mitomycin and Anemia, Fanconi studies

Mitomycin: An antineoplastic antibiotic produced by Streptomyces caespitosus. It is one of the bi- or tri-functional ALKYLATING AGENTS causing cross-linking of DNA and inhibition of DNA synthesis.
mitomycin : A family of aziridine-containing natural products isolated from Streptomyces caespitosus or Streptomyces lavendulae.

Research Excerpts

Excerpt	Relevance	Reference
" DNA interstrand cross-links (ICLs), one of the most severe forms of DNA damage caused by anticancer drugs such as cisplatin and mitomycin C (MMC), activates the Fanconi anemia (FA)/BRCA DNA repair pathway."	7.79	Ouabain, a cardiac glycoside, inhibits the Fanconi anemia/BRCA pathway activated by DNA interstrand cross-linking agents. ( Hwang, M; Hwang, SK; Jun, DW; Kim, HJ; Kim, S; Lee, CH, 2013)
"Lymphocytes of Fanconi anemia (FA) show an increased sensitivity to the alkylating agents such as mitomycin C (MMC), but their responses to gamma-irradiation is controversial."	7.75	DNA damage in leukocytes from Fanconi anemia (FA) patients and heterozygotes induced by mitomycin C and ionizing radiation as assessed by the comet and comet-FISH assay. ( Mohseni Meybodi, A; Mozdarani, H, 2009)
"It is well known that Fanconi anemia (FA) patients show a hypersensitivity to the effect of cross-linking agents such as mitomycin C (MMC) and diepoxybutane (DEB), while the sensitivity of these patients to ionizing radiation is still controversial."	7.74	Cytogenetic sensitivity of G0 lymphocytes of Fanconi anemia patients and obligate carriers to mitomycin C and ionizing radiation. ( Mohseni-Meybodi, A; Mozdarani, H; Vosough, P, 2007)
"This study was conducted to differentiate between Fanconi anemia (FA) and "idiopathic" aplastic anemia on the basis of induced chromosomal breakage study with mitomycin C (MMC)."	7.72	Differentiation of Fanconi anemia from idiopathic aplastic anemia by induced chromosomal breakage study using mitomycin-C (MMC). ( Choudhry, VP; Kucheria, K; Talwar, R, 2004)
"Fanconi anemia (FA) is a genetic disorder defined by cellular hypersensitivity to DNA cross-linking agents, such as mitomycin C (MMC)."	7.70	Assessment of mitomycin C sensitivity in Fanconi anemia complementation group C gene (Fac) knock-out mouse cells. ( Demuth, I; Digweed, M; Liu, JM; Otsuki, T; Wang, J, 1998)
"A striking feature of Fanconi anemia (FA) cells is their hypersensitivity towards crosslinking agents such as mitomycin C (MMC)."	7.69	Apoptosis is not involved in the hypersensitivity of Fanconi anemia cells to mitomycin C. ( Müller, H; Rey, JP; Scott, R, 1994)
"Fanconi anemia (FA) is a clinically and genetically heterogenous disease that is usually diagnosed on the basis of chromosomal instability reflecting the hypersensitivity towards the DNA cross-linking agents diepoxybutane (DEB) and/or mitomycin C."	7.69	Comparative evaluation of diepoxybutane sensitivity and cell cycle blockage in the diagnosis of Fanconi anemia. ( Friedl, R; Hentze, S; Hoehn, H; Schindler, D; Schroeder-Kurth, T; Seyschab, H; Sun, Y, 1995)
"The authors studied the effect of mitomycin C (MMC) and bromodeoxyuridine (BrdU) on the induction of chromosome aberrations on lymphocytes of four patients with Fanconi anemia (FA) and of one normal subject."	7.68	Effect of mitomycin C and bromodeoxyuridine on Fanconi anemia lymphocytes. ( Carnevale, A; Frias, S; Mendoza, S; Molina, B, 1991)
"Crosslink repair of mitomycin C-induced interstrand crosslinks was studied in exponentially growing and confluent normal human, transformed W138CT-1, Fanconi's anemia (FA) and xeroderma pigmentosum (XP) group-A fibroblasts by the assay methods of alkaline sucrose centrifugation, hydroxyapatite column chromatography and S1-nuclease digestion."	7.66	Defective repair of mitomycin C crosslinks in Fanconi's anemia and loss in confluent normal human and xeroderma pigmentosum cells. ( Fujiwara, Y, 1982)
"Hydroxyurea (HU) is an agent that induces replicative stress by inhibiting ribonucleotide reductase (RNR), which synthesizes deoxyribonucleotide triphosphates (dNTPs) necessary for DNA replication and repair."	5.42	Hydroxyurea induces chromosomal damage in G2 and enhances the clastogenic effect of mitomycin C in Fanconi anemia cells. ( Altamirano-Lozano, M; Carnevale, A; Frias, S; Gómez, L; Marchetti, F; Molina, B; Ortiz, R; Ramos, S; Torres, L, 2015)
"Chromosomal breakage was induced by MMC 0 ng/ml, 40 ng/ml, and 80 ng/ml."	5.39	[Correlation of single-cell gel electrophoresis and mitomycin C-induced chromosomal breakage for chromosomal instabiligy in children with Fanconi anemia]. ( Cai, XJ; Chen, XJ; Chen, YM; Guo, Y; Liu, F; Liu, Q; Liu, TF; Liu, XM; Ruan, M; Wang, SC; Yang, WY; Zhang, JY; Zhang, L; Zhu, XF; Zou, Y, 2013)
"Induced chromosomal breakage study was successful in 171 out of 205 aplastic anemia (AA) patients."	5.39	Differentiation of Fanconi anemia and aplastic anemia using mitomycin C test in Tunisia. ( Abdelhak, S; Abidli, N; Aissaoui, L; Amouri, A; Ayed, W; Bejaoui, M; Ben Halim, N; Ben Othmane, T; Ben Romdhane, N; Ben Youssef, Y; Chemkhi, I; Elloumi, M; Guermani, H; Hadiji, S; Hentati, S; Kammoun, L; Kilani, O; Mellouli, F; Talmoudi, F; Torjmane, L, 2013)
"Chromosomal aberrations were first measured after exposure to mitomicyn C (MMC) or hydroxyurea (HU)."	5.35	Differential expression of TP53 associated genes in Fanconi anemia cells after mitomycin C and hydroxyurea treatment. ( Acuña, H; Coleman, MA; Frias, S; Gómez, L; Hinz, JM; Jones, IM; Martinez, A; Molina, B, 2008)
"Curcumin was previously identified as a weak inhibitor of FANCD2-Ub."	5.35	Monoketone analogs of curcumin, a new class of Fanconi anemia pathway inhibitors. ( Hiddingh, S; Hoatlin, ME; Landais, I; McCarroll, M; Snyder, JP; Sun, A; Turker, MS; Yang, C, 2009)
"Seckel syndrome is a rare autosomal recessive disorder."	5.30	Normal expression of the Fanconi anemia proteins FAA and FAC and sensitivity to mitomycin C in two patients with Seckel syndrome. ( Abou-Zahr, F; Bacino, C; Bejjani, B; Kruyt, FA; Kurg, R; Shapira, SK; Youssoufian, H, 1999)
"However, spontaneous chromosomal breakage was not affected."	5.30	Overexpression of thioredoxin in Fanconi anemia fibroblasts prevents the cytotoxic and DNA damaging effect of mitomycin C and diepoxybutane. ( Hirsch-Kauffmann, M; Meisslitzer, C; Ruppitsch, W; Schweiger, M, 1998)
" Chromosomal breakage was induced by (i) Diepoxybutane 0."	5.13	Correlation of thyroid and growth hormones to chromosomal instability in Egyptian Fanconi anemia patients. ( Al-Haggar, M; Al-Morsy, Z; Chalaby, N; Mesbah, A; Ragab, A; Yahia, S, 2008)
"Activation of the Fanconi anemia (FA) pathway after treatment with mitomycin C (MMC) is essential for preventing chromosome translocations termed "radials."	4.31	Fanconi anemia-associated chromosomal radial formation is dependent on POLθ-mediated alternative end joining. ( Bielinsky, AK; Hendrickson, EA; Kram, RE; Lin, K; Myers, CL; Rogers, CB; Sobeck, A, 2023)
" The diagnostic feature of FA is increased chromosomal breakage in blood lymphocytes cultured with diepoxybutane or mitomycin C."	3.80	Comparison of chromosome breakage in non-mosaic and mosaic patients with Fanconi anemia, relatives, and patients with other inherited bone marrow failure syndromes. ( Alter, BP; Fargo, JH; Giri, N; Olson, SB; Rochowski, A; Savage, SA, 2014)
" Using a newly identified small-molecule inhibitor of WRN helicase (NSC 617145), we investigated the role of WRN in the interstrand cross-link (ICL) response in cells derived from patients with Fanconi anemia, a hereditary disorder characterized by bone marrow failure and cancer."	3.79	Werner syndrome helicase has a critical role in DNA damage responses in the absence of a functional fanconi anemia pathway. ( Aggarwal, M; Banerjee, T; Brosh, RM; Iannascoli, C; Pichierri, P; Shoemaker, RH; Sommers, JA, 2013)
" Specifically, pharmacological inhibition of WRN helicase activity in human cells defective in the Fanconi anemia (FA) pathway of interstrand cross-link (ICL) repair are sensitized to the DNA cross-linking agent and chemotherapy drug mitomycin C (MMC) by the WRN helicase inhibitor NSC 617145."	3.79	Targeting an Achilles' heel of cancer with a WRN helicase inhibitor. ( Aggarwal, M; Banerjee, T; Brosh, RM; Sommers, JA, 2013)
" DNA interstrand cross-links (ICLs), one of the most severe forms of DNA damage caused by anticancer drugs such as cisplatin and mitomycin C (MMC), activates the Fanconi anemia (FA)/BRCA DNA repair pathway."	3.79	Ouabain, a cardiac glycoside, inhibits the Fanconi anemia/BRCA pathway activated by DNA interstrand cross-linking agents. ( Hwang, M; Hwang, SK; Jun, DW; Kim, HJ; Kim, S; Lee, CH, 2013)
"Investigation of mitomycin C-induced chromosomal breakage was carried out in 163 pediatric patients with AA and siblings of the cases where diagnosis of FA was confirmed."	3.79	Cytogenetic assessment of Fanconi anemia in children with aplastic anemia in Tunisia. ( Abdelhak, S; Aissaoui, L; Amouri, A; Bejaoui, M; Benhalim, N; Dellagi, K; Hdiji, S; Kammoun, L; Lakhal, A; Meddeb, M; Mellouli, F; Othmen, TB; Ouederni, M; Talmoudi, F; Torjemane, L, 2013)
"Lymphocytes of Fanconi anemia (FA) show an increased sensitivity to the alkylating agents such as mitomycin C (MMC), but their responses to gamma-irradiation is controversial."	3.75	DNA damage in leukocytes from Fanconi anemia (FA) patients and heterozygotes induced by mitomycin C and ionizing radiation as assessed by the comet and comet-FISH assay. ( Mohseni Meybodi, A; Mozdarani, H, 2009)
"We evaluated Fanconi anemia diagnosis on blood lymphocytes and skin fibroblasts from a cohort of 87 bone marrow failure patients (55 children and 32 adults) with no obvious full clinical picture of Fanconi anemia, by performing a combination of chromosomal breakage tests, FANCD2-monoubiquitination assays, a new flow cytometry-based mitomycin C sensitivity test in fibroblasts, and, when Fanconi anemia was diagnosed, complementation group and mutation analyses."	3.75	Diagnosis of Fanconi anemia in patients with bone marrow failure. ( Baruchel, A; Brethon, B; Cassinat, B; Chamousset, D; de Villartay, JP; Gluckman, E; Larghero, J; Le Roux, G; Leblanc, T; Pinto, FO; Socié, G; Soulier, J; Stoppa-Lyonnet, D, 2009)
"It is well known that Fanconi anemia (FA) patients show a hypersensitivity to the effect of cross-linking agents such as mitomycin C (MMC) and diepoxybutane (DEB), while the sensitivity of these patients to ionizing radiation is still controversial."	3.74	Cytogenetic sensitivity of G0 lymphocytes of Fanconi anemia patients and obligate carriers to mitomycin C and ionizing radiation. ( Mohseni-Meybodi, A; Mozdarani, H; Vosough, P, 2007)
"Fanconi anemia (FA) is an autosomal recessive disorder characterized by aplastic anemia, cancer susceptibility, and cellular sensitivity to mitomycin C."	3.73	The WD40 repeats of FANCL are required for Fanconi anemia core complex assembly. ( D'Andrea, AD; Gurtan, AM; Stuckert, P, 2006)
"Fanconi anemia (FA) results from mutations in a group of genes whose products, including BRCA2 and BACH1/BRIP1, are known to function in one common pathway (the FA-BRCA pathway) to guard genome integrity, especially when challenged by DNA crosslinking agents, such as Cisplatin and mitomycin C (MMC)."	3.73	Altered expression of FANCL confers mitomycin C sensitivity in Calu-6 lung cancer cells. ( Couch, FJ; Fei, P; Lin, CJ; Wang, X; Zhang, J, 2006)
" Moreover, in human cells exposed to mitomycin C, short interfering RNA-mediated knock-down of BRIP1 leads to a substantial increase in chromosome aberrations, a characteristic phenotype of cells derived from individuals with Fanconi anemia."	3.73	The BRIP1 helicase functions independently of BRCA1 in the Fanconi anemia pathway for DNA crosslink repair. ( Bridge, WL; Franklin, RJ; Hiom, K; Vandenberg, CJ, 2005)
" Mitomycin C (MMC) was used as a DNA cross-linker to study chromosomal breakage."	3.73	Cytogenetic investigation in Iranian patients suspected with Fanconi anemia. ( Hormozian, F; Mahjoubi, F; Manoochehri, F; Mortezapour, F; Nasiri, F; Rahnama, M; Razazian, F; Seyedmortaz, L; Soleymani, S; Tootian, S; Zamanian, M, 2006)
"The human FANCG/XRCC9 gene, which is defective in Fanconi anemia complementation group G (FA-G) cells, was first cloned by genetic complementation of the mitomycin C (MMC) sensitivity of CHO mutant UV40."	3.72	Characterization of the hamster FancG/Xrcc9 gene and mutations in CHO UV40 and NM3. ( Christian, AT; George, JW; Jones, NJ; Lamerdin, JE; Souza, B; Thompson, LH; Yamada, NA, 2004)
"This study was conducted to differentiate between Fanconi anemia (FA) and "idiopathic" aplastic anemia on the basis of induced chromosomal breakage study with mitomycin C (MMC)."	3.72	Differentiation of Fanconi anemia from idiopathic aplastic anemia by induced chromosomal breakage study using mitomycin-C (MMC). ( Choudhry, VP; Kucheria, K; Talwar, R, 2004)
"Fanconi anemia (FA) cells are characteristically hypersensitive to bifunctional alkylating agents, notably mitomycin C (MMC), causing increased programmed cell death (PCD)."	3.72	Fanconi's anemia cell lines show distinct mechanisms of cell death in response to mitomycin C or agonistic anti-Fas antibodies. ( Clarke, AA; Gibson, FM; Myatt, N; Rutherford, TR; Scott, J, 2004)
"Fanconi anemia (FA) is a human autosomal recessive cancer susceptibility disorder characterized by cellular sensitivity to mitomycin C and ionizing radiation."	3.71	Targeted disruption of the murine Fanconi anemia gene, Fancg/Xrcc9. ( D'Andrea, AD; Hays, T; Kuang, Y; Lu, N; Montes De Oca, R; Moreau, L; Seed, B; Yang, Y, 2001)
"Fanconi anemia (FA) is a human autosomal recessive cancer susceptibility disorder characterized by cellular sensitivity to mitomycin C and ionizing radiation."	3.71	Interaction of the Fanconi anemia proteins and BRCA1 in a common pathway. ( D'Andrea, AD; Ganesan, S; Garcia-Higuera, I; Grompe, M; Hejna, J; Meyn, MS; Taniguchi, T; Timmers, C, 2001)
"Cells harvested from Fanconi anemia (FA) patients show an increased hypersensitivity to the multifunctional DNA damaging agent mitomycin C (MMC), which causes cross-links in DNA as well as 7,8-dihydro-8-oxoguanine (8-oxoG) adducts indicative of escalated oxidative DNA damage."	3.71	The Drosophila S3 multifunctional DNA repair/ribosomal protein protects Fanconi anemia cells against oxidative DNA damaging agents. ( Clapp, DW; Deutsch, WA; Freie, B; Kelley, MR; New, S; Tritt, R; Xu, Y, 2001)
" The current diagnostic test for FA consists of cytogenetic quantitation of chromosomal breakage in response to diepoxybutane (DEB) or mitomycin C (MMC)."	3.71	A novel diagnostic screen for defects in the Fanconi anemia pathway. ( D'Andrea, AD; Haining, N; Montes de Oca, R; Moreau, LA; Nathan, DG; Shimamura, A; Svenson, JL, 2002)
"Fanconi anemia is a hereditary cancer susceptibility disorder characterized at the cellular level by spontaneous chromosomal instability and specific hypersensitivity to DNA cross-linking agents such as mitomycin C."	3.71	Impaired DNA damage-induced nuclear Rad51 foci formation uniquely characterizes Fanconi anemia group D1. ( Artwert, F; Godthelp, BC; Joenje, H; Zdzienicka, MZ, 2002)
"Fanconi anemia (FA) is a human autosomal-recessive cancer susceptibility disorder characterized by multiple congenital abnormalities, progressive bone marrow failure, and cellular sensitivity to mitomycin C (MMC)."	3.71	Function of the Fanconi anemia pathway in Fanconi anemia complementation group F and D1 cells. ( D'Andrea, AD; Grompe, M; Nakanishi, K; Siddique, MA; Taniguchi, T, 2001)
"Fanconi anemia (FA) is a human autosomal disorder characterized by cancer susceptibility and cellular sensitivity to DNA crosslinking agents such as mitomycin C and diepoxybutane."	3.71	The Chinese hamster FANCG/XRCC9 mutant NM3 fails to express the monoubiquitinated form of the FANCD2 protein, is hypersensitive to a range of DNA damaging agents and exhibits a normal level of spontaneous sister chromatid exchange. ( Bryant, PE; D'Andrea, AD; Johnson, MA; Jones, NJ; May, S; Meyn, RE; Stuckert, AP; Trueman, KL; Wilson, JB, 2001)
"Fanconi anemia (FA) is a rare autosomal recessive cancer susceptibility disorder characterized by cellular hypersensitivity to mitomycin C (MMC)."	3.71	Biallelic inactivation of BRCA2 in Fanconi anemia. ( Cox, B; D'Andrea, AD; De Die-Smulders, C; Fox, EA; Grompe, M; Howlett, NG; Ikeda, H; Joenje, H; Olson, S; Pals, G; Persky, N; Taniguchi, T; Waisfisz, Q, 2002)
"Fanconi anemia (FA) is a genetic disorder defined by cellular hypersensitivity to DNA cross-linking agents, such as mitomycin C (MMC)."	3.70	Assessment of mitomycin C sensitivity in Fanconi anemia complementation group C gene (Fac) knock-out mouse cells. ( Demuth, I; Digweed, M; Liu, JM; Otsuki, T; Wang, J, 1998)
"Fanconi anemia (FA) cells are hypersensitive to cytotoxicity, cell cycle arrest, and chromosomal aberrations induced by DNA cross-linking agents, such as mitomycin C (MMC) and nitrogen mustard (HN2)."	3.69	The Fanconi anemia complementation group C protein corrects DNA interstrand cross-link-specific apoptosis in HSC536N cells. ( Ashmun, RA; Brent, TP; Howell, SR; Marathi, UK, 1996)
"Fanconi anemia (FA) cells, complementation group D, which had been transfected with mouse genomic DNA were partially corrected for their mitomycin C (MMC) hypersensitivity."	3.69	Identification and chromosomal localization of a DNA fragment implicated in the partial correction of the Fanconi anemia group D cellular defect. ( Diatloff-Zito, C; Duchaud, E; Fraser, D; Moustacchi, E; Viegas-Pequignot, E, 1994)
"Fanconi anemia (FA) is a clinically and genetically heterogenous disease that is usually diagnosed on the basis of chromosomal instability reflecting the hypersensitivity towards the DNA cross-linking agents diepoxybutane (DEB) and/or mitomycin C."	3.69	Comparative evaluation of diepoxybutane sensitivity and cell cycle blockage in the diagnosis of Fanconi anemia. ( Friedl, R; Hentze, S; Hoehn, H; Schindler, D; Schroeder-Kurth, T; Seyschab, H; Sun, Y, 1995)
"A striking feature of Fanconi anemia (FA) cells is their hypersensitivity towards crosslinking agents such as mitomycin C (MMC)."	3.69	Apoptosis is not involved in the hypersensitivity of Fanconi anemia cells to mitomycin C. ( Müller, H; Rey, JP; Scott, R, 1994)
"Cells from Fanconi anemia (FA) patients have defective DNA repair and are hypersensitive to DNA crosslinking agents such as mitomycin C (MMC)."	3.69	Fanconi anemia cells have a normal gene structure for topoisomerase I. ( Grompe, M; Jakobs, PM; Moses, RE; Neeley, TL; Saito, H, 1994)
"Cells from patients with Fanconi anemia (FA) frequently show an increased sensitivity to DNA crosslinking agents such as mitomycin C (MMC)."	3.68	Hypersensitivity to oxygen is a uniform and secondary defect in Fanconi anemia cells. ( Hammond, AT; Moses, RE; Saito, H, 1993)
"The correction of chromosomal hypersensitivity to mitomycin C (MMC) in Fanconi anemia (FA) human lymphoblasts is observed by growth in a medium conditioned by normal human cells."	3.68	Abnormal lymphokine production: a novel feature of the genetic disease Fanconi anemia. I. Involvement of interleukin-6. ( Moustacchi, E; Rosselli, F; Sanceau, J; Wietzerbin, J, 1992)
"The authors studied the effect of mitomycin C (MMC) and bromodeoxyuridine (BrdU) on the induction of chromosome aberrations on lymphocytes of four patients with Fanconi anemia (FA) and of one normal subject."	3.68	Effect of mitomycin C and bromodeoxyuridine on Fanconi anemia lymphocytes. ( Carnevale, A; Frias, S; Mendoza, S; Molina, B, 1991)
"V-H4, a mitomycin C (MMC)-sensitive Chinese hamster cell mutant, is phenotypically very similar to Fanconi anemia (FA) cells."	3.68	The Chinese hamster cell mutant V-H4 is homologous to Fanconi anemia (complementation group A). ( Arwert, F; Rooimans, MA; Simons, JW; Westerveld, A; Zdzienicka, MZ, 1991)
"By comparing fibroblast strains derived from individuals exhibiting chromosome instability and/or mutagen hypersensitivity (Cockayne syndrome, ataxia telangiectasia, and Fanconi anemia) with strains derived from healthy donors, the fibroblast micronucleus assay has been established as a reproducible measure of the genotypic variation in spontaneous or mitomycin C (MMC)-induced chromosomal instability."	3.67	Micronucleus assay in human fibroblasts: a measure of spontaneous chromosomal instability and mutagen hypersensitivity. ( Dimnik, LS; Greentree, CL; Hennig, UG; Hoar, DI; Rudd, NL, 1988)
"Crosslink repair of mitomycin C-induced interstrand crosslinks was studied in exponentially growing and confluent normal human, transformed W138CT-1, Fanconi's anemia (FA) and xeroderma pigmentosum (XP) group-A fibroblasts by the assay methods of alkaline sucrose centrifugation, hydroxyapatite column chromatography and S1-nuclease digestion."	3.66	Defective repair of mitomycin C crosslinks in Fanconi's anemia and loss in confluent normal human and xeroderma pigmentosum cells. ( Fujiwara, Y, 1982)
" We screened cancer patients' tumors for FA functional defects then aimed to establish the safety/feasibility of administering PARP inhibitors as monotherapy and combined with a DNA-breaking agent."	2.82	Veliparib Alone or in Combination with Mitomycin C in Patients with Solid Tumors With Functional Deficiency in Homologous Recombination Repair. ( Bekaii-Saab, T; Chen, A; Duan, W; Ji, J; Lustberg, M; Marshall, J; Rose, J; Schaaf, LJ; Shilo, K; Thurmond, J; Timmers, C; Villalona-Calero, MA; Westman, JA; Xiaobai, L; Zhao, W, 2016)
"Oral squamous cell carcinoma (OSCC) may develop in young adults."	1.43	Sensitivity to chromosomal breakage as risk factor in young adults with oral squamous cell carcinoma. ( Braakhuis, BJ; Brakenhoff, RH; Flach, GB; Graveland, AP; Joenje, H; Leemans, CR; Nieuwint, AW; Oostra, AB, 2016)
"Hydroxyurea (HU) is an agent that induces replicative stress by inhibiting ribonucleotide reductase (RNR), which synthesizes deoxyribonucleotide triphosphates (dNTPs) necessary for DNA replication and repair."	1.42	Hydroxyurea induces chromosomal damage in G2 and enhances the clastogenic effect of mitomycin C in Fanconi anemia cells. ( Altamirano-Lozano, M; Carnevale, A; Frias, S; Gómez, L; Marchetti, F; Molina, B; Ortiz, R; Ramos, S; Torres, L, 2015)
"Chromosomal breakage was induced by MMC 0 ng/ml, 40 ng/ml, and 80 ng/ml."	1.39	[Correlation of single-cell gel electrophoresis and mitomycin C-induced chromosomal breakage for chromosomal instabiligy in children with Fanconi anemia]. ( Cai, XJ; Chen, XJ; Chen, YM; Guo, Y; Liu, F; Liu, Q; Liu, TF; Liu, XM; Ruan, M; Wang, SC; Yang, WY; Zhang, JY; Zhang, L; Zhu, XF; Zou, Y, 2013)
"Induced chromosomal breakage study was successful in 171 out of 205 aplastic anemia (AA) patients."	1.39	Differentiation of Fanconi anemia and aplastic anemia using mitomycin C test in Tunisia. ( Abdelhak, S; Abidli, N; Aissaoui, L; Amouri, A; Ayed, W; Bejaoui, M; Ben Halim, N; Ben Othmane, T; Ben Romdhane, N; Ben Youssef, Y; Chemkhi, I; Elloumi, M; Guermani, H; Hadiji, S; Hentati, S; Kammoun, L; Kilani, O; Mellouli, F; Talmoudi, F; Torjmane, L, 2013)
"Ectopic expression of FAVL in bladder cancer cells as well as normal human cells confer an impaired FA pathway and hypersensitivity to Mitomycin C, similar to those found in FA cells, indicating that FAVL elevation may possess the same tumor promotion potential as an impaired FA pathway harbored in FA cells."	1.38	FAVL impairment of the Fanconi anemia pathway promotes the development of human bladder cancer. ( Dudimah, FD; Fei, P; Panneerselvam, J; Park, HK; Wang, H; Zhang, J; Zhang, P, 2012)
" Thus, appropriately dosed Cy may provide a suitable conditioning regimen for FA patients undergoing HSC gene therapy."	1.38	Cyclophosphamide promotes engraftment of gene-modified cells in a mouse model of Fanconi anemia without causing cytogenetic abnormalities. ( Adair, JE; Beard, BC; Becker, PS; Chien, S; Fang, M; Kiem, HP; Taylor, JA; Trobridge, GD; Wohlfahrt, ME; Zhao, X, 2012)
"The disease Fanconi anemia is a genome instability syndrome characterized by cellular sensitivity to DNA interstrand cross-linking agents, manifest by decreased cellular survival and chromosomal aberrations after such treatment."	1.35	Tip60 is required for DNA interstrand cross-link repair in the Fanconi anemia pathway. ( Al-Dhalimy, M; Hejna, J; Hemphill, A; Hines, J; Holtorf, M; Mathewson, L; Moses, RE; Olson, SB, 2008)
"Chromosomal aberrations were first measured after exposure to mitomicyn C (MMC) or hydroxyurea (HU)."	1.35	Differential expression of TP53 associated genes in Fanconi anemia cells after mitomycin C and hydroxyurea treatment. ( Acuña, H; Coleman, MA; Frias, S; Gómez, L; Hinz, JM; Jones, IM; Martinez, A; Molina, B, 2008)
"Since the Fanconi anemia-breast cancer associated (FANC-BRCA) DNA damage response network plays a crucial role in protecting cells against ICLs, in the present work we tested this hypothesis by exposing cells to AA and monitoring activation of this network."	1.35	Acetaldehyde stimulates FANCD2 monoubiquitination, H2AX phosphorylation, and BRCA1 phosphorylation in human cells in vitro: implications for alcohol-related carcinogenesis. ( Brooks, PJ; Lamerdin, JE; Marietta, C; Thompson, LH, 2009)
"Curcumin was previously identified as a weak inhibitor of FANCD2-Ub."	1.35	Monoketone analogs of curcumin, a new class of Fanconi anemia pathway inhibitors. ( Hiddingh, S; Hoatlin, ME; Landais, I; McCarroll, M; Snyder, JP; Sun, A; Turker, MS; Yang, C, 2009)
"Patients with advanced stage invasive cervical cancer (CC) exhibit highly complex genomic alterations and respond poorly to conventional treatment protocols."	1.32	Promoter hypermethylation of FANCF: disruption of Fanconi Anemia-BRCA pathway in cervical cancer. ( Arias-Pulido, H; Basso, K; Dürst, M; Gissmann, L; Mansukhani, M; Meyer, L; Murty, VV; Nandula, SV; Narayan, G; Pothuri, B; Schneider, A; Sugirtharaj, DD; Vargas, H; Villella, J, 2004)
"N-Ethylmaleimide treatment abolishes multimerization and interaction of FANCA and FANCG in vitro."	1.32	Oxidative stress/damage induces multimerization and interaction of Fanconi anemia proteins. ( Beck, BD; Ciccone, SL; Clapp, DW; Freie, B; Hwang, B; Lee, SH; Park, SJ, 2004)
"Fanconi anemia is characterized by bone marrow failure secondary to stem cell dysfunction."	1.31	Functional correction of fanconi anemia group C hematopoietic cells by the use of a novel lentiviral vector. ( Olsen, JC; Patel, M; Rao, KW; Walsh, CE; Yamada, K, 2001)
"The mitomycin C-treated Fancc(-/-) mouse provides a valuable model to address long-term efficacy of such treatment."	1.31	Short-term granulocyte colony-stimulating factor and erythropoietin treatment enhances hematopoiesis and survival in the mitomycin C-conditioned Fancc(-/-) mouse model, while long-term treatment is ineffective. ( Buchwald, M; Carreau, M; Dick, JE; Gan, OI; Hitzler, JK; Liu, L, 2002)
"However, spontaneous chromosomal breakage was not affected."	1.30	Overexpression of thioredoxin in Fanconi anemia fibroblasts prevents the cytotoxic and DNA damaging effect of mitomycin C and diepoxybutane. ( Hirsch-Kauffmann, M; Meisslitzer, C; Ruppitsch, W; Schweiger, M, 1998)
" Thus, at low doses of MMC, FA-C cells exhibit a unique cyclin B1/cdc2 response that is not observed in wild-type cells treated with an equitoxic high dosage of cross-linker."	1.30	Involvement of the Fanconi's anemia protein FAC in a pathway that signals to the cyclin B/cdc2 kinase. ( Arwert, F; Dijkmans, LM; Joenje, H; Kruyt, FA, 1997)
"Seckel syndrome is a rare autosomal recessive disorder."	1.30	Normal expression of the Fanconi anemia proteins FAA and FAC and sensitivity to mitomycin C in two patients with Seckel syndrome. ( Abou-Zahr, F; Bacino, C; Bejjani, B; Kruyt, FA; Kurg, R; Shapira, SK; Youssoufian, H, 1999)
"Fanconi anemia is a rare autosomal recessive disease characterized by developmental defects of the thumb and radius, childhood onset of pancytopenic anemia and increased risk of leukemia."	1.30	Complementation group assignments in Fanconi anemia fibroblast cell lines from North America. ( Fiddler-Odell, E; Grompe, M; Jakobs, PM; Moses, RE; Olson, S; Reifsteck, C, 1997)
"Fanconi anemia is a cancer-prone disease characterized by progressive loss of blood cells, skeletal defects and stunted growth."	1.28	Alteration of a nuclease in Fanconi anemia. ( Boyd, JB; Buchwald, M; Harris, PV; Ryan, C; Sakaguchi, K, 1991)
"These included cells from patients with Fanconi's anemia (FA), dyskeratosis congenita (DC) a disorder related to FA, Gardner's syndrome (GS) and xeroderma pigmentosum grop C (XPC)."	1.27	Suppression of cytotoxic effect of mitomycin-C by superoxide dismutase in Fanconi's anemia and dyskeratosis congenita fibroblasts. ( Little, JB; Nagasawa, H, 1983)
"Lymphocytes from two sisters with Fanconi's anemia (FA) were studied for cell cycle kinetics, sister chromatid exchanges (SCEs), and chromosomal aberrations when they had undergone one, two, or three or more divisions in mitomycin C (MMC)-treated cultures."	1.27	Proliferative kinetics and mitomycin C-induced chromosome damage in Fanconi's anemia lymphocytes. ( Koizumi, A; Miura, K; Morimoto, K, 1983)
"The results indicate that Fanconi's anemia lymphocytes fail to exhibit an increased sensitivity to the antimitotic and clastogenic effects of paraquat and streptonigrin."	1.27	Cytogenetic toxicity of paraquat and streptonigrin in Fanconi's anemia. ( Arwert, F; de Koning, H; Joenje, H; Nieuwint, AW; Oostra, AB; Roozendaal, KJ, 1987)
"In order to develop the usefulness of Fanconi's anemia (FA) lymphoblast lines for biochemical and genetic studies, we have determined their sensitivity to a variety of DNA-damaging chemicals."	1.26	Susceptibility of Fanconi's anemia lymphoblasts to DNA-cross-linking and alkylating agents. ( Buchwald, M; Ishida, R, 1982)

Timeframe	Studies, this research(%)	All Research%
pre-1990	31 (14.69)	18.7374
1990's	56 (26.54)	18.2507
2000's	73 (34.60)	29.6817
2010's	44 (20.85)	24.3611
2020's	7 (3.32)	2.80

Trial			Phase	Enrollment	Study Type	Start Date	Status
Retroviral Mediated Gene Transfer of the Fanconi Anemia Complementation Group C Gene to Hematopoietic Progenitors of Group C Patients[NCT00001399]			Phase 1	9 participants	Interventional	1993-12-03	Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Article	Year
Re-definition and supporting evidence toward Fanconi Anemia as a mitochondrial disease: Prospects for new design in clinical management. Redox biology, 2021, Volume: 40 Topics: Fanconi Anemia; Humans; Mitochondrial Diseases; Mitomycin; Phenotype; Proteins	2021
Fanconi anemia and its diagnosis. Mutation research, 2009, Jul-31, Volume: 668, Issue:1-2 Topics: Congenital Abnormalities; DNA Damage; Endocrine System Diseases; Epoxy Compounds; Fanconi Anemia; Ge	2009
Molecular genetics and Fanconi anaemia: new insights into old problems. British journal of haematology, 1998, Volume: 103, Issue:2 Topics: Apoptosis; Cell Cycle Proteins; Cytokines; DNA Repair; DNA-Binding Proteins; Fanconi Anemia; Fanconi	1998
Mitomycins. Cancer chemotherapy and biological response modifiers, 1999, Volume: 18 Topics: Animals; Antibiotics, Antineoplastic; Apoptosis; Biotransformation; DNA Damage; Drug Interactions; F	1999
The genetics of Fanconi's anaemia. Bailliere's best practice & research. Clinical haematology, 2000, Volume: 13, Issue:3 Topics: Cells, Cultured; Chromosome Breakage; DNA Damage; Epoxy Compounds; Fanconi Anemia; Genetic Testing;	2000
Prospects for nutritional interventions in the clinical management of Fanconi anemia. Cancer causes & control : CCC, 2000, Volume: 11, Issue:10 Topics: Anemia, Aplastic; Antibiotics, Antineoplastic; Cell Transformation, Neoplastic; Disease Progression;	2000

Article	Year
Veliparib Alone or in Combination with Mitomycin C in Patients with Solid Tumors With Functional Deficiency in Homologous Recombination Repair. Journal of the National Cancer Institute, 2016, Volume: 108, Issue:7 Topics: Adult; Aged; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Benzimidazoles;	2016
Correlation of thyroid and growth hormones to chromosomal instability in Egyptian Fanconi anemia patients. Indian journal of pediatrics, 2008, Volume: 75, Issue:7 Topics: Adolescent; Cells, Cultured; Child; Child, Preschool; Chromosomal Instability; Chromosome Breakage;	2008
Fanconi anemia screening by diepoxybutane and mitomicin C tests in Korean children with bone marrow failure syndromes. Journal of Korean medical science, 1998, Volume: 13, Issue:6 Topics: Adolescent; Bone Marrow Diseases; Child; Child, Preschool; Epoxy Compounds; Fanconi Anemia; Female;	1998

mitomycin and Anemia, Fanconi

Research Excerpts

Research

Studies (211)

Authors

Clinical Trials (1)

Trial Overview

Reviews

Trials

Other Studies

Authors	Studies
Fahey, K	1
O'Donovan, L	1
Carr, M	1
Carty, MP	1
Aldabbagh, F	1
Rogers, CB	1
Kram, RE	1
Lin, K	1
Myers, CL	1
Sobeck, A	1
Hendrickson, EA	1
Bielinsky, AK	1
Farkas, G	1
Székely, G	1
Goda, V	1
Kállay, KM	1
Kocsis, ZS	1
Szakszon, K	1
Benyó, G	1
Erdélyi, D	1
Liptai, Z	1
Csordás, K	1
Kertész, G	1
Szegedi, I	1
Kriván, G	1
Takácsi-Nagy, Z	1
Polgár, C	1
Jurányi, Z	1
Codilupi, T	1
Taube, D	1
Naegeli, H	1
Frost, MG	1
Mazloumi Aboukheili, AM	1
Toth, R	1
Walden, H	1
Brannvoll, A	1
Xue, X	1
Kwon, Y	1
Kompocholi, S	1
Simonsen, AKW	1
Viswalingam, KS	1
Gonzalez, L	1
Hickson, ID	2
Oestergaard, VH	2
Mankouri, HW	1
Sung, P	1
Lisby, M	1
Hammarsten, O	1
Muslimovic, A	1
Thunström, S	1
Ek, T	1
Johansson, P	1
Nolan, M	1
Knudson, K	1
Holz, MK	1
Chaudhury, I	1
Pagano, G	5
Tiano, L	1
Pallardó, FV	1
Lyakhovich, A	1
Mukhopadhyay, SS	2
Di Bartolomeo, P	1
Zatterale, A	2
Trifuoggi, M	1
Inano, S	1
Sato, K	1
Katsuki, Y	1
Kobayashi, W	1
Tanaka, H	1
Nakajima, K	1
Nakada, S	1
Miyoshi, H	1
Knies, K	1
Takaori-Kondo, A	1
Schindler, D	6
Ishiai, M	2
Kurumizaka, H	1
Takata, M	3
Francies, FZ	1
Wainwright, R	1
Poole, J	1
De Leeneer, K	1
Coene, I	1
Wieme, G	1
Poirel, HA	1
Brichard, B	1
Vermeulen, S	1
Vral, A	1
Slabbert, J	1
Claes, K	1
Baeyens, A	1
Dutta, A	2
De, R	1
Dolai, TK	1
Pal, P	1
Ghosh, S	1
Mitra, PK	1
Halder, A	1
Röhrig, S	1
Dorn, A	1
Enderle, J	1
Schindele, A	1
Herrmann, NJ	1
Knoll, A	1
Puchta, H	1
Zhang, L	1
Liu, Q	1
Zou, Y	1
Liu, XM	1
Zhang, JY	1
Wang, SC	1
Chen, XJ	1
Guo, Y	1
Yang, WY	1
Ruan, M	1
Liu, TF	1
Liu, F	1
Cai, XJ	1
Chen, YM	1
Zhu, XF	1
Talmoudi, F	2
Kilani, O	1
Ayed, W	1
Ben Halim, N	1
Mellouli, F	2
Torjmane, L	1
Aissaoui, L	2
Ben Youssef, Y	1
Kammoun, L	2
Ben Othmane, T	1
Bejaoui, M	2
Ben Romdhane, N	1
Elloumi, M	1
Hadiji, S	1
Hentati, S	1
Chemkhi, I	1
Abidli, N	1
Guermani, H	1
Abdelhak, S	2
Amouri, A	2
Aggarwal, M	2
Banerjee, T	2
Sommers, JA	2
Iannascoli, C	1
Pichierri, P	1
Shoemaker, RH	1
Brosh, RM	2
Selenti, N	1
Sofocleous, C	1
Kattamis, A	1
Kolialexi, A	1
Kitsiou, S	1
Fryssira, E	1
Polychronopoulou, S	1
Kanavakis, E	1
Mavrou, A	1
Martínez, S	1
Pérez, L	2
Galmarini, CM	1
Aracil, M	1
Tercero, JC	2
Gago, F	2
Albella, B	2
Bueren, JA	6
Takata, K	1
Reh, S	1
Tomida, J	1
Person, MD	1
Wood, RD	1
Jun, DW	1
Hwang, M	1
Kim, HJ	1
Hwang, SK	1
Kim, S	1
Lee, CH	1
Chang, L	1
Yuan, W	1
Zeng, H	1
Zhou, Q	1
Wei, W	1
Zhou, J	1
Li, M	1
Wang, X	4
Xu, M	1
Yang, F	1
Yang, Y	2
Cheng, T	1
Zhu, X	1
Fargo, JH	1
Rochowski, A	1
Giri, N	1
Savage, SA	1
Olson, SB	6
Alter, BP	1
Molina, B	5
Marchetti, F	1
Gómez, L	3
Ramos, S	1
Torres, L	2
Ortiz, R	2
Altamirano-Lozano, M	1
Carnevale, A	3
Frias, S	6
Braakhuis, BJ	1
Nieuwint, AW	3
Oostra, AB	5
Joenje, H	18
Flach, GB	1
Graveland, AP	1
Brakenhoff, RH	1
Leemans, CR	1
Rodríguez, A	1
Juárez, U	1
Sosa, D	1
Azpeitia, E	1
García-de Teresa, B	1
Cortés, E	1
Salazar, AM	1
Ostrosky-Wegman, P	2
Mendoza, L	1
Garbati, MR	1
Hays, LE	1
Rathbun, RK	3
Jillette, N	1
Chin, K	1
Al-Dhalimy, M	3
Agarwal, A	1
Newell, AE	1
Bagby, GC	4
Renaud, E	1
Barascu, A	1
Rosselli, F	5
Hashimoto, K	1
Wada, K	1
Matsumoto, K	1
Moriya, M	1
Matsuzaki, K	1
Borel, V	1
Adelman, CA	1
Boulton, SJ	1
Du, W	1
Amarachintha, S	1
Erden, O	1
Wilson, A	1
Meetei, AR	1
Andreassen, PR	3
Namekawa, SH	1
Pang, Q	2
Villalona-Calero, MA	1
Duan, W	1
Zhao, W	1
Shilo, K	1
Schaaf, LJ	1
Thurmond, J	1
Westman, JA	1
Marshall, J	1
Xiaobai, L	1
Ji, J	1
Rose, J	1
Lustberg, M	1
Bekaii-Saab, T	1
Chen, A	1
Timmers, C	3
Tremblay, CS	2
Huang, FF	1
Habi, O	1
Huard, CC	1
Godin, C	2
Lévesque, G	2
Carreau, M	5
Martinez, A	1
Hinz, JM	1
Acuña, H	1
Jones, IM	1
Coleman, MA	1
Al-Haggar, M	1
Al-Morsy, Z	1
Yahia, S	1
Chalaby, N	1
Ragab, A	1
Mesbah, A	1
Wang, LC	1
Stone, S	1
Hoatlin, ME	4
Gautier, J	1
Camelo, RM	1
Kehdy, FS	1
Salas, CE	1
Lopes, MT	1
Xiao, H	1
Zhang, K	1
Xia, B	1
Collins, NB	1
Wilson, JB	2
Bush, T	1
Thomashevski, A	1
Roberts, KJ	1
Jones, NJ	4
Kupfer, GM	4
Mohseni Meybodi, A	1
Mozdarani, H	2
Pinto, FO	1
Leblanc, T	1
Chamousset, D	1
Le Roux, G	1
Brethon, B	1
Cassinat, B	1
Larghero, J	1
de Villartay, JP	1
Stoppa-Lyonnet, D	1
Baruchel, A	1
Socié, G	1
Gluckman, E	2
Soulier, J	1
Marietta, C	1
Thompson, LH	2
Lamerdin, JE	2
Brooks, PJ	1
Auerbach, AD	3
Howlett, NG	3
Harney, JA	2
Rego, MA	2
Kolling, FW	1
Glover, TW	1
Hemphill, AW	1
Akkari, Y	1
Newell, AH	1
Schultz, RA	1
Grompe, M	16
North, PS	1
Jakobs, PM	4
Rennie, S	1
Pauw, D	1
Hejna, J	4
Moses, RE	7
van de Vrugt, HJ	3
Eaton, L	1
Hanlon Newell, A	1
Liskay, RM	1
Landais, I	1
Hiddingh, S	1
McCarroll, M	1
Yang, C	1
Sun, A	1
Turker, MS	1
Snyder, JP	1
Korgaonkar, S	1
Ghosh, K	1
Vundinti, BR	1
Becker, PS	2
Taylor, JA	2
Trobridge, GD	2
Zhao, X	2
Beard, BC	2
Chien, S	2
Adair, J	1
Kohn, DB	1
Wagner, JE	1
Shimamura, A	2
Kiem, HP	2
Smogorzewska, A	2
Desetty, R	1
Saito, TT	1
Schlabach, M	1
Lach, FP	2
Sowa, ME	1
Clark, AB	1
Kunkel, TA	1
Harper, JW	1
Colaiácovo, MP	1
Elledge, SJ	2
Castella, M	2
Pujol, R	1
Callén, E	3
Ramírez, MJ	2
Casado, JA	4
Talavera, M	1
Ferro, T	2
Muñoz, A	2
Sevilla, J	2
Madero, L	2
Cela, E	2
Beléndez, C	1
de Heredia, CD	1
Olivé, T	3
de Toledo, JS	1
Badell, I	3
Estella, J	2
Dasí, Á	2
Rodríguez-Villa, A	2
Gómez, P	1
Tapia, M	2
Molinés, A	2
Figuera, Á	1
Surrallés, J	4
Stoepker, C	1
Hain, K	1
Schuster, B	1
Hilhorst-Hofstee, Y	1
Rooimans, MA	3
Steltenpool, J	1
Eirich, K	1
Korthof, ET	1
Jaspers, NG	2
Bettecken, T	1
Rouse, J	1
de Winter, JP	1
Kim, TM	1
Ko, JH	1
Choi, YJ	1
Hu, L	1
Hasty, P	1
Mason, JM	1
Sekiguchi, JM	1
Mauro, M	1
Shen, M	1
Abo-Elwafa, HA	1
Attia, FM	1
Sharaf, AE	1
Bernard, ME	1
Kim, H	1
Berhane, H	1
Epperly, MW	1
Franicola, D	1
Zhang, X	1
Houghton, F	1
Shields, D	1
Wang, H	2
Bakkenist, CJ	1
Frantz, MC	1
Forbeck, EM	1
Goff, JP	1
Wipf, P	1
Greenberger, JS	1
Leung, JW	1
Wang, Y	1
Fong, KW	1
Huen, MS	1
Li, L	1
Chen, J	1
Adair, JE	1
Fang, M	1
Wohlfahrt, ME	1
Nishimura, K	1
Horikawa, K	1
Fukagawa, T	1
Takisawa, H	1
Kanemaki, MT	1
Panneerselvam, J	1
Park, HK	1
Zhang, J	2
Dudimah, FD	1
Zhang, P	1
Fei, P	2
Prieto-Remón, I	1
Sánchez-Carrera, D	1
López-Duarte, M	1
Richard, C	1
Pipaón, C	1
Salewsky, B	1
Schmiester, M	1
Digweed, M	3
Demuth, I	2
Kim, Y	1
Spitz, GS	1
Veturi, U	1
Benhalim, N	1
Torjemane, L	1
Ouederni, M	1
Lakhal, A	1
Othmen, TB	1
Meddeb, M	1
Dellagi, K	1
Hdiji, S	1
Godthelp, BC	3
Artwert, F	1
Zdzienicka, MZ	5
Liu, L	2
Gan, OI	2
Hitzler, JK	1
Dick, JE	2
Buchwald, M	14
Stewart, G	1
Creus, A	1
Marcos, R	1
Ortega, JJ	1
Río, P	3
Segovia, JC	3
Hanenberg, H	3
Martínez, J	1
Göttsche, K	2
Cheng, NC	2
Arwert, F	11
Montes de Oca, R	3
Svenson, JL	1
Haining, N	1
Moreau, LA	2
Nathan, DG	1
D'Andrea, AD	18
Nakanishi, K	2
Taniguchi, T	7
Ranganathan, V	1
New, HV	1
Stotsky, M	1
Mathew, CG	3
Kastan, MB	2
Weaver, DT	1
Ramirez, MH	1
Adelfalk, C	1
Kontou, M	1
Hirsch-Kauffmann, M	2
Schweiger, M	2
Hussain, S	1
Witt, E	1
Huber, PA	1
Medhurst, AL	1
Ashworth, A	1
Brodeur, I	1
Goulet, I	1
Charbonneau, C	1
Delisle, MC	1
Huard, C	1
Khandjian, EW	1
Clarke, AA	3
Gibson, FM	1
Scott, J	1
Myatt, N	1
Rutherford, TR	3
Van Der Heijden, MS	2
Brody, JR	2
Kern, SE	2
Yamada, NA	1
George, JW	1
Souza, B	1
Christian, AT	1
Narayan, G	1
Arias-Pulido, H	1
Nandula, SV	1
Basso, K	1
Sugirtharaj, DD	1
Vargas, H	1
Mansukhani, M	1
Villella, J	1
Meyer, L	1
Schneider, A	1
Gissmann, L	1
Dürst, M	1
Pothuri, B	1
Murty, VV	1
Park, SJ	1
Ciccone, SL	1
Beck, BD	1
Hwang, B	1
Freie, B	2
Clapp, DW	3
Lee, SH	1
Talwar, R	1
Choudhry, VP	1
Kucheria, K	1
Gallmeier, E	1
Cunningham, SC	1
Dezentje, DA	1
Shen, D	1
Hruban, RH	1
Margossian, SP	1
Gregory, RC	2
Houghtaling, S	1
Nijman, SM	1
Huang, TT	1
Dirac, AM	1
Brummelkamp, TR	1
Kerkhoven, RM	1
Bernards, R	1
Bridge, WL	1
Vandenberg, CJ	1
Franklin, RJ	1
Hiom, K	1
Gordon, SM	1
Alon, N	1
Gurtan, AM	2
Stuckert, P	2
Navarro, S	1
Meza, NW	1
Quintana-Bustamante, O	1
Jacome, A	2
McAllister, K	1
Puerto, S	1
Machida, YJ	1
Machida, Y	1
Chen, Y	2
van Buul, PP	1
Elghalbzouri-Maghrani, E	1
van Duijn-Goedhart, A	1
Leung, KS	1
Hicks, MJ	1
Hastings, PJ	1
Youssoufian, H	8
Plon, SE	1
Antonio Casado, J	1
Lobitz, S	2
Cantalejo, A	1
Cervera, J	1
Sánchez-Calero, J	1
José Ortega, J	1
Neveling, K	1
Kalb, R	1
Lin, CJ	1
Couch, FJ	1
Tootian, S	1
Mahjoubi, F	1
Rahnama, M	1
Hormozian, F	1
Mortezapour, F	1
Razazian, F	1
Manoochehri, F	1
Zamanian, M	1
Nasiri, F	1
Soleymani, S	1
Seyedmortaz, L	1
Kennedy, RD	1
Ray, K	1
Ellenberger, T	1
Langevin, F	1
Kuiken, HJ	1
Pace, P	1
Niedzwiedz, W	1
Simpson, LJ	1
Ohzeki, M	1
Sale, JE	1
Patel, KJ	1
Mohseni-Meybodi, A	1
Vosough, P	1
Holtorf, M	1
Hines, J	1
Mathewson, L	1
Hemphill, A	1
Müller, LU	1
Milsom, MD	1
Kim, MO	1
Schambach, A	1
Schuesler, T	1
Williams, DA	2
Mirchandani, KD	1
McCaffrey, RM	1
Marco, E	1
García-Hernández, V	1
Domingo, A	1
Vaquero, JJ	1
Cohen, MM	2
Fruchtman, CE	1
Simpson, SJ	2
Martin, AO	2
Miura, K	2
Morimoto, K	2
Koizumi, A	2
Nagasawa, H	2
Little, JB	2
Zakrzewski, S	2
Koch, M	1
Sperling, K	2
Cervenka, J	1
Hirsch, BA	1
Kwee, ML	2
Poll, EH	2
van de Kamp, JJ	1
de Koning, H	2
Eriksson, AW	2
Duckworth-Rysiecki, G	4
Hultén, M	1
Mann, J	1
Taylor, AM	1
Kortbeek, HT	1
Little, FF	1
Burke, MJ	1
McCone, EF	1
Targovnik, HS	1
Chan, GL	1
Fujiwara, Y	3
Kano, Y	2
Yamamoto, Y	1
Kaneko, T	1
Iijima, K	1
Sato, M	1
Latt, SA	2
Schreck, RR	1
D'Andrea, A	2
Kaiser, TN	2
Schlesinger, F	1
Lester, S	1
Sakai, K	1
Lojewski, A	1
Dougherty, C	1
Juergens, L	1
Sahar, E	1
Ishida, R	1
Honig, GR	1
Maurer, HS	1
Nicklas, JW	1
Diatloff-Zito, C	2
Duchaud, E	2
Viegas-Pequignot, E	1
Fraser, D	1
Moustacchi, E	6
Yamashita, T	2
Barber, DL	1
Zhu, Y	1
Wu, N	2
Gibbons, B	1
Scott, D	1
Hungerford, JL	1
Cheung, KL	1
Harrison, C	1
Attard-Montalto, S	1
Evans, M	1
Birch, JM	1
Kingston, JE	1
Telleman, P	1
Overkamp, WJ	1
van Wessel, N	1
Studzian, K	1
Wetselaar, L	1
Natarajan, AT	1
Rey, JP	2
Scott, R	2
Müller, H	2
Saito, H	3
Hammond, AT	1
Seyschab, H	1
Friedl, R	1
Sun, Y	1
Hoehn, H	2
Hentze, S	1
Schroeder-Kurth, T	1
Walsh, CE	3
Nienhuis, AW	1
Samulski, RJ	1
Brown, MG	2
Miller, JL	1
Young, NS	1
Liu, JM	4
Evans, DG	1
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Spreadborough, A	1
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Kruyt, FA	7
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Reifsteck, C	5
Olson, S	6
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Jaiswal, AK	1
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Li, X	1
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Hong, WP	1
Kim, CJ	1
Park, JY	1
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Ryang, DW	1
Hwang, TJ	1
Korkina, LG	2
Abou-Zahr, F	2
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Bagby, G	1
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Garcia-Higuera, I	3
Pearson, T	2
van Berkel, CG	1
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Kelley, MR	1
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