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2. Development and Initial Validation of the Macrophage Activation Syndrome/Primary Hemophagocytic Lymphohistiocytosis Score, a Diagnostic Tool that Differentiates Primary Hemophagocytic Lymphohistiocytosis from Macrophage Activation Syndrome

Author

Abinun, Mario, Aggarwal, Amita, Akikusa, Jonathan, Al-Mayouf, Sulaiman, Alessio, Maria, Anton, Jordi, Apaz, Maria Teresa, Astigarraga, Itziar, Avcin, Tadej, Ayaz, Nuray Aktay, Barone, Patrizia, Bica, Bianca, Bolt, Isabel, Bovis, Francesca, Breda, Luciana, Chasnyk, Vyacheslav, Cimaz, Rolando, Corona, Fabrizia, Cron, Randy Q., Cuttica, Ruben, Davì, Sergio, Davidsone, Zane, De Cunto, Carmen, De Inocencio, Jaime, Demirkaya, Erkan, Eisenstein, Eli M., Enciso, Sandra, Espada, Graciela, Fischbach, Michel, Frosch, Michael, Gallizzi, Romina, Gamir, Maria Luz, Gao, Yi-Jin, Griffin, Thomas, Grom, Alexei, Hashad, Soad, Hennon, Teresa, Henter, Jan-Inge, Horne, AnnaCarin, Horneff, Gerd, Huasong, Zeng, Huber, Adam, Ilowite, Norman, Insalaco, Antonella, Ioseliani, Maka, Jeng, Michael, Kapović, Agneza Marija, Kasapcopur, Ozgur, Khubchandani, Raju, Kitoh, Toshiyuki, Koné-Paut, Isabelle, de Oliveira, Sheila Knupp Feitosa, Lattanzi, Bianca, Lehmberg, Kai, Lepore, Loredana, Li, Caifeng, Lipton, Jeffrey M., Magni-Manzoni, Silvia, Maritsi, Despoina, Martini, Alberto, McCurdy, Deborah, Merino, Rosa, Micalizzi, Concetta, Miettunen, Paivi, Minoia, Francesca, Mulaosmanovic, Velma, Nichols, Kim E., Nielsen, Susan, Ozen, Seza, Pal, Priyankar, Prahalad, Sampath, Ravelli, Angelo, Rigante, Donato, Rumba-Rozenfelde, Ingrida, Ruperto, Nicolino, Russo, Ricardo, Magalhães, Claudia Saad, Sanner, Helga, Sewairi, Wafaa Mohamed Saad, Shenoi, Susan, Artur Silva, Clovis, Stanevicha, Valda, Sterba, Gary, Stine, Kimo C., Susic, Gordana, Sztajnbok, Flavio, Takei, Syuji, Trauzeddel, Ralf, Tsitsami, Elena, Unsal, Erbil, Uziel, Yosef, Vougiouka, Olga, Wallace, Carol A., Weaver, Lehn, E. Weiss, Jennifer, Weitzman, Sheila, Wouters, Carine, Wulffraat, Nico, Zletni, Mabruka, Arico, Maurizio, Egeler, R. Maarten, Filipovich, Alexandra H., Gadner, Helmut, Imashuku, Shinsaku, Janka, Gritta, Ladisch, Stephan, McClain, Ken L., and Webb, David

Published
2017
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3. 2016 Classification Criteria for Macrophage Activation Syndrome Complicating Systemic Juvenile Idiopathic Arthritis: A European League Against Rheumatism/American College of Rheumatology/Paediatric Rheumatology International Trials Organisation Collaborative Initiative

Author

Ravelli, Angelo, Minoia, Francesca, Davì, Sergio, Horne, AnnaCarin, Bovis, Francesca, Pistorio, Angela, Aricò, Maurizio, Avcin, Tadej, Behrens, Edward M., De Benedetti, Fabrizio, Filipovic, Lisa, Grom, Alexei A., Henter, Jan-Inge, Ilowite, Norman T., Jordan, Michael B., Khubchandani, Raju, Kitoh, Toshiyuki, Lehmberg, Kai, Lovell, Daniel J., Miettunen, Paivi, Nichols, Kim E., Ozen, Seza, Schmid, Jana Pachlopnik, Ramanan, Athimalaipet V., Russo, Ricardo, Schneider, Rayfel, Sterba, Gary, Uziel, Yosef, Wallace, Carol, Wouters, Carine, Wulffraat, Nico, Demirkaya, Erkan, Brunner, Hermine I., Martini, Alberto, Ruperto, Nicolino, Cron, Randy Q., Abinun, Mario, Aggarwal, Amita, Akikusa, Jonathan, Al-Mayouf, Sulaiman M., Alessio, Maria, Anton, Jordi, Apaz, Maria Teresa, Astigarraga, Itziar, Ayaz, Nuray A., Barone, Patrizia, Bica, Blanca, Bolt, Isabel, Breda, Luciana, Chasnyk, Vyacheslav, Cimaz, Rolando, Corona, Fabrizia, Cuttica, Ruben, DʼAngelo, Gianfranco, Davidsone, Zane, De Cunto, Carmen, De Inocencio, Jaime, Eisenstein, Eli, Enciso, Sandra, Espada, Graciela, Fischbach, Michel, Frosch, Michael, Gallizzi, Romina, Gamir, Maria Luz, Gao, Yi-Jin, Griffin, Thomas, Hashad, Soad, Hennon, Teresa, Horneff, Gerd, Huasong, Zeng, Huber, Adam, Ilowite, Norman, Insalaco, Antonella, Ioseliani, Maka, Jelusic-Drazic, Marijia, Jeng, Michael, Kapovic, Agneza, Kasapcopur, Ozgur, Kone-Paut, Isabelle, de Oliveira, Sheila Knupp Feitosa, Lattanzi, Bianca, Lepore, Loredana, Li, Caifeng, Lipton, Jeffrey M., Magni-Manzoni, Silvia, Maritsi, Despoina, McCurdy, Deborah, Merino, Rosa, Mulaosmanovic, Velma, Nielsen, Susan, Pal, Priyankar, Prahalad, Sampath, Rigante, Donato, Rumba-Rozenfelde, Ingrida, Magalhaes, Claudia Saad, Sanner, Helga, Sawhney, Sujata, Sewairi, Wafaa M., Shakoory, Bita, Shenoi, Susan, Clovis, Artur Silva, Stanevicha, Valda, Stine, Kimo C., Susic, Gordana, Sztajnbok, Flavio, Takei, Syuji, Tezer, Hasan, Trauzeddel, Ralf, Tsitsami, Elena, Unsal, Erbil, Vougiouka, Olga, Weaver, Lehn K., Weiss, Jennifer, Weitzman, Sheila, and Zletni, Mabruka

Published
2016
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4. Development and Initial Validation of the Macrophage Activation Syndrome/Primary Hemophagocytic Lymphohistiocytosis Score, a Diagnostic Tool that Differentiates Primary Hemophagocytic Lymphohistiocytosis from Macrophage Activation Syndrome

Author

Minoia, Francesca, Bovis, Francesca, Davì, Sergio, Insalaco, Antonella, Lehmberg, Kai, Shenoi, Susan, Weitzman, Sheila, Espada, Graciela, Gao, Yi-Jin, Anton, Jordi, Kitoh, Toshiyuki, Kasapcopur, Ozgur, Sanner, Helga, Merino, Rosa, Astigarraga, Itziar, Alessio, Maria, Jeng, Michael, Chasnyk, Vyacheslav, Nichols, Kim E., Huasong, Zeng, Li, Caifeng, Micalizzi, Concetta, Ruperto, Nicolino, Martini, Alberto, Cron, Randy Q., Ravelli, Angelo, Horne, AnnaCarin, Abinun, Mario, Aggarwal, Amita, Akikusa, Jonathan, Al-Mayouf, Sulaiman, Apaz, Maria Teresa, Avcin, Tadej, Ayaz, Nuray Aktay, Barone, Patrizia, Bica, Bianca, Bolt, Isabel, Breda, Luciana, Cimaz, Rolando, Corona, Fabrizia, Cuttica, Ruben, Davidsone, Zane, De Cunto, Carmen, De Inocencio, Jaime, Demirkaya, Erkan, Eisenstein, Eli M., Enciso, Sandra, Fischbach, Michel, Frosch, Michael, Gallizzi, Romina, Gamir, Maria Luz, Griffin, Thomas, Grom, Alexei, Hashad, Soad, Hennon, Teresa, Henter, Jan-Inge, Horne, AnnaCarin, Horneff, Gerd, Huber, Adam, Ilowite, Norman, Ioseliani, Maka, Kapović, Agneza Marija, Khubchandani, Raju, Koné-Paut, Isabelle, de Oliveira, Sheila Knupp Feitosa, Lattanzi, Bianca, Lepore, Loredana, Lipton, Jeffrey M., Magni-Manzoni, Silvia, Maritsi, Despoina, McCurdy, Deborah, Miettunen, Paivi, Mulaosmanovic, Velma, Nielsen, Susan, Ozen, Seza, Pal, Priyankar, Prahalad, Sampath, Rigante, Donato, Rumba-Rozenfelde, Ingrida, Ruperto, Nicolino, Russo, Ricardo, Magalhães, Claudia Saad, Sewairi, Wafaa Mohamed Saad, Silva, Clovis Artur, Stanevicha, Valda, Sterba, Gary, Stine, Kimo C., Susic, Gordana, Sztajnbok, Flavio, Takei, Syuji, Trauzeddel, Ralf, Tsitsami, Elena, Unsal, Erbil, Uziel, Yosef, Vougiouka, Olga, Wallace, Carol A., Weaver, Lehn, Weiss, Jennifer E., Wouters, Carine, Wulffraat, Nico, Zletni, Mabruka, Arico, Maurizio, Egeler, Maarten R., Filipovich, Alexandra H., Gadner, Helmut, Imashuku, Shinsaku, Janka, Gritta, Ladisch, Stephan, McClain, Ken L., and Webb, David

Published
2017
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6. Doxorubicin‐induced delayed‐onset subclinical cardiotoxicity in mice.

Author

Desai, Varsha G., Vijay, Vikrant, Han, Tao, Moland, Carrie L., Phanavanh, Bounleut, Lee, Taewon, Davis, Kelly J., Muskhelishvili, Levan, Stine, Kimo C., and Fuscoe, James C.

Subjects
DOXORUBICIN, CARDIOTOXICITY, VENTRICULAR ejection fraction, SARCOPLASMIC reticulum, HEART diseases, MICE
Abstract

Subclinical cardiotoxicity at low total cumulative doxorubicin (DOX) doses can manifest into cardiomyopathy in long‐term cancer survivors. However, the underlying mechanisms are poorly understood. In male B6C3F1 mice, assessment of cardiac function by echocardiography was performed at 1, 4, 10, 17, and 24 weeks after exposure to 6, 9, 12, and 24 mg/kg total cumulative DOX doses or saline (SAL) to monitor development of delayed‐onset cardiotoxicity. The 6‐ or 9‐mg/kg total cumulative doses resulted in a significant time‐dependent decline in systolic function (left ventricular ejection fraction (LVEF) and fractional shortening (FS)) during the 24‐week recovery although there was not a significant alteration in % LVEF or % FS at any specific time point during the recovery. A significant decline in systolic function was elicited by the cardiotoxic cumulative DOX dose (24 mg/kg) during the 4‐ to 24‐week period after treatment compared to SAL‐treated counterparts. At 24 weeks after DOX treatment, a significant dose‐related decrease in the expression of genes and proteins involved in sarcoplasmic reticulum (SR) calcium homeostasis (Ryr2 and Serca2) was associated with a dose‐related increase in the transcript level of Casp12 (SR‐specific apoptosis) in hearts. These mice also showed enhanced apoptotic activity in hearts indicated by a significant dose‐related elevation in the number of apoptotic cardiomyocytes compared to SAL‐treated counterparts. These findings collectively suggest that a steady decline in SR calcium handling and apoptosis might be involved in the development of subclinical cardiotoxicity that can evolve into irreversible cardiomyopathy later in life. Subclinical cardiotoxicity elicited by low total cumulative doxorubicin (DOX) doses can occur years after treatment in cancer patients. In male B6C3F1 mice, a progressive deterioration in heart function measured by echocardiography was evidenced by a significant time‐dependent decline in systolic function during 24 weeks after treatment with 6‐ or 9‐mg/kg total cumulative DOX doses. A significant dose‐related downregulation of Ryr2 and Serca2 and increased number of apoptotic cardiomyocytes at 24 weeks after treatment may underlie delayed‐onset subclinical cardiac dysfunction. [ABSTRACT FROM AUTHOR]

Published
2022
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14. Impact of Dietary Yogurt on Immune Function

Author

Wheeler, J. Gary, Bogle, Margaret L., Shema, Sarah J., Shirrell, M. Annette, Stine, Kimo C., Pittler, Arlyn J., Burks, A. Wesley, and Helm, Ricki M.

Published
1997

15. Telomere fusion as a mechanism for the progressive loss of the short arm of chromosome 11 in an anaplastic Wilms' tumor

Author

Sawyer, Jeffrey R., Goosen, Linda S., Stine, Kimo C., and Thomas, James R.

Subjects
Telomeres -- Health aspects, Nephroblastoma -- Genetic aspects, Chromosome deletion -- Health aspects, Health
Abstract

Wilms' tumor (WT) is associated with chromosomal deletions and loss of heterozygosity (LOH) of alleles at 11p13. The authors report the youngest known patient with diffusely anaplastic WT and, to their knowledge, the first case to demonstrate telomeric fusions as a chromosomal mechanism for the loss of bands 11p13 and 11p15 in WT. Recurrent clonal telomeric association (tas) initiated breakage/fusion cycles that resulted in deletions of chromosome bands 11p15, 11p13, and, subsequently, the entire short arm of chromosome 11. In addition, tas involving the long arms of chromosomes 7 and 9 resulted in the subsequent deletion of the long arm of chromosome 7. This report expands the spectrum of chromosomal mechanisms that can account for the loss of alleles on the short arm of chromosome 11 in WT by providing evidence that the progressive loss of critical chromosome regions associated with tumor suppression may occur as a result of chromosomal instability initiated by tas. Cancer 1994; 74: 767-73.

Published
1994

17. Alterations in antibody-dependent cellular cytotoxicity during the course of HIV-1 infection

Author

Tyler, Douglas S., Stanley, S. David, Nastala, Chet A., Austin, Arthur A., Bartlett, John A., Stine, Kimo C., Lyerly, H. Kim, Bolognesi, Dani P., and Weinhold, Kent J.

Subjects
Immunotherapy -- Research, Cellular immunity -- Physiological aspects, HIV (Viruses) -- Physiological aspects, AIDS (Disease) -- Physiological aspects, Health
Abstract

Cell-mediated cytotoxicity (CMC) specific for human immunodeficiency virus (HIV) is a type of antibody dependent cellular cytotoxicity (ADCC) activity, in which antibodies to HIV bind to immune cells, known as natural killer (NK) cells, enabling them to kill any cell containing HIV antigens. This type of cellular immunity occurs in early stages of the disease, but decreases with the progression of HIV. The factors that contribute to the decline of this activity were examined by studying the various conditions under which antibodies bind to the NK cells. Sera from patients with HIV infection were tested for the presence of antibodies that allow ADCC activity and for the binding of antibody to NK cells. HIV-infected patients without symptoms of AIDS had low levels of antibodies for ADCC, but did not have antibodies that could bind to NK cells. However, patients with AIDS had large amounts of antibodies for ADCC activity, but did not have antibodies that could bind to NK cells. There was also a group of patients who had low levels of CMC, but large amounts of antibodies which could bind to NK cells. This indicates that other factors besides the amount of antibody specific to HIV are involved in the decrease of CMC. Lymphocytes from AIDS patients had lower levels of ADCC and NK activity, compared with normal individuals, even if there was a lot of antibody present so that these cells could be armed. Therefore, in patients who are infected with HIV, there are defects in both the types and levels of antibodies and in the cells themselves. These defects result in the decline of CMC activity. To know what conditions would allow the arming of NK cells is important, since this information could be used to develop a type of immunotherapy for HIV infection or AIDS. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1990

18. A Novel Germline TP53Mutation in a Patient With Li-Fraumeni Syndrome: Resolving a Variant of Uncertain Significance

Author

Douglass, David P., Stine, Kimo C., and Farrar, Jason E.

Abstract

Increasing availability of genomic testing poses new challenges to clinicians, particularly where variant interpretation from commercial sources may be equivocal. The authors report a patient with recurrent rhabdomyosarcoma and subsequent bilateral breast cancer who was found to harbor a previously undescribed germline TP53sequence alteration annotated by the commercial laboratory as a variant of uncertain significance. By investigating publicly available databases of aggregated normal germline and malignant somatic genomic sequences, the authors conclude that this missense variant, c.476C>T (p.A159V), is a novel, pathogenic Li-Fraumeni syndrome mutation and demonstrate the utility of these resources in clinical pediatric hematology and oncology practice.

Published
2021
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19. The genomic landscape of juvenile myelomonocytic leukemia

Author

Mahoney, Donald H, Yu, Ariel, Stewart, Chip, Costello, Joseph F, Stine, Kimo C, Stieglitz, Elliot, Cooper, Todd, Liu, Y Lucy, Olshen, Adam B, Gerbing, Robert B, Goyal, Rakesh K, Hugge, Christopher, Beckman, Kyle, Brown, Patrick A, Toretsky, Jeffrey A, Briones, Michael, Ma, Jing, Nemecek, Eneida R, Roehrs, Philip A, Abusin, Ghada, Schore, Reuven J, Hitzler, Johann, Li, Yongjin, Hayashi, Robert J, Monteleone, Philip, Carcamo, Benjamin, Emanuel, Peter D, Messinger, Yoav H, Archambeault, Sophie L, Takemoto, Clifford M, Fluchel, Mark N, and Dahl, Gary V

Abstract

Juvenile myelomonocytic leukemia (JMML) is a myeloproliferative neoplasm (MPN) of childhood with a poor prognosis. Mutations in NF1, NRAS, KRAS, PTPN11 and CBL occur in 85% of patients, yet there are currently no risk stratification algorithms capable of predicting which patients will be refractory to conventional treatment and therefore be candidates for experimental therapies. In addition, there have been few other molecular pathways identified aside from the Ras/MAPK pathway to serve as the basis for such novel therapeutic strategies. We therefore sought to genomically characterize serial samples from patients at diagnosis through relapse and transformation to acute myeloid leukemia in order to expand our knowledge of the mutational spectrum in JMML. We identified recurrent mutations in genes involved in signal transduction, gene splicing, the polycomb repressive complex 2 (PRC2) and transcription. Importantly, the number of somatic alterations present at diagnosis appears to be the major determinant of outcome.

Published
2015
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20. Nutlin-3 treatment spares cisplatin-induced inhibition of bone healing while maintaining osteosarcoma toxicity

Author

Stine, Kimo C., primary, Wahl, Elizabeth C., additional, Liu, Lichu, additional, Skinner, Robert A., additional, VanderSchilden, Jaclyn, additional, Bunn, Robert C., additional, Montgomery, Corey O., additional, Aronson, James, additional, Becton, David L., additional, Nicholas, Richard W., additional, Swearingen, Christopher J., additional, Suva, Larry J., additional, and Lumpkin, Charles K., additional

Published
2016
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21. Correction: Corrigendum: The genomic landscape of juvenile myelomonocytic leukemia

Author

Stieglitz, Elliot, primary, Taylor-Weiner, Amaro N, additional, Chang, Tiffany Y, additional, Gelston, Laura C, additional, Wang, Yong-Dong, additional, Mazor, Tali, additional, Esquivel, Emilio, additional, Yu, Ariel, additional, Seepo, Sara, additional, Olsen, Scott R, additional, Rosenberg, Mara, additional, Archambeault, Sophie L, additional, Abusin, Ghada, additional, Beckman, Kyle, additional, Brown, Patrick A, additional, Briones, Michael, additional, Carcamo, Benjamin, additional, Cooper, Todd, additional, Dahl, Gary V, additional, Emanuel, Peter D, additional, Fluchel, Mark N, additional, Goyal, Rakesh K, additional, Hayashi, Robert J, additional, Hitzler, Johann, additional, Hugge, Christopher, additional, Liu, Y Lucy, additional, Messinger, Yoav H, additional, Mahoney, Donald H, additional, Monteleone, Philip, additional, Nemecek, Eneida R, additional, Roehrs, Philip A, additional, Schore, Reuven J, additional, Stine, Kimo C, additional, Takemoto, Clifford M, additional, Toretsky, Jeffrey A, additional, Costello, Joseph F, additional, Olshen, Adam B, additional, Stewart, Chip, additional, Li, Yongjin, additional, Ma, Jing, additional, Gerbing, Robert B, additional, Alonzo, Todd A, additional, Getz, Gad, additional, Gruber, Tanja A, additional, Golub, Todd R, additional, Stegmaier, Kimberly, additional, and Loh, Mignon L, additional

Published
2016
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22. The genomic landscape of juvenile myelomonocytic leukemia

Author

Stieglitz, Elliot, primary, Taylor-Weiner, Amaro N, additional, Chang, Tiffany Y, additional, Gelston, Laura C, additional, Wang, Yong-Dong, additional, Mazor, Tali, additional, Esquivel, Emilio, additional, Yu, Ariel, additional, Seepo, Sara, additional, Olsen, Scott R, additional, Rosenberg, Mara, additional, Archambeault, Sophie L, additional, Abusin, Ghada, additional, Beckman, Kyle, additional, Brown, Patrick A, additional, Briones, Michael, additional, Carcamo, Benjamin, additional, Cooper, Todd, additional, Dahl, Gary V, additional, Emanuel, Peter D, additional, Fluchel, Mark N, additional, Goyal, Rakesh K, additional, Hayashi, Robert J, additional, Hitzler, Johann, additional, Hugge, Christopher, additional, Liu, Y Lucy, additional, Messinger, Yoav H, additional, Mahoney, Donald H, additional, Monteleone, Philip, additional, Nemecek, Eneida R, additional, Roehrs, Philip A, additional, Schore, Reuven J, additional, Stine, Kimo C, additional, Takemoto, Clifford M, additional, Toretsky, Jeffrey A, additional, Costello, Joseph F, additional, Olshen, Adam B, additional, Stewart, Chip, additional, Li, Yongjin, additional, Ma, Jing, additional, Gerbing, Robert B, additional, Alonzo, Todd A, additional, Getz, Gad, additional, Gruber, Tanja A, additional, Golub, Todd R, additional, Stegmaier, Kimberly, additional, and Loh, Mignon L, additional

Published
2015
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24. Dissecting the Heterogeneity of Macrophage Activation Syndrome Complicating Systemic Juvenile Idiopathic Arthritis

Author

Minoia, Francesca, primary, Davì, Sergio, additional, Horne, AnnaCarin, additional, Bovis, Francesca, additional, Demirkaya, Erkan, additional, Akikusa, Jonathan, additional, Ayaz, Nuray A., additional, Al-Mayouf, Sulaiman M., additional, Barone, Patrizia, additional, Bica, Bianca, additional, Bolt, Isabel, additional, Breda, Luciana, additional, De Cunto, Carmen, additional, Enciso, Sandra, additional, Gallizzi, Romina, additional, Griffin, Thomas, additional, Hennon, Teresa, additional, Horneff, Gerd, additional, Jeng, Michael, additional, Kapovic, Ageza M., additional, Lipton, Jeffrey M., additional, Magni Manzoni, Silvia, additional, Rumba-Rozenfelde, Ingrida, additional, Magalhaes, Claudia Saad, additional, Sewairi, Wafaa M., additional, Stine, Kimo C., additional, Vougiouka, Olga, additional, Weaver, Lehn K., additional, Davidsone, Zane, additional, De Inocencio, Jaime, additional, Ioseliani, Maka, additional, Lattanzi, Bianca, additional, Tezer, Hasan, additional, Buoncompagni, Antonella, additional, Picco, Paolo, additional, Ruperto, Nicolino, additional, Martini, Alberto, additional, Cron, Randy Q., additional, and Ravelli, Angelo, additional

Published
2015
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25. Dissecting the heterogeneity of macrophage activation syndrome

Author

Davì, Sergio, primary, Minoia, Francesca, additional, Horne, AnnaCarin, additional, Bovis, Francesca, additional, Demirkaya, Erkan, additional, Akikusa, Jonathan, additional, Ayaz, Nuray Aktay, additional, Barone, Patrizia, additional, Bica, Bianca, additional, Bolt, Isabel, additional, Breda, Luciana, additional, Davidsone, Zane, additional, De Cunto, Carmen, additional, De Inocencio, Jaime, additional, Enciso, Sandra, additional, Gallizzi, Romina, additional, Griffin, Thomas, additional, Hennon, Teresa, additional, Horneff, Gerd, additional, Ioseliani, Maka, additional, Jeng, Michael, additional, Kapovic, Agneza Marja, additional, Lattanzi, Bianca, additional, Lipton, Jeffrey M, additional, Magni-Manzoni, Silvia, additional, Nassif, Clarissa, additional, Rumba, Ingrida, additional, Magalhaes, Claudia Saad, additional, Al-Mayouf, Sulaiman, additional, Sewairi, Wafaa Mohammed, additional, Stine, Kimo C, additional, Vougiouka, Olga, additional, Weaver, Lehn, additional, Zletni, Mabruka Ahmed, additional, Ruperto, Nicola, additional, Martini, Alberto, additional, Cron, Randy Q, additional, and Ravelli, Angelo, additional

Published
2014
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27. Cellular anti-GP120 cytolytic reactivities in HIV-1 seropositive individuals

Author

Weinhold, Kent J., Matthews, Thomas J., Ahearne, Paul M., Langlois, Alphonse J., Lyerly, H. Kim, Tyler, Douglas S., Stine, Kimo C., Bolognesi, Dani P., and Durack, David T.

Subjects
AIDS virus carriers -- Research, Cell-mediated cytotoxicity -- Research, HIV (Viruses) -- Research, Glycoproteins -- Research
Published
1988

28. Cisplatin inhibits bone healing during distraction osteogenesis

Author

Stine, Kimo C., primary, Wahl, Elizabeth C., additional, Liu, Lichu, additional, Skinner, Robert A., additional, VanderSchilden, Jacquelyn, additional, Bunn, Robert C., additional, Montgomery, Corey O., additional, Suva, Larry J., additional, Aronson, James, additional, Becton, David L., additional, Nicholas, Richard W., additional, Swearingen, Christopher J., additional, and Lumpkin, Charles K., additional

Published
2013
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36. Cisplatin inhibits bone healing during distraction osteogenesis.

Author

Stine, Kimo C., Wahl, Elizabeth C., Liu, Lichu, Skinner, Robert A., VanderSchilden, Jacquelyn, Bunn, Robert C., Montgomery, Corey O., Suva, Larry J., Aronson, James, Becton, David L., Nicholas, Richard W., Swearingen, Christopher J., and Lumpkin, Charles K.

Subjects
*CISPLATIN, *BONE growth, *WOUND healing, *OSTEOSARCOMA, *BONE tumors, *HOMOGRAFTS
Abstract

ABSTRACT Osteosarcoma (OS) is the most common malignant bone tumor affecting children and adolescents. Many patients are treated with a combination of chemotherapy, resection, and limb salvage protocols. Surgical reconstructions after tumor resection include structural allografts, non-cemented endoprostheses, and distraction osteogenesis (DO), which require direct bone formation. Although cisplatin (CDP) is extensively used for OS chemotherapy, the effects on bone regeneration are not well studied. The effects of CDP on direct bone formation in DO were compared using two dosing regimens and both C57BL/6 (B6) and tumor necrosis factor receptor 1 knockout (TNFR1KO) mice, as CDP toxicity is associated with elevated TNF levels. Detailed evaluation of the five-dose CDP regimen (2 mg/kg/day), demonstrated significant decreases in new bone formation in the DO gaps of CDP treated versus vehicle treated mice ( p < 0.001). Further, no significant inhibitory effects from the five-dose CDP regimen were observed in TNFR1KO mice. The two-dose regimen significantly inhibited new bone formation in B6 mice. These results demonstrate that CDP has profound short term negative effects on the process of bone repair in DO. These data provide the mechanistic basis for modeling peri-operative chemotherapy doses and schedules and may provide new opportunities to identify molecules that spare normal cells from the inhibitory effects of CDP. © 2013 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 32:464-470, 2014. [ABSTRACT FROM AUTHOR]

Published
2014
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39. Impact of Dietary Yogurt on Immune Function*

Author

Gary Wheeler, J., primary, Bogle, Margaret L., additional, Shema, Sarah J., additional, Annette Shirrell, M., additional, Stine, Kimo C., additional, Pittler, Arlyn J., additional, Wesley Burks, A., additional, and Helm, Ricki M., additional

Published
1997
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43. Randomized use of cyclosporin A (CsA) to modulate P-glycoprotein in children with AML in remission: Pediatric Oncology Group Study 9421

Author

Becton, David, Dahl, Gary V., Ravindranath, Yaddanapudi, Chang, Myron N., Behm, Fred G., Raimondi, Susana C., Head, David R., Stine, Kimo C., Lacayo, Norman J., Sikic, Branimir Ivan, Arceci, Robert J., and Weinstein, Howard

Abstract

Relapse is a major obstacle in the cure of acute myeloid leukemia (AML). The Pediatric Oncology Group AML Study 9421 tested 2 different strategies to improve event-free survival (EFS) and overall survival (OS). Patients were randomized to receive standard-dose DAT (daunorubicin, cytarabine, and thioguanine) or high-dose DAT during induction. To interfere with P-glycoprotein (P-gp)-dependent drug efflux, the second randomization tested the benefit of cyclosporine (CsA) added to consolidation chemotherapy. Of the 282 children randomly assigned to receive standard DAT induction, 248 (87.9%) achieved remission compared to 253 (91%) of the 278 receiving high-dose DAT (P= ns). Children with HLA-identical sibling donors who achieved a complete remission received an allogeneic bone marrow transplant as consolidation. For the 83 patients receiving a matched related donor bone marrow transplantation (BMT), the 3-year disease-free survival (DFS) is 67%. Of the 418 children who achieved remission and went on to consolidation with and without CsA, the DFS was 40.6% and 33.9%, respectively (P= .24). Overexpression of P-gp was infrequent (14%) in this pediatric population. In this study, intensifying induction with high-dose DAT and the addition of CsA to consolidation chemotherapy did not prolong the durations of remission or improve overall survival for children with AML.

Published
2006
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45. Spontaneous Remission of Cryptosporidiosis in a Child with Acute Lymphocytic Leukemia.

Author

Stine, Kimo C., Harris, Jo-Ann S., Lindsey, Norma J., and Cho, Cheng T.

Subjects
CRYPTOSPORIDIOSIS, LYMPHOCYTIC leukemia, LEUKEMIA in children, JUVENILE diseases, PEDIATRICS
Abstract

Cryptosporidiosis has been documented in pediatric patients with various forms of congenital and acquired immunodeficiency. This is a report of cryptosporidiosis in a child with acute lymphocytic leukemia. Cryptosporidiosis. an uncommon cause of diarrhea, may produce severe diarrhea in children with acute lymphocytic leukemia. [ABSTRACT FROM AUTHOR]

Published
1985
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50. Corrigendum: The genomic landscape of juvenile myelomonocytic leukemia

Author

Stieglitz, Elliot, Taylor-Weiner, Amaro N, Chang, Tiffany Y, Gelston, Laura C, Wang, Yong-Dong, Mazor, Tali, Esquivel, Emilio, Yu, Ariel, Seepo, Sara, Olsen, Scott R, Rosenberg, Mara, Archambeault, Sophie L, Abusin, Ghada, Beckman, Kyle, Brown, Patrick A, Briones, Michael, Carcamo, Benjamin, Cooper, Todd, Dahl, Gary V, Emanuel, Peter D, Fluchel, Mark N, Goyal, Rakesh K, Hayashi, Robert J, Hitzler, Johann, Hugge, Christopher, Liu, Y Lucy, Messinger, Yoav H, Mahoney, Donald H, Monteleone, Philip, Nemecek, Eneida R, Roehrs, Philip A, Schore, Reuven J, Stine, Kimo C, Takemoto, Clifford M, Toretsky, Jeffrey A, Costello, Joseph F, Olshen, Adam B, Stewart, Chip, Li, Yongjin, Ma, Jing, Gerbing, Robert B, Alonzo, Todd A, Getz, Gad, Gruber, Tanja A, Golub, Todd R, Stegmaier, Kimberly, and Loh, Mignon L

Published
2016
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