested for the ability to inhibit the growth of Balb 3T3 mouse fibroblast cells and CAOV3 human ovarian carcinoma cells. Polymers of 2-chloro-1,4-benzenediamine and the same organotin dichloride were synthesized and tested as well....
Show moreA large number of metal-containing compounds show significant activity against cancer cells and incorporating a metal into a polymer offers several possible advantages. Compounds of the type R2SnCl2 (R = methyl, ethyl, propyl, butyl, t-butyl, octyl and phenyl) were tested for the ability to inhibit the growth of Balb 3T3 mouse fibroblast cells and CAOV3 human ovarian carcinoma cells. Polymers of 2-chloro-1,4-benzenediamine and the same organotin dichloride were synthesized and tested as well. For both monomers and polymers, the pattern of growth inhibition relative to the R group was butyl > propyl = t-butyl = octyl = phenyl > ethyl > methyl. This and other aspects of the structure-activity relationship of the monomers and polymers were examined.
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Date Issued: 2006
PURL: http://purl.flvc.org/fcla/dt/13410
Subject Headings: Apoptosis--Molecular aspects, Polymeric composites, Organometallic compounds, Cancer--Molecular aspects, Antineoplastic agents--Testing, Polymers in medicine
Format: Document (PDF)

Title: The Impact of Pharmacological Targeting of Abnormal Tumor Metabolism with 3-Bromopyruvate on Dendritic Cell Mediated Tumoral Immunity.
Creator: Lang, Kevin, Hartmann, James X., Florida Atlantic University, Charles E. Schmidt College of Science, Department of Biological Sciences
Abstract/Description: Studies have shown that tumor cells are susceptible to pharmacological targeting of their altered glycolytic metabolism with a variety of compounds that result in apoptosis. One such compound, 3-bromopyruvate (3-BP), has been shown to eradicate cancer in an animal model. However, no studies have shown whether the apoptotic fragments resulting from 3-BP treatment have the capacity to elicit an immunogenic cell death that activates dendritic cells, the primary antigen presenting cell in the...
Show moreStudies have shown that tumor cells are susceptible to pharmacological targeting of their altered glycolytic metabolism with a variety of compounds that result in apoptosis. One such compound, 3-bromopyruvate (3-BP), has been shown to eradicate cancer in an animal model. However, no studies have shown whether the apoptotic fragments resulting from 3-BP treatment have the capacity to elicit an immunogenic cell death that activates dendritic cells, the primary antigen presenting cell in the immune system. Immunogenic cell death is critical to eliciting an effective adaptive immune response that selectively kills additional target cells and generates immunological memory. We demonstrated that 3-bromopyruvate induced apoptosis in a number of different murine breast cancer cell lines, including the highly metastatic 4T1 line. The dying tumor cells stimulated immature dendritic cells (DCs) of the immortal JAWS II cell line to produce high levels of the pro-inflammatory cytokine IL-12, and increased their expression of key co-stimulatory molecules CD80 and CD86. The activated dendritic cells showed increased uptake of fragments from dying tumor cells that correlated with the increased levels of calreticulin on the surface and release of high group motility box 1 (HMGB1) of the latter following 3-BP treatment. Additionally, the anti-phagocytic signal CD47 present on breast cancer cells was reduced by treatment with 3-bromopyruvate when compared to the levels on untreated 4T1 cells. 3-BP treated breast cancer cells were able to activate dendritic cells through TLR4 signaling. Signaling was dependent on both the expression of surface calreticulin and on the extracellular release of high mobility group box 1 protein (HMGB1) during the process of immunogenic cell death. Killing by 3-BP was compared to mitoxantrone and doxorubicin, among the few chemotherapeutics that induce immunogenic cell death. 3-BP killing was likewise compared to camptothecin, a compound that fails to induce immunogenic cell death. Importantly, 3-BP did not markedly decrease the levels of the key peptide presenting molecule MHC I on DCs that were co-cultivated with dying tumor cells. Treatment of the highly aggressive triple negative BT-20 human breast cancer cell line with 3-BP also induced an immunogenic cell death, activating human dendritic cells in vitro.
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Date Issued: 2017
PURL: http://purl.flvc.org/fau/fd/FA00004834
Subject Headings: Apoptosis., Cellular signal transduction., Cell death., Breast--Cancer--Treatment., Carrier proteins., Cancer--Molecular aspects., Biological interfaces.
Format: Document (PDF)

Title: Investigating the Role of CHI3L1 in Promoting Tumor Growth and Metastasis Using Mammary Tumor Models.
Creator: Libreros, Stephania, Iragavarapu-Charyulu, Vijaya, Florida Atlantic University, Charles E. Schmidt College of Medicine, Department of Biomedical Science
Abstract/Description: Metastasis is the primary cause of mortality in women with breast cancer. Recently, elevated serum levels of a glycoprotein known as chitinase-3 likeprotein- 1 (CHI3L1) has been correlated with poor prognosis and shorter survival of patients with cancer and inflammatory diseases. The biological and physiological functions of CHI3L1 in tumor progression have not yet been elucidated. In this document, we describe the role of CHI3L1 in tumor growth and metastasis and its relationship with...
Show moreMetastasis is the primary cause of mortality in women with breast cancer. Recently, elevated serum levels of a glycoprotein known as chitinase-3 likeprotein- 1 (CHI3L1) has been correlated with poor prognosis and shorter survival of patients with cancer and inflammatory diseases. The biological and physiological functions of CHI3L1 in tumor progression have not yet been elucidated. In this document, we describe the role of CHI3L1 in tumor growth and metastasis and its relationship with inflammation. Using well-established models of breast cancer, we show that CHI3L1 is increased in the serum of tumor bearing mice. We found that CHI3L1 levels are increased at both the “pre-metastatic” and “metastatic stage” and that tumor cells, splenic, alveolar and interstitial macrophages; and myeloid derived population produce CHI3L1. Furthermore, we demonstrated that CHI3L1 has an inhibitory role on the expression of interferon-gamma (IFN γ) by T cells, while enhancing the production of pro-inflammatory mediators by macrophages such as Cchemokine ligand 2 (CCL2/MCP-1), Chemokine CX motif ligand 2 (CXCL2/IL-8) and matrix metalloproteinase-9 (MMP-9), all of which promote tumor growth and metastasis. We demonstrated that in vivo treatment of tumor-bearing mice with chitin microparticles, a TH1 adjuvant and a substrate for CHI3L1, promoted immune effector functions with increased production of IFN-γ but decreased CCL2/MCP-1, CXCL2/IL-8 and MMP-9 expression by splenic and pulmonary macrophages. Significantly, in vivo administration of chitin microparticles decreased tumor growth and pulmonary metastasis in mammary tumor bearing mice. These results suggest that CHI3L1 may play a role in tumor progression. Inflammation plays a pivotal role during tumor progression and metastasis by promoting the production of pro-inflammatory molecules such as CHI3L1. However, little is known about how CHI3L1 expression can affect secondary sites to enhance metastasis. In these studies, we demonstrated that CHI3L1 alters the cellular composition and inflammatory mediators that aid in the establishment of a metastatic niche for the support of infiltrating tumor cells leading to accelerated tumor progression. Since previous studies showed that CHI3L1 modulates inflammation, we determined the role of CHI3L1 in the context of pre-existing inflammation and metastasis. We found that CHI3L1 deficient mice with preexisting inflammation had decreased pro-inflammatory mediators, and significant reduction in tumor volume and metastasis compared to wild type controls. Preexisting inflammation and CHI3L1 may be driving the establishment of a premetastatic milieu in the lungs and aiding in the establishment of metastasis. Understanding the role of CHI3L1 in inflammation during tumor progression could result in the design of targeted therapies for breast cancer patients.
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Date Issued: 2015
PURL: http://purl.flvc.org/fau/fd/FA00004517, http://purl.flvc.org/fau/fd/FA00004517
Subject Headings: Biopharmaceutics, Breast -- Cancer -- Etiology, Breast -- Cancer -- Molecular aspects, Cell differentiation, Chitinase, Glycoproteins -- Metabolism, Inflammation, Mice as laboratory animals
Format: Document (PDF)

Title: Enhancement of the Chemopreventive and Chemotherapeutic Effects of Genistein and Beta-lapachone in Human Prostate Cancer Cells by Pyroelectrically Generated Very Low Dose Ionizing Radiation.
Creator: Oseni, Saheed Oluwasina, Kumi-Diaka, James, Florida Atlantic University, Charles E. Schmidt College of Science, Department of Biological Sciences
Abstract/Description: An estimated 220,800 new prostate cancer cases and 27,540 deaths are expected to occur in US men by the end of 2015. Despite the increased treatment modes for prostate cancer, there is still no definite cure, and prognosis remains, at best, cautiously optimistic. The explicit amalgamation of two or more cancer therapeutic modalities such as surgery, radiation, and chemotherapy, has been one of the main interests of clinical investigation for several decades. Genistein (GN) and Beta-lapachone ...
Show moreAn estimated 220,800 new prostate cancer cases and 27,540 deaths are expected to occur in US men by the end of 2015. Despite the increased treatment modes for prostate cancer, there is still no definite cure, and prognosis remains, at best, cautiously optimistic. The explicit amalgamation of two or more cancer therapeutic modalities such as surgery, radiation, and chemotherapy, has been one of the main interests of clinical investigation for several decades. Genistein (GN) and Beta-lapachone (BL) are two of the most promising anticancer phytochemical compounds. However, the anticancer activities of BL have been correlated with the enzyme activity of NQO1. The aim of this study was to investigate the enhancing effects of VLDR derived from a portable pyroelectric crystal generator on the chemopreventive and/or chemotherapeutic effects of GN and BL in NQO1+ PC3 and NQO1± (deficient) LNCaP prostate cancer cells (PCa) in vitro. The combination treat ment-induced cytotoxicity was investigated via MTT and Trypan blue exclusion assays. Dicoumarol (an NQO1 inhibitor) was co-administered to assess the effect of VLDR on NQO1 modulation. Nitro-blue tetrazolium assay was used to assess the intracellular ROS levels. Fluorescence microscopy was also used to assess the mode of cell death. In this study, a novel quantitative modeling approach was employed to comparably assess the cytotoxic effects of specific drugs used alone or in combinations with VLDR and to predict the potential synergistic therapeutic combinations. The data suggests that VLDR induced a rise in ROS levels, followed by upregulation in NQO1 levels. Pharmacodynamic indices were developed to quantify and characterize the combination treatment as synergistic, additive or antagonistic per dose or time-interval. Synergism was found to be dose and time-interval dependent. The major mode of cell death by this combination therapeutic regimen was found to be via apoptosis . In conclusion, our results confirm that VLDR enhanced cytotoxicity effects of both drugs dose- and time-dependently.
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Date Issued: 2015
PURL: http://purl.flvc.org/fau/fd/FA00004530, http://purl.flvc.org/fau/fd/FA00004530
Subject Headings: Apoptosis -- Molecular aspects, Genistein -- Therapeutic use, Phytochemicals -- Physiological effect, Phytochemicals -- Therapeutic use, Prostate -- Cancer -- Adjuvant treatment, Prostate -- Cancer -- Cryptopathology, Prostate -- Cancer -- Molecular aspects
Format: Document (PDF)

Title: Impact of Vitamin C on Genistein-Induced Apoptosis in Prostate Cancer.
Creator: Famuyiwa, Toluleke, Kumi-Diaka, James, Florida Atlantic University, Charles E. Schmidt College of Science, Department of Biological Sciences
Abstract/Description: This study determined the impact of vitamin C dose on genistein-induced apoptosis in LNCaP cancer cells at various treatment regimens in vitro. Although the linear regression of viability assay (MTT) indicated a p-value = 0.11; NBT assay reveal a declining SOD activity during cell death. Apoptosis induction was the main mode of treatment induced cell death. The overall data showed the trend of treatment efficacy as;(Gen 10uM + Vit C 40uM) > (Gen 30uM + Vit C 40uM) > (Gen 70uM + Vit C 40uM) >...
Show moreThis study determined the impact of vitamin C dose on genistein-induced apoptosis in LNCaP cancer cells at various treatment regimens in vitro. Although the linear regression of viability assay (MTT) indicated a p-value = 0.11; NBT assay reveal a declining SOD activity during cell death. Apoptosis induction was the main mode of treatment induced cell death. The overall data showed the trend of treatment efficacy as;(Gen 10uM + Vit C 40uM) > (Gen 30uM + Vit C 40uM) > (Gen 70uM + Vit C 40uM) > 10uM genistein > 70uM genistein. The chi-square test for comparing necrosis, apoptosis and life cells showed that Vitamin C could impact genistein-induced apoptosis in LNCaP cells (p = 0.0003). This study forms the basis for in vivo studies of the impact of vitamin C on genistein-induced apoptosis in LNCaP prostate cancer cells.
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Date Issued: 2015
PURL: http://purl.flvc.org/fau/fd/FA00004497, http://purl.flvc.org/fau/fd/FA00004497
Subject Headings: Apoptosis -- Molecular aspects, Cellular signal transduction, Genistein -- Therapeutic use, Phytochemicals -- Physiological effect, Phytochemicals -- Therapeutic use, Prostate -- Cancer -- Adjuvant treatment, Prostate -- Cancer -- Molecular aspects, Vitamin C -- Therapeutic use
Format: Document (PDF)

Title: Therapeutic potential of pomegranate and genistein for human breast cancer.
Creator: Louis Jeune, Marie Adeline, Florida Atlantic University, Kumi-Diaka, James
Abstract/Description: The therapeutic potential of pomegranate and genistein on growth inhibition of human breast cancer cells was investigated. Methods. Cells (MCF-7) were initially cultured for 48 hr to achieve 80% confluence; and then exposed to the agents in single and combination treatments. Post-treatment analysis was done by using a series of bioassays, including LDH, MTS, AcrO-EthBr, Annexin-FITC and TUNEL assays for growth inhibition and apoptosis detection; and Caspase-3 and NQO1 for molecular pathways...
Show moreThe therapeutic potential of pomegranate and genistein on growth inhibition of human breast cancer cells was investigated. Methods. Cells (MCF-7) were initially cultured for 48 hr to achieve 80% confluence; and then exposed to the agents in single and combination treatments. Post-treatment analysis was done by using a series of bioassays, including LDH, MTS, AcrO-EthBr, Annexin-FITC and TUNEL assays for growth inhibition and apoptosis detection; and Caspase-3 and NQO1 for molecular pathways of apoptosis. Results. Pomegranate and genistein showed significant dose- and time-dependent cytotoxic and growth inhibition effects as well as apoptosis induction in MCF-7 cancer cells, with significantly higher ( P < 0.01) effects in the combination treatments than in the single treatments. Both drugs induced apoptosis through a caspase-mediated mechanism and independent of NQO1. Discussion and conclusions. Pomegranate and genistein inhibit the growth of MCF-7 breast cancer cells through induction of apoptosis with combination treatment being more efficacious than single treatments.
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Date Issued: 2004
PURL: http://purl.flvc.org/fcla/dt/13130
Subject Headings: Phytochemicals--Physiological effect, Breast--Cancer--Molecular aspects, Women--Diseases--Alternative treatment, Apoptosis--Molecular aspects, Breast--Cancer--Treatment
Format: Document (PDF)

Title: Genistein targets only proliferating but not quiescent cells: Potential therapeutic significance in breast cancer.
Creator: Bodepudi, Sreedevi., Florida Atlantic University, Kumi-Diaka, James
Abstract/Description: Phytochemicals are biologically active secondary plant metabolites that could mimic biological activities. In this study genistein isoflavone, a phytochemical present in soy was investigated to determine its effect on the growth of human breast cancer cell line GI-101 and normal breast epithelial cells in vitro. The cells were exposed to varying concentrations of genistein isoflavone for 24 and 48 hour time periods and the effect was determined using post-treatment assays: MTT and Trypan Blue...
Show morePhytochemicals are biologically active secondary plant metabolites that could mimic biological activities. In this study genistein isoflavone, a phytochemical present in soy was investigated to determine its effect on the growth of human breast cancer cell line GI-101 and normal breast epithelial cells in vitro. The cells were exposed to varying concentrations of genistein isoflavone for 24 and 48 hour time periods and the effect was determined using post-treatment assays: MTT and Trypan Blue for cell viability; LDH assay for cytotoxicity; Rhodamine 123/Propidium Iodide and Ethidium Bromide/Acridine Orange assays for treatment-induced apoptosis and FAM Poly caspase assay for mechanism of action. The overall results revealed that genistein inhibited cell growth and proliferation through apoptosis in the cells in both time and dose-dependent manner. Normal breast epithelial cells were not significantly affected by genistein at the corresponding dosages. Based on the results obtained, it was concluded that genistein isoflavone could offer therapeutic efficacy in human breast carcinoma without significantly affecting the normal breast epithelial cells.
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Date Issued: 2006
PURL: http://purl.flvc.org/fcla/dt/13315
Subject Headings: Phytochemicals--Physiological effect, Breast--Cancer--Molecular aspects, Women--Diseases--Alternative treatment, Breast--Cancer--Treatment, Apoptosis--Molecular aspects
Format: Document (PDF)

Apoptosis--Molecular aspects (4)	+ -
Phytochemicals--Physiological effect (3)	+ -
Apoptosis -- Molecular aspects (2)	+ -
Breast--Cancer--Molecular aspects (2)	+ -
Breast--Cancer--Treatment (2)	+ -

Breast--Cancer--Treatment. (2)	+ -
Cancer--Molecular aspects. (2)	+ -
Phytochemicals -- Physiological effect (2)	+ -
Phytochemicals -- Therapeutic use (2)	+ -
Prostate--Cancer--Molecular aspects (2)	+ -
Women--Diseases--Alternative treatment (2)	+ -
Antineoplastic agents--Testing (1)	+ -
Apoptosis (1)	+ -
Apoptosis. (1)	+ -
Biological interfaces. (1)	+ -
Biological response modifiers. (1)	+ -
Biopharmaceutics (1)	+ -
Breast -- Cancer -- Etiology (1)	+ -
Breast -- Cancer -- Molecular aspects (1)	+ -
Cancer--Immunological aspects. (1)	+ -
Cancer--Molecular aspects (1)	+ -
Carrier proteins. (1)	+ -
Cell death. (1)	+ -
Cell differentiation (1)	+ -
Cellular signal transduction (1)	+ -
Cellular signal transduction. (1)	+ -
Chitinase (1)	+ -
Genistein -- Therapeutic use (1)	+ -
Genistein -- Therapeutic use (1)	+ -
Glycoproteins -- Metabolism (1)	+ -

Florida Atlantic University (10)	+ -
Kumi-Diaka, James (6)	+ -
Charles E. Schmidt College of Science (4)	+ -
Department of Biological Sciences (4)	+ -
Hartmann, James X. (2)	+ -

Bodepudi, Sreedevi. (1)	+ -
Charles E. Schmidt College of Medicine (1)	+ -
Department of Biomedical Science (1)	+ -
Doucette, Randy D. (1)	+ -
Famuyiwa, Toluleke (1)	+ -
Iragavarapu-Charyulu, Vijaya (1)	+ -
Lang, Kevin (1)	+ -
Libreros, Stephania (1)	+ -
Liddle, Genevieve M. (1)	+ -
Louda, Deborah W. (1)	+ -
Louis Jeune, Marie Adeline (1)	+ -
Merchant, Kendra T. (1)	+ -
Oseni, Saheed Oluwasina (1)	+ -
Saddler, Shawnette Simone (1)	+ -

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