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1. Mild Beta-Thalassemia intermedia Caused by Compound Heterozygosity for Gγ(Aγδβ)o/β-Thalassemia and Molecular Characterization of the Defect in Four Chinese Families

Author

Yong Chui Wee, Mary Anne Tan Jin Ai, Yean Ching Wong, Juan Loong Kok, Sook Fan Yap, and Kim Lian Tan

Subjects
Hemolytic anemia, congenital, hereditary, and neonatal diseases and abnormalities, Mutation, Beta thalassemia, Hematology, General Medicine, Biology, Compound heterozygosity, medicine.disease, medicine.disease_cause, Molecular biology, Loss of heterozygosity, Hemoglobinopathy, hemic and lymphatic diseases, Genotype, medicine, BETA-THALASSEMIA INTERMEDIA
Abstract

Molecular characterization of the compound heterozygous condition – Gγ(Aγδβ)o/β-thalassemia – in four families showing mild β-thalassemia intermedia was carried out using DNA amplification techniques. Using the Amplification Refractory Mutation System (ARMS) to confirm the β-mutations and DNA amplification to detect the 100-kb Chinese-specific Gγ(Aγδβ)o-deletion, two families were confirmed to possess Gγ(Aγδβ)o/β-thalassemia with the IVSII No. 654 β+-allele. In the third family, the Gγ(Aγδβ)o-deletion was confirmed in the father and the mother was a β-thalassemia carrier with the cd 41–42 βo-allele. Their affected child with Gγ(Aγδβ)o/β-thalassemia was found to be transfusion dependent. The same Gγ(Aγδβ)o-deletion and β-thalassemia (cd 41–42) was also confirmed in a fourth family. In addition, the mother was also diagnosed with Hb H disease (genotype -α3.7/–SEA). Both the children were found to possess Gγ(Aγδβ)o/β-thalassemia but they were not transfusion dependent and this could be due to co-inheritance of α-thalassemia-2 (genotype-α3.7/αα) in the children together with their compound heterozygous condition.

Published
2003

2. Molecular characterisation and frequency of Ggamma Xmn I polymorphism in Chinese and Malay beta-thalassaemia patients in Malaysia

Author

Yean Ching, Wong, Elizabeth, George, Kim Lian, Tan, Sook Fan, Yap, Lee Lee, Chan, and Jin Ai Mary Anne, Tan

Subjects
Polymorphism, Genetic, Asian People, beta-Thalassemia, Malaysia, Humans, Deoxyribonucleases, Type II Site-Specific, Polymerase Chain Reaction
Abstract

The molecular basis of variable phenotypes in P-thalassaemia patients with identical genotypes has been associated with co-inheritance of alpha-thalassaemia and persistence of HbF production in adult life. The Xmn I restriction site at -158 position of the Ggamma-gene is associated with increased expression of the Ggamma-globin gene and higher production of HbF This study aims to determine the frequency of the digammaferent genotypes of the Ggamma Xmn I polymorphism in P-thalassaemia patients in two ethnic groups in Malaysia. Molecular characterisation and frequency of the Ggamma Xmn I polymorphism were studied in fifty-eight Chinese and forty-nine beta-thalassaemia Malay patients by Xmn I digestion after DNA amplification of a 650 bp sequence. The in-house developed technique did not require further purification or concentration of amplified DNA before restriction enzyme digestion. The cheaper Seakem LE agarose was used instead of Nusieve agarose and distinct well separated bands were observed. Genotyping showed that the most frequent genotype observed in the Malaysian Chinese was homozygosity for the absence of the Xmn I site (-/-) (89.7%). In the Malays, heterozygosity of the Xmn I site (+/-) was most common (63.3%). Homozygosity for the Xmn I site (+/+) was absent in the Chinese, but was confirmed in 8.2% of the Malays. The ratio of the (+) allele (presence of the Xmn I site) to the (-) allele (absence of the Xmn I site)) was higher in the Malays (0.66) compared to the Chinese (0.05). The (+/-) and (+/+) genotypes are more commonly observed in the Malays than the Chinese in Malaysia.

Published
2007

3. Contents Vol. 109, 2003

Author

Daniel H. Kett, Wenche Jy, Naoko Miwa, Alessandra Rusignuolo, H. Müller, N. Papadopoulos, A. Cheva, Yean Ching Wong, Hiroshi Nihei, Akira Kawashima, Giovanna Meloni, Sook Fan Yap, Lajos Gergely, Éva Remenyik, Dalia Stagler, Mayukh Das, C. Schneider, D. Tamiolakis, Paolo de Fabritiis, Kosaku Nitta, J. Thiele, Naoki Kobayashi, Yoshinori Iwatani, Franco Mandelli, E. Varus, Giovanna Palumbo, Edgardop S. Santos, László Váróczy, Arnon Nagler, Shigeru Otsubo, Akitoshi Imai, Lidia De Felice, Keiko Uchida, A. Mank, P. Bakker, A. Semin-Goossens, Osamu Kabutomori, Roshan B. Cohla, Keisuke Sato, A. Kotini, Takahumi Ogawa, Joaquin J. Jimenez, Giacinto La Verde, Toshio Higa, Masahiro Imamura, Tomomi Toubai, Moshe Gmori, Ulrich Kaiser, Shimon Slavin, F. Simone, Giuseppe Avvisati, Lawrence L. Horstman, D. Mohanty, Yoshio Kiyama, Györgyi Vadász, Junji Tanaka, Yuzuru Kanakura, Shlomi Konstantini, Maria Teresa Petrucci, C. Wickenhauser, Kim Lian Tan, P. Skaphida, Wako Yumura, Juan Loong Kok, J. v.d. Lelie, Árpád Illés, Masahiro Ogasawara, R. Vos, B.P. Dash, M.R. Ranjit, Naoki Kimata, G.P. Chhotray, Takashi Akiba, H.M. Kvasnicka, Mary Anne Tan Jin Ai, Yoshihiko Watanabe, Noriyuki Miyokawa, Yong Chui Wee, D.W. Beelen, Michela Ribersani, Teresa Gagliano-DeCesare, T. Jivannakis, Masaharu Kasai, Zoneddy Ruiz-Dayao, Yoko Kondo, Yeon S. Ahn, Yuriko Otsubo, and Soumya Panigrahi

Subjects
Hematology, General Medicine
Published
2003

4. Subject Index Vol. 109, 2003

Author

Yoshihiko Watanabe, Daniel H. Kett, Paolo de Fabritiis, Györgyi Vadász, Maria Teresa Petrucci, C. Wickenhauser, Alessandra Rusignuolo, P. Bakker, Yoshio Kiyama, M.R. Ranjit, Noriyuki Miyokawa, Lawrence L. Horstman, T. Jivannakis, Yong Chui Wee, Ulrich Kaiser, Yean Ching Wong, Dalia Stagler, D. Tamiolakis, Masaharu Kasai, Toshio Higa, Kim Lian Tan, Masahiro Ogasawara, G.P. Chhotray, Edgardop S. Santos, Naoki Kimata, Mayukh Das, Yuriko Otsubo, P. Skaphida, D.W. Beelen, Soumya Panigrahi, J. Thiele, Wako Yumura, Naoki Kobayashi, Shlomi Konstantini, Teresa Gagliano-DeCesare, H.M. Kvasnicka, F. Simone, Michela Ribersani, Keiko Uchida, A. Kotini, Juan Loong Kok, Takashi Akiba, László Váróczy, Naoko Miwa, Takahumi Ogawa, Arnon Nagler, Akitoshi Imai, Masahiro Imamura, Mary Anne Tan Jin Ai, N. Papadopoulos, A. Mank, J. v.d. Lelie, Junji Tanaka, Éva Remenyik, Árpád Illés, B.P. Dash, Yoko Kondo, Yuzuru Kanakura, Roshan B. Cohla, Tomomi Toubai, Osamu Kabutomori, Zoneddy Ruiz-Dayao, C. Schneider, Joaquin J. Jimenez, Kosaku Nitta, Franco Mandelli, Moshe Gmori, Shigeru Otsubo, Sook Fan Yap, Keisuke Sato, Shimon Slavin, Yeon S. Ahn, D. Mohanty, R. Vos, Wenche Jy, H. Müller, E. Varus, Lidia De Felice, A. Cheva, Hiroshi Nihei, Akira Kawashima, Yoshinori Iwatani, A. Semin-Goossens, Giovanna Meloni, Lajos Gergely, Giovanna Palumbo, Giacinto La Verde, and Giuseppe Avvisati

Subjects
Index (economics), Statistics, Subject (documents), Hematology, General Medicine, Mathematics
Published
2003

5. Mild Beta-Thalassemia intermedia Caused by Compound Heterozygosity for [supG]ϒ([supA]ϒδβ)°/ β-Thalassemia and Molecular Characterization of the Defect in Four Chinese Families.

Author

Tan Jin Ai, Mary Anne, Sook Fan Yap, Kim Lian Tan, Yean Ching Wong, Yong Chui Wee, and Juan Loong Kok

Subjects
THALASSEMIA, GENETIC disorders, GENETIC polymorphisms, DNA, GENETIC mutation
Abstract

Molecular characterization of the compound heterozygous condition--[supG]γ([supA]γδΒ)[supo]/Β-thalassemia--in four families showing mild Β-thalassemia intermedia was carried out using DNA amplification techniques. Using the Amplification Refractory Mutation System (ARMS) to confirm the Β-mutations and DNA amplification to detect the 100-kb Chinese-specific [supG]γ([supA]γδΒ)[supo]-deletion, two families were confirmed to possess [supG]γ([supA]γδΒ)[supo]/&Beta-thalassemia with the IVSII No. 654 Β[sup+]-allele. In the third family, the [supG]γ([supA]γδΒ)[supo]-deletion was confirmed in the father and the mother was a Β-thalassemia carrier with the cd 41-42 Β[supo]-allele. Their affected child with [supG]γ([supA]γδΒ)[supo]/Β-thalassemia was found to be transfusion dependent. The same [supG]γ([supA]γδΒ)[supo]-deletion and Β-thalassemia (cd 41-42) was also confirmed in a fourth family. In addition, the mother was also diagnosed with Hb H disease (genotype-α[sup3.7]/[sup-SEA]). Both the children were found to possess [supG]γ([supA]γδΒ)[supo]/Β-thalassemia but they were not transfusion dependent and this could be due to co-inheritance of α-thalassemia-2 (genotype-α[sup3.7]/αα) in the children together with their compound heterozygous condition. [ABSTRACT FROM AUTHOR]

Published
2003
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