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351. Genotypic Variation and Phenotypic Characterization of Granzyme B Gene Polymorphisms

Author

Girnita, Diana M., primary, Webber, Steven A., additional, Brooks, Maria M., additional, Ferrell, Robert, additional, Girnita, Alin L., additional, Burckart, Gilbert J., additional, Chinnock, Richard, additional, Canter, Charles, additional, Addonizio, Linda, additional, Bernstein, Daniel, additional, Kirklin, James K., additional, Naftel, David, additional, and Zeevi, Adriana, additional

Published
2009
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352. 532: Genetic Polymorphisms Impact the Risk of Infection in Pediatric Heart Transplantation – A Multi-Center Study

Author

Girnita, D.M., primary, Brooks, M.M., additional, Webber, S.A., additional, Burckart, G.J., additional, Ferrell, R., additional, Girnita, A.L., additional, Chinnock, R., additional, Canter, C., additional, Addonizio, L., additional, Bernstein, D., additional, Kirklin, J.K., additional, Naftel, D., additional, and Zeevi, A., additional

Published
2009
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353. Prospective Iterative Trial of Proteasome Inhibitor-Based Desensitization

Author

Woodle, E.S., primary, Shields, A.R., additional, Ejaz, N.S., additional, Sadaka, B., additional, Girnita, A., additional, Walsh, R.C., additional, Alloway, R.R., additional, Brailey, P., additional, Cardi, M.A., additional, Abu Jawdeh, B.G., additional, Roy-Chaudhury, P., additional, Govil, A., additional, and Mogilishetty, G., additional

Published
2015
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354. Graft versus host disease in intestinal transplantation

Author

Alin Girnita, George V. Mazariegos, Geoffrey Bond, Jorge Reyes, Kareem Abu-Elmagd, Camila Macedo, Ronald Jaffe, Rakesh Sindhi, John Peters, and L Martin

Subjects
Adult, Male, medicine.medical_specialty, Adolescent, medicine.medical_treatment, Graft vs Host Disease, Gastroenterology, Internal medicine, medicine, Immunology and Allergy, Humans, Transplantation, Homologous, Pharmacology (medical), Oral mucosa, Child, Retrospective Studies, Transplantation, business.industry, Infant, Retrospective cohort study, Immunosuppression, Middle Aged, medicine.disease, Rash, Tacrolimus, Surgery, Intestines, Diarrhea, surgical procedures, operative, Graft-versus-host disease, medicine.anatomical_structure, Child, Preschool, Drug Therapy, Combination, Female, medicine.symptom, business, Immunosuppressive Agents
Abstract

Our aim was to analyze the clinical course and outcome of patients with graft vs. host disease (GVHD) after intestinal transplantation (ITx). All patients receiving ITx between May, 1990 and December, 2003 were retrospectively reviewed for evidence of GVHD. Two hundred and fifty patients underwent ITx during the study period. Graft vs. host disease was suspected clinically in 23 patients on the clinical basis of presentation such as skin rash, ulceration of oral mucosa, diarrhea, lymphadenopathy, or native liver dysfunction. Fourteen (eight children and six adults) patients (5.6% of total patient population) had GVHD confirmed by histopathological criteria including keratinocyte necrosis (n = 9), epithelial apoptosis of the native gastrointestinal tract (n = 4), and epithelial cell necrosis of oral mucosa (n = 1). Donor-cell tissue infiltration or extensive peripheral blood donor-cell chimerism was documented on seven occasions. The majority of cases of GVHD resolved with steroid administration and optimization of tacrolimus immunosuppression. The incidence of histologically proven GVHD after clinical intestinal transplantation is 6.5% (8/122) in children and 4.7% (6/128) in adults. Successful clinical management requires a high index of suspicion to minimize morbidity and mortality. Diagnostic and treatment strategies based on this experience are proposed.

Published
2004

355. Impact of ELISA-detected anti-HLA antibodies on pediatric cardiac allograft outcome

Author

Sylvie Di Filippo, Susan A. Miller, Adriana Zeevi, Steven A. Webber, Alin Girnita, Sanjiv K. Gandhi, Gerard J. Boyle, and Sabrina Tsao

Subjects
Graft Rejection, Heart Defects, Congenital, Male, medicine.medical_specialty, Adolescent, medicine.medical_treatment, Immunology, Enzyme-Linked Immunosorbent Assay, Human leukocyte antigen, Gastroenterology, Antibodies, Coronary artery disease, HLA Antigens, Internal medicine, medicine, Immunology and Allergy, Lung transplantation, Humans, Transplantation, Homologous, Hla antibodies, Child, biology, Cardiac allograft, business.industry, Graft Survival, Histocompatibility Antigens Class I, Histocompatibility Antigens Class II, Infant, General Medicine, medicine.disease, Transplantation, Treatment Outcome, Child, Preschool, biology.protein, Heart Transplantation, Female, Antibody, Pediatric heart transplantation, business, Cardiomyopathies
Abstract

In this study, we determine whether the presence of enzyme-linked immunosorbent assay (ELISA) detected anti-human leukocyte antigen (HLA) antibodies correlates with acute and chronic rejection in pediatric heart transplantation (Tx). Forty-five patients, who had serial ELISA pre- and posttransplantation, were studied. Age at Tx was 8.2 +/- 7.2 years. Acute rejection (AR) was defined as International Society for Heart and Lung Transplantation Grade > or =3a. Patients were defined as rejectors (22 cases) if they had recurrent AR or steroid-resistant AR within the first year post-Tx; the other cases (23) were defined as nonrejectors. Overall, 219 samples were analyzed. Twenty-two of the 45 had pre- or post-Tx anti-HLA antibodies: 77% in rejectors (17/22) and only 22% in nonrejectors (5/23), p = 0.0002. Pre-Tx HLA antibodies were present in 12 cases (27%). Presensitization was more frequent in rejectors (11/22, 50%) than in nonrejectors (1/23, 4%, p = 0.0005). Nineteen cases retained (9 cases) or developed (10 cases) anti-HLA antibodies post-Tx: 14 in rejectors (63.6%) and 5 in nonrejectors (21.7%), p = 0.003. Four of eight cases with coronary artery disease (50%) had preformed anti-HLA antibodies compared with 8 of 37 without coronary artery disease (25.6%) (p = 0.09). Preformed, persistent, and de novo ELISA-detected anti-HLA antibodies were correlated with first-year acute rejection profile.

Published
2004

358. 26-OR: Impact of genetic polymorphisms on rejection with hemodynamic compromise – A multi-institutional study

Author

Girnita, D.M., primary, Webber, S.A., additional, Brooks, M.M., additional, Burckart, G.J., additional, Ferrell, R., additional, Chinnock, R., additional, Canter, C., additional, Addonizio, L., additional, Bernstein, D., additional, Kirklin, J.K., additional, Naftel, D., additional, Girnita, A.L., additional, and Zeevi, A., additional

Published
2008
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362. Genetic Polymorphisms Impact the Risk of Acute Rejection in Pediatric Heart Transplantation: A Multi-Institutional Study

Author

Girnita, Diana M., primary, Brooks, Maria M., additional, Webber, Steven A., additional, Burckart, Gilbert J., additional, Ferrell, Robert, additional, Zdanowicz, Gina, additional, DeCroo, Susan, additional, Smith, Louise, additional, Chinnock, Richard, additional, Canter, Charles, additional, Addonizio, Linda, additional, Bernstein, Daniel, additional, Kirklin, James K., additional, Ranganathan, Sarangarajan, additional, Naftel, David, additional, Girnita, Alin L., additional, and Zeevi, Adriana, additional

Published
2008
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363. GP2-2: The deubiquitinating enzyme, USP9X positively regulates insulin-like growth factor (IGF)-dependent cell growth by inhibition of degradation of IGF-I receptor (IGF-IR) and insulin receptor substrate (IRS)-2 in prostate cancer cells

Author

Furuta, H., primary, Yoshihara, H., additional, Fukushima, T., additional, Saeki, Y.S., additional, Ito, A., additional, Worrall, C., additional, Girnita, L., additional, Tanaka, K., additional, Yoshida, M., additional, Asano, T., additional, Chida, K., additional, Hakuno, F., additional, and Takahashi, S.-I., additional

Published
2014
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365. 314: Genotypic Variation and Phenotypic Characterization of Granzyme B Gene Polymorphisms

Author

Girnita, D.M., primary, Webber, S.A., additional, Ferrell, R., additional, Brooks, M.M., additional, DeCroo, S., additional, Burckart, G., additional, Zdanowicz, G., additional, Chinnock, R., additional, Canter, C., additional, Addonizio, L., additional, Bernstein, D., additional, Kirklin, J.K., additional, Naftel, D., additional, Smith, L., additional, Girnita, A.L., additional, and Zeevi, A., additional

Published
2008
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368. CD44s adhesive function spontaneous and PMA-inducible CD44 cleavage are regulated at post-translational level in cells of melanocytic lineage

Author

Armando Bartolazzi, F Del Prete, Leonard Girnita, P. G. Natali, Marco Paolo Martegani, and Alessandra Gasbarri

Subjects
Cancer Research, Glycosylation, Skin Neoplasms, Antimetabolites, Cell, Down-Regulation, Dermatology, Biology, Cleavage (embryo), medicine, Tumor Cells, Cultured, Humans, Hyaluronic Acid, Receptor, Melanoma, Genetics, Regulation of gene expression, Metalloproteinase, Alternative splicing, CD44, Cell biology, Neoplasm Proteins, Gene Expression Regulation, Neoplastic, medicine.anatomical_structure, Hyaluronan Receptors, Oncology, Ectodomain, biology.protein, Metalloproteases, Mutagenesis, Site-Directed, Tetradecanoylphorbol Acetate, Protein Processing, Post-Translational, Protein Binding
Abstract

Adhesion between the CD44s receptor and hyaluronic acid plays an important role in cell migration, tumour growth and progression. Although the alternative splicing of CD44 variant exons represents the principal regulatory mechanism of CD44-mediated functions, CD44v spliced variants are scantily expressed in melanoma cells. For this reason, we have investigated the possibility that post-translational modifications of the CD44 standard receptor could play a pivotal role in regulating CD44-mediated functions in melanoma. Using metabolic inhibitors of N- and O-glycosylation, as well as melanoma transfectants expressing CD44s O-glycosylation site-specific mutants, we performed structural and functional analysis of N- and O-deglycosylated CD44s molecules expressed in melanoma cells. We discovered that complete N- and O-glycosylation is not required by CD44s to be correctly expressed on the melanoma cell surface. Indeed, variably glycosylated and functionally different CD44s molecules were constitutively expressed in primary and metastatic lesions. Furthermore, we observed that changes in N- and O-glycosylation of CD44s could modulate its cleavage. In fact, spontaneous CD44s shedding was dependent on the presence of partial or complete O-glycosylation of four serine-glycine motifs localized in the membrane-proximal CD44 ectodomain. Mutation of these serine residues, as well as an extensive metabolic O-deglycosylation, strongly impaired spontaneous CD44 shedding. Furthermore, an O-glycosylation-independent mechanism of CD44 cleavage has been identified. This alternative mechanism of receptor cleavage is phorbol 12-myristate-13-acetate (PMA) inducible, mediated by metalloproteinase and requires the presence of N-linked sugar residues. Our findings demonstrate that the post-translational modification of CD44s represents the principal regulatory mechanism of CD44s-mediated functions in melanoma.

Published
2003

369. Genome-Wide Screen for MicroRNAs Reveals a Role for miR-203 in Melanoma Metastasis

Author

Lohcharoenkal, Warangkana, Das Mahapatra, Kunal, Pasquali, Lorenzo, Crudden, Caitrin, Kular, Lara, Akkaya Ulum, Yeliz Z., Zhang, Lingyun, Xu Landén, Ning, Girnita, Leonard, Jagodic, Maja, Ståhle, Mona, Sonkoly, Enikö, and Pivarcsi, Andor

Abstract

Melanoma is one of the deadliest human cancers with limited therapeutic options. MicroRNAs are a class of short noncoding RNAs regulating gene expression at the post-transcriptional level. To identify important miRNAs in melanoma, we compared the miRNome of primary and metastatic melanomas in The Cancer Genome Atlas dataset and found lower miR-203 abundance in metastatic melanoma. Lower level of miR-203 was associated with poor overall survival in metastatic disease. We found that the methylation levels of several CpGs in the MIR203promoter negatively correlated with miR-203 expression and that treatment with the demethylating agent 5-aza-2-deoxycytidine induced miR-203 expression, which was associated with demethylation of the promoter CpGs, in melanoma cell lines. In vitro, there was a decreased expression of miR-203 in melanoma cell lines in comparison with primary melanocytes. Ectopic overexpression of miR-203 suppressed cell motility, colony formation, and sphere formation as well as the angiogenesis-inducing capacity of melanoma cells. In vivo, miR-203 inhibited xenograft tumor growth and reduced lymph node and lung metastasis. SLUG was shown as a target of miR-203, and knockdown of SLUG recapitulated the effects of miR-203, whereas its restoration was able to reverse the miR-203-mediated suppression of cell motility. These results establish a role for miR-203 as a tumor suppressor in melanoma which suppresses both early and late steps of metastasis. Hence, restoration of miR-203 has therapeutic potential in melanoma.

Published
2018
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372. P66 Role of IGF-1R signaling in uveal melanoma

Author

Leonard Girnita, H. Zheng, T. Lin, H. Shen, Ada Girnita, and C. Worrall

Subjects
Endocrinology, business.industry, Endocrinology, Diabetes and Metabolism, Melanoma, Cancer research, medicine, medicine.disease, business
Published
2010
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374. 40-OR: The combination high VEGF/high IL-6 and low IL-10 gene polymorphism impact the risk of acute rejection in pediatric heart transplantation – a multicenter study

Author

Girnita, D.M., primary, Brooks, M., additional, Webber, S., additional, Burckart, G., additional, Ferrell, R., additional, Zdanowicz, G., additional, Chinnock, R., additional, Canter, C., additional, Addonizio, L., additional, Bernstein, D., additional, Kirklin, J., additional, Naftel, D., additional, Girnita, A., additional, and Zeevi, A., additional

Published
2007
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382. Insulin-like growth factor-1 receptor in uveal melanoma: a predictor for metastatic disease and a potential therapeutic target

Author

Charlotta, All-Ericsson, Leonard, Girnita, Stefan, Seregard, Armando, Bartolazzi, Martine J, Jager, and Olle, Larsson

Subjects
Adult, Aged, 80 and over, Male, Uveal Neoplasms, Cell Survival, Blotting, Western, Middle Aged, Precipitin Tests, Receptor, IGF Type 1, Immunoenzyme Techniques, Survival Rate, Biomarkers, Tumor, Tumor Cells, Cultured, Humans, Female, Neoplasm Metastasis, Melanoma, Cell Division, Aged
Abstract

To investigate the expression of the insulin-like growth factor-1 receptor (IGF-1R) with special focus on its role in cell growth in uveal melanoma.Paraffin material from 36 clinicopathologically well characterized cases of primary uveal melanomas (18 of which had metastasized to the liver) with more than 15 years' follow-up was used for immunohistochemical analysis. In the experimental studies, three uveal melanoma cell lines (OCM-1, OCM-3, and 92-1) were used. The expression level of IGF-1R in the cell lines was modulated by glycosylation inhibitors, and the IGF-1R was neutralized with the antibody alphaIR-3. Expression of IGF-1R was assayed by Western blot analysis and immunohistochemistry. Cell growth and survival were analyzed by cell counting, thymidine incorporation, and viability assays.Western blot analysis and immunohistochemistry confirmed that IGF-1R is expressed in uveal melanoma. Although 10 of 18 patients who died of metastasizing disease showed high IGF-1R expression, only 5 of 18 tumors from patients who survived for 15 years or more after enucleation exhibited a high IGF-1R expression. Kaplan-Meier analysis showed a significant association (P = 0.035) between a high IGF-1R expression and death due to metastatic uveal melanoma. Using in vitro experimental models, we found that inhibition of the IGF-1R activity (tyrosine phosphorylation) was associated with a drastic decrease in uveal melanoma cell viability.These data suggest an important role of IGF-1R in uveal melanoma. The significant association between high IGF-1R expression and death due to metastatic disease may be explained by the fact that IGF-1 is mainly produced in the liver, which is the preferential site for uveal melanoma metastases. These data also point to the possibility of therapeutically interfering with IGF-1R, which appears to be expressed preferentially in uveal melanomas that appear to follow an aggressive clinical course.

Published
2002

384. 532: Genetic Polymorphisms Impact the Risk of Infection in Pediatric Heart Transplantation – A Multi-Center Study

Author

Daniel Bernstein, Steven A. Webber, A. Zeevi, James K. Kirklin, Charles E. Canter, Alin Girnita, D. Naftel, Gilbert J. Burckart, Robert E. Ferrell, Richard E. Chinnock, Linda J. Addonizio, Maria M. Brooks, and Diana M. Girnita

Subjects
Pulmonary and Respiratory Medicine, Transplantation, Pediatrics, medicine.medical_specialty, business.industry, Multi center study, Risk of infection, Medicine, Surgery, Pediatric heart transplantation, Cardiology and Cardiovascular Medicine, business
Published
2009
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385. Disparate Distribution of 16 Candidate Single Nucleotide Polymorphisms Among Racial and Ethnic Groups of Pediatric Heart Transplant Patients

Author

Girnita, Diana M., primary, Webber, Steven A., additional, Ferrell, Robert, additional, Burckart, Gilbert J., additional, Brooks, Maria M., additional, McDade, Kevin K., additional, Chinnock, Richard, additional, Canter, Charles, additional, Addonizio, Linda, additional, Bernstein, Daniel, additional, Kirklin, James K., additional, Girnita, Alin L., additional, and Zeevi, Adriana, additional

Published
2006
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391. GP2-2: The deubiquitinating enzyme, USP9X positively regulates insulin-like growth factor (IGF)-dependent cell growth by inhibition of degradation of IGF-I receptor (IGF-IR) and insulin receptor substrate (IRS)-2 in prostate cancer cells

Author

Hidehito Yoshihara, K. Tanaka, Fumihiko Hakuno, Toshiaki Fukushima, C. Worrall, S.-I. Takahashi, Leonard Girnita, M. Yoshida, Haruka Furuta, Y. Saeki, Tomoichiro Asano, A. Ito, and K. Chida

Subjects
biology, Cell growth, Chemistry, Endocrinology, Diabetes and Metabolism, medicine.medical_treatment, medicine.disease, Deubiquitinating enzyme, Prostate cancer, Insulin-like growth factor, Endocrinology, Growth factor receptor, Insulin receptor substrate, biology.protein, medicine, Cancer research, Growth factor receptor inhibitor, Insulin-like growth factor 1 receptor
Published
2014
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392. Expression and Growth Dependency of the Insulin-Like Growth Factor I Receptor in Craniopharyngioma Cells: A Novel Therapeutic Approach

Author

Ulfarsson, Elfar, primary, Karström, Alexandra, additional, Yin, Shucheng, additional, Girnita, Ada, additional, Vasilcanu, Daiana, additional, Thoren, Marja, additional, Kratz, Gunnar, additional, Hillman, Jan, additional, Axelson, Magnus, additional, Larsson, Olle, additional, and Girnita, Leonard, additional

Published
2005
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395. 26-OR: Impact of genetic polymorphisms on rejection with hemodynamic compromise – A multi-institutional study

Author

Richard E. Chinnock, Linda J. Addonizio, Charles E. Canter, Diana M. Girnita, David C. Naftel, A. Zeevi, Steven A. Webber, Alin Girnita, Maria M. Brooks, Gilbert J. Burckart, James K. Kirklin, Daniel Bernstein, and Robert E. Ferrell

Subjects
Hemodynamic compromise, medicine.medical_specialty, business.industry, Internal medicine, Immunology, medicine, Cardiology, Immunology and Allergy, General Medicine, business
Published
2008
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398. Inhibition of N-linked glycosylation down-regulates insulin-like growth factor-1 receptor at the cell surface and kills Ewing's sarcoma cells: therapeutic implications

Author

L, Girnita, M, Wang, Y, Xie, G, Nilsson, A, Dricu, J, Wejde, and O, Larsson

Subjects
Glycosylation, Cell Survival, Tunicamycin, Tumor Cells, Cultured, Down-Regulation, Humans, Antineoplastic Agents, Lovastatin, Sarcoma, Ewing, Cell Division, Receptor, IGF Type 1
Abstract

The insulin-like growth factor-1 receptor (IGF-1R) has been shown to be of critical importance for tumor development and tumor cell survival of various types of malignancies. We have previously demonstrated that an adequate N-linked glycosylation of IGF-1R is required for its translocation to the cell surface in melanoma cells. This raises the possibility of using glycosylation inhibitors as therapeutic agents against IGF-1R-dependent malignancies. In this study we show that inhibition of N-linked glycosylation using tunicamycin or the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor lovastatin resulted in down-regulation of IGF-1R at the cell surface in Ewing's sarcoma cell lines (RD-ES and ES-1 cells). The down-regulation of plasma membrane-bound IGF-1R was correlated with a drastic decrease in IGF-1R autophosphorylation, suggesting biochemical inactivation of the receptor. Whereas RD-ES and ES-1 cells responded differently with regard to DNA synthesis, the decrease in IGF-1R expression was accompanied by a rapid and substantial decrease in survival of both cell lines. Our data suggest that relatively untoxic HMG-CoA reductase inhibitors (e.g. lovastatin) could have therapeutic significance in IGF-1R-dependent neoplasms like Ewing's sarcoma.

Published
2000

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