San San Lum

Summary

Affiliation: National Cancer Centre
Country: Singapore

Publications

  1. ncbi request reprint Defective MHC class I antigen surface expression promotes cellular survival through elevated ER stress and modulation of p53 function
    K Sabapathy
    Laboratory of Molecular Carcinogenesis, Division of Cellular and Molecular Research, Humphrey Oei Institute of Cancer Research, National Cancer Centre Singapore, 11 Hospital Drive, Singapore
    Cell Death Differ 15:1364-74. 2008
  2. pmc Cancer-derived p53 mutants suppress p53-target gene expression--potential mechanism for gain of function of mutant p53
    Faina Vikhanskaya
    Laboratory of Molecular Carcinogenesis, National Cancer Centre, Singapore 169610, Singapore
    Nucleic Acids Res 35:2093-104. 2007
  3. pmc TAp73beta and DNp73beta activate the expression of the pro-survival caspase-2S
    Wen Hong Toh
    Division of Cellular and Molecular Research, Humphrey Oei Institute of Cancer Research, National Cancer Centre, 11, Hospital Drive, Singapore 169610, Singapore
    Nucleic Acids Res 36:4498-509. 2008
  4. pmc Characterization of novel and uncharacterized p53 SNPs in the Chinese population--intron 2 SNP co-segregates with the common codon 72 polymorphism
    Beng Hooi Phang
    Division of Cellular and Molecular Research, Humphrey Oei Institute of Cancer Research, National Cancer Centre, Singapore, Singapore
    PLoS ONE 6:e15320. 2011
  5. ncbi request reprint Distinct roles for JNK1 and JNK2 in regulating JNK activity and c-Jun-dependent cell proliferation
    Kanaga Sabapathy
    Research Institute of Molecular Pathology, Dr Bohrgasse 7, A 1030 Vienna, Austria
    Mol Cell 15:713-25. 2004
  6. pmc Effect of MDM2 SNP309 and p53 codon 72 polymorphisms on lung cancer risk and survival among non-smoking Chinese women in Singapore
    Hui Wan Chua
    Division of Cellular and Molecular Research, Humphrey Oei Institute of Cancer Research, National Cancer Centre, 11 Hospital Drive, Singapore
    BMC Cancer 10:88. 2010
  7. ncbi request reprint JNK2: a negative regulator of cellular proliferation
    Kanaga Sabapathy
    National Cancer Centre, Singapore, Singapore
    Cell Cycle 3:1520-3. 2004
  8. pmc Jun N-terminal kinase 2 modulates thymocyte apoptosis and T cell activation through c-Jun and nuclear factor of activated T cell (NF-AT)
    A Behrens
    Research Institute of Molecular Pathology, Dr Bohr Gasse 7, A 1030 Vienna, Austria
    Proc Natl Acad Sci U S A 98:1769-74. 2001
  9. pmc c-Jun NH2-terminal kinase (JNK)1 and JNK2 have similar and stage-dependent roles in regulating T cell apoptosis and proliferation
    K Sabapathy
    Research Institute of Molecular Pathology, Vienna A 1030, Austria
    J Exp Med 193:317-28. 2001
  10. doi request reprint MDM2 SNP309 G allele increases risk but the T allele is associated with earlier onset age of sporadic breast cancers in the Chinese population
    San San Lum
    Laboratory of Molecular Carcinogenesis, Division of Cellular and Molecular Research, Humphrey Oei Institute of Cancer Research, National Cancer Centre, 11 Hospital Drive, Singapore 169610, Singapore
    Carcinogenesis 29:754-61. 2008

Collaborators

  • Michael Karin
  • E F Wagner
  • Laurent Corcos
  • Daniel Ng
  • Konrad Hochedlinger
  • W M Tong
  • Z Q Wang
  • L Chang
  • J T Zhang
  • Huihua Li
  • T Kallunki
  • J A Trapani
  • Karen H Vousden
  • R W Johnstone
  • Baojie Li
  • Jeremy P E Spencer
  • Satoru Kyo
  • Adeline Seow
  • S Linder
  • Kanaga Sabapathy
  • K Sabapathy
  • Ming Kei Lee
  • Wen Hong Toh
  • Faina Vikhanskaya
  • S Y Nam
  • Shin Yuen Nam
  • Iqbal Dulloo
  • Hui Wan Chua
  • M K Lee
  • Ju Tao Chen
  • Beng Hooi Phang
  • Kai Wei Lin
  • W H Toh
  • Sergey N Kolomeichuk
  • Xin Mei Li
  • Daniel J Gough
  • K Hettinger
  • B H Phang
  • Matthew Whiteman
  • Massimo Broggini
  • Di Yun Ruan
  • Linda Strandberg Ihrlund
  • M Siddique
  • Lakshmanane Boominathan
  • Yuanyu Hu
  • Geqiang Li
  • Jean Pierre David
  • I Graef
  • A Behrens
  • Yeh Ching Linn
  • Serena Choo
  • Li Ying Soh
  • Christopher S Lyle
  • Emmanuelle Logette
  • Timothy C Chambers
  • David T Terrano
  • I de Belle
  • Christopher J P Clarke
  • Jia Ling Siau
  • Peter Rose
  • Robert D Schreiber
  • Jeffrey S Armstrong
  • Siew Hwa Chu
  • Shan Shan Yu
  • M K Poh
  • Marco Mazzoletti
  • S A G Reddy
  • F Vikhanskaya
  • Qiang Wu
  • Huck Hui Ng
  • Chen Chen Li
  • Helen A Arthur
  • Nam Sang Cheung
  • Jan Thorsten Schantz
  • Enoch Yi No Ko
  • Theocharis Panaretakis
  • Gabor Barna
  • Emma Hernlund
  • Maria C Shoshan
  • Kristina Viktorsson
  • Da Hua Lu
  • Chern Pang Chia
  • M Prakash Hande
  • Stephen P Goff
  • De Yu Cai
  • Zhi Cheng Xiao
  • Mobin M Siddique
  • Eduardo J Firpo
  • Xueying Wang
  • Li Zeng

Detail Information

Publications37

  1. ncbi request reprint Defective MHC class I antigen surface expression promotes cellular survival through elevated ER stress and modulation of p53 function
    K Sabapathy
    Laboratory of Molecular Carcinogenesis, Division of Cellular and Molecular Research, Humphrey Oei Institute of Cancer Research, National Cancer Centre Singapore, 11 Hospital Drive, Singapore
    Cell Death Differ 15:1364-74. 2008
    ....
  2. pmc Cancer-derived p53 mutants suppress p53-target gene expression--potential mechanism for gain of function of mutant p53
    Faina Vikhanskaya
    Laboratory of Molecular Carcinogenesis, National Cancer Centre, Singapore 169610, Singapore
    Nucleic Acids Res 35:2093-104. 2007
    ..Together, the results demonstrate another mechanism through which p53 mutants could promote cellular growth...
  3. pmc TAp73beta and DNp73beta activate the expression of the pro-survival caspase-2S
    Wen Hong Toh
    Division of Cellular and Molecular Research, Humphrey Oei Institute of Cancer Research, National Cancer Centre, 11, Hospital Drive, Singapore 169610, Singapore
    Nucleic Acids Res 36:4498-509. 2008
    ..Together, the data identifies caspase-2(S) as a novel transcriptional target common to both TAp73 and DNp73, and raises the possibility that TAp73 may be over-expressed in cancers to promote survival...
  4. pmc Characterization of novel and uncharacterized p53 SNPs in the Chinese population--intron 2 SNP co-segregates with the common codon 72 polymorphism
    Beng Hooi Phang
    Division of Cellular and Molecular Research, Humphrey Oei Institute of Cancer Research, National Cancer Centre, Singapore, Singapore
    PLoS ONE 6:e15320. 2011
    ..97 (1.32, 3.394)]. These data together demonstrate high SNP diversity in p53 gene between different populations, highlighting ethnicity-based differences, and their association with cancer risk...
  5. ncbi request reprint Distinct roles for JNK1 and JNK2 in regulating JNK activity and c-Jun-dependent cell proliferation
    Kanaga Sabapathy
    Research Institute of Molecular Pathology, Dr Bohrgasse 7, A 1030 Vienna, Austria
    Mol Cell 15:713-25. 2004
    ..In contrast, JNK1 becomes the major c-Jun interacting kinase after cell stimulation. These data provide mechanistic insights into the distinct roles of different JNK isoforms...
  6. pmc Effect of MDM2 SNP309 and p53 codon 72 polymorphisms on lung cancer risk and survival among non-smoking Chinese women in Singapore
    Hui Wan Chua
    Division of Cellular and Molecular Research, Humphrey Oei Institute of Cancer Research, National Cancer Centre, 11 Hospital Drive, Singapore
    BMC Cancer 10:88. 2010
    ..An increasing trend has been observed in the prevalence of lung cancers in non-smokers, especially females, though the underlying genetic basis is unclear...
  7. ncbi request reprint JNK2: a negative regulator of cellular proliferation
    Kanaga Sabapathy
    National Cancer Centre, Singapore, Singapore
    Cell Cycle 3:1520-3. 2004
    ..These data therefore suggests that JNK2, in contrast to JNK1, is a negative regulator of cellular proliferation in multiple cell types...
  8. pmc Jun N-terminal kinase 2 modulates thymocyte apoptosis and T cell activation through c-Jun and nuclear factor of activated T cell (NF-AT)
    A Behrens
    Research Institute of Molecular Pathology, Dr Bohr Gasse 7, A 1030 Vienna, Austria
    Proc Natl Acad Sci U S A 98:1769-74. 2001
    ..These results demonstrate that JNK signaling differentially uses c-Jun and NF-AT as molecular effectors during thymocyte apoptosis and T cell proliferation...
  9. pmc c-Jun NH2-terminal kinase (JNK)1 and JNK2 have similar and stage-dependent roles in regulating T cell apoptosis and proliferation
    K Sabapathy
    Research Institute of Molecular Pathology, Vienna A 1030, Austria
    J Exp Med 193:317-28. 2001
    ..Thus, JNK1 and JNK2 control similar functions during T cell maturation through differential targeting of distinct substrates...
  10. doi request reprint MDM2 SNP309 G allele increases risk but the T allele is associated with earlier onset age of sporadic breast cancers in the Chinese population
    San San Lum
    Laboratory of Molecular Carcinogenesis, Division of Cellular and Molecular Research, Humphrey Oei Institute of Cancer Research, National Cancer Centre, 11 Hospital Drive, Singapore 169610, Singapore
    Carcinogenesis 29:754-61. 2008
    ....
  11. doi request reprint An essential role for p73 in regulating mitotic cell death
    W H Toh
    Humphrey Oei Institute of Cancer Research, National Cancer Centre, Singapore, Singapore
    Cell Death Differ 17:787-800. 2010
    ..Taken together, the data show an important role for the p73-Bim axis in regulating cell death during mitosis that is independent of p53...
  12. ncbi request reprint The codon 72 polymorphism-specific effects of human p53 are absent in mouse cells: implications on generation of mouse models
    B H Phang
    Laboratory of Molecular Carcinogenesis, Division of Cellular and Molecular Research, National Cancer Centre, Singapore, Singapore
    Oncogene 26:2964-74. 2007
    ....
  13. ncbi request reprint c-Jun promotes cellular survival by suppression of PTEN
    K Hettinger
    Laboratory of Molecular Carcinogenesis, Division of Cellular and Molecular Research, National Cancer Centre, 11, Hospital Drive, Singapore 169610, Singapore
    Cell Death Differ 14:218-29. 2007
    ..Together, the data demonstrate that c-Jun contributes to the promotion of cellular survival by regulating the expression of PTEN...
  14. pmc Serine 312 phosphorylation is dispensable for wild-type p53 functions in vivo
    M K Lee
    Laboratory of Molecular Carcinogenesis, Division of Cellular and Molecular Research, Humphrey Oei Institute of Cancer Research, National Cancer Centre, 11 Hospital Drive, Singapore 169610, Singapore
    Cell Death Differ 18:214-21. 2011
    ....
  15. ncbi request reprint Defective neural tube morphogenesis and altered apoptosis in the absence of both JNK1 and JNK2
    K Sabapathy
    Research Institute of Molecular Pathology, Dr Bohr Gasse 7, A 1030, Vienna, Austria
    Mech Dev 89:115-24. 1999
    ..These results assign both pro- and anti-apoptotic functions for JNK1 and JNK2 in the development of the fetal brain...
  16. ncbi request reprint Trp53-dependent DNA-repair is affected by the codon 72 polymorphism
    M Siddique
    Laboratory of Molecular Carcinogenesis, National Cancer Centre, Singapore
    Oncogene 25:3489-500. 2006
    ..Together, the data highlight the functional differences between the Trp53 polymorphic variants, and suggest that their expression status may influence cancer risk...
  17. doi request reprint p53 promotes cellular survival in a context-dependent manner by directly inducing the expression of haeme-oxygenase-1
    S Y Nam
    Division of Cellular and Molecular Research, Humphrey Oei Institute of Cancer Research, National Cancer Centre, Singapore
    Oncogene 30:4476-86. 2011
    ..Taken together, these data demonstrate a direct role for p53 in promoting cellular survival in a context-specific manner through the activation of a direct transcriptional target, HO-1...
  18. doi request reprint Distinct signaling pathways of microtubule inhibitors--vinblastine and Taxol induce JNK-dependent cell death but through AP-1-dependent and AP-1-independent mechanisms, respectively
    Sergey N Kolomeichuk
    Department of Biochemistry and Molecular Biology, University of Arkansas for Medical Sciences, 4301 W Markham Street, Little Rock, AR 72205, USA
    FEBS J 275:1889-99. 2008
    ..In addition, these results show, contrary to popular belief, that JNK activation is not necessarily accompanied by c-Jun activation, and thus c-Jun is not an obligate substrate of JNK...
  19. ncbi request reprint c-Jun regulates the stability and activity of the p53 homologue, p73
    Wen Hong Toh
    Laboratory of Molecular Carcinogenesis, Division of Cellular and Molecular Research, National Cancer Centre, 11, Hospital Drive, Singapore 169610, Singapore
    J Biol Chem 279:44713-22. 2004
    ..Together, these findings demonstrate a possible role for c-Jun in regulating p73 function and highlight the importance of the cooperativity between transcription factors in potentiating apoptosis...
  20. ncbi request reprint An apoptotic signaling pathway in the interferon antiviral response mediated by RNase L and c-Jun NH2-terminal kinase
    Geqiang Li
    Department of Biochemistry, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106, USA
    J Biol Chem 279:1123-31. 2004
    ..These findings suggest that JNK and RNase L function in an integrated signaling pathway during the IFN response that leads to elimination of virus-infected cells through apoptosis...
  21. pmc Phosphorylation at carboxyl-terminal S373 and S375 residues and 14-3-3 binding are not required for mouse p53 function
    Ming Kei Lee
    Laboratory of Molecular Carcinogenesis, National Cancer Center, Singapore 169610, Singapore
    Neoplasia 9:690-8. 2007
    ..Together, the data suggest that despite a high homology with human p53, neither phosphorylation status at S373 and S375 nor 14-3-3 binding may be a critical event for mouse p53 to be functional...
  22. ncbi request reprint p73 supports cellular growth through c-Jun-dependent AP-1 transactivation
    Faina Vikhanskaya
    Laboratory of Molecular Carcinogenesis, National Cancer Centre, 11 Hospital Drive, Singapore 169610, Singapore
    Nat Cell Biol 9:698-705. 2007
    ..Collectively, our data demonstrates a novel and unexpected role of p73 in augmenting AP-1 transcriptional activity through which it supports cellular growth...
  23. ncbi request reprint Impaired long-term potentiation in c-Jun N-terminal kinase 2-deficient mice
    Ju Tao Chen
    Department of Clinical Research, Singapore General Hospital, Singapore
    J Neurochem 93:463-73. 2005
    ..Together, the data highlight the specific role of JNK2 in hippocampal synaptic plasticity during development...
  24. ncbi request reprint JNK1 contributes to metabotropic glutamate receptor-dependent long-term depression and short-term synaptic plasticity in the mice area hippocampal CA1
    Xin Mei Li
    Department of Neurobiology and Biophysics, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230027, PR China
    Eur J Neurosci 25:391-6. 2007
    ..These results demonstrated that JNK1 played a crucial role in the short-term synaptic plasticity and mGluR-dependent LTD, whereas hippocampus LTP was not affected by JNK1 deficiency...
  25. ncbi request reprint JNK1 modulates osteoclastogenesis through both c-Jun phosphorylation-dependent and -independent mechanisms
    Jean Pierre David
    Research Institute of Molecular Pathology, Dr Bohr Gasse 7, A 1030 Vienna, Austria
    J Cell Sci 115:4317-25. 2002
    ..Thus, these data provide genetic evidence that JNK1 activation modulates osteoclastogenesis through both c-Jun-phosphorylation-dependent and -independent mechanisms...
  26. ncbi request reprint Differential effects of JNK1 and JNK2 on signal specific induction of apoptosis
    Konrad Hochedlinger
    Research Institute of Molecular Pathology IMP, Dr Bohrgasse 7, A 1030 Vienna, Austria
    Oncogene 21:2441-5. 2002
    ....
  27. ncbi request reprint A novel c-Jun-dependent signal transduction pathway necessary for the transcriptional activation of interferon gamma response genes
    Daniel J Gough
    Peter MacCallum Cancer Centre, St Andrews Place, East Melbourne, and University of Melbourne, Parkville 3054, Victoria, Australia
    J Biol Chem 282:938-46. 2007
    ..This represents a novel signal transduction pathway induced by IFNgamma that proceeds in parallel with conventional JAK/STAT signaling to activate ISGs...
  28. pmc ERK phosphorylates p66shcA on Ser36 and subsequently regulates p27kip1 expression via the Akt-FOXO3a pathway: implication of p27kip1 in cell response to oxidative stress
    Yuanyu Hu
    The Institute of Molecular and Cell Biology, Proteos, Singapore 138673, Singapore
    Mol Biol Cell 16:3705-18. 2005
    ..Taken together, the data suggest there exists an interplay between ERK and ShcA proteins, which modulates the expression of p27 and cell response to oxidative stress...
  29. ncbi request reprint Two distinct steps of Bak regulation during apoptotic stress signaling: different roles of MEKK1 and JNK1
    Linda Strandberg Ihrlund
    Department Oncology Pathology, Cancer Center Karolinska, Karolinska Institute R8 03, S 171 76 Stockholm, Sweden
    Exp Cell Res 312:1581-9. 2006
    ..The two-step regulation of Bak revealed here may be important for tight control of mitochondrial factor release and apoptosis...
  30. pmc Multiple stress signals induce p73beta accumulation
    Kai Wei Lin
    Laboratory of Molecular Carcinogenesis, National Cancer Centre, 11 Hospital, Drive, Singapore 169610, Singapore
    Neoplasia 6:546-57. 2004
    ..Together, the data demonstrate that several stress signals can signal to p73 in vivo, which raises the possibility of eradicating cancers with an unmutated p73 gene by activating them with stress-inducing agents or their mimetics...
  31. ncbi request reprint Ectopic mTERT expression in mouse embryonic stem cells does not affect differentiation but confers resistance to differentiation- and stress-induced p53-dependent apoptosis
    Ming Kei Lee
    National Cancer Centre, 11, Hospital Drive, Singapore 169610, Republic of Singapore
    J Cell Sci 118:819-29. 2005
    ....
  32. doi request reprint The R246S hot-spot p53 mutant exerts dominant-negative effects in embryonic stem cells in vitro and in vivo
    Ming Kei Lee
    Division of Cellular and Molecular Research, Humphrey Oei Institute of Cancer Research, National Cancer Centre, Singapore
    J Cell Sci 121:1899-906. 2008
    ..These data therefore indicate that the DN effects of mutant p53 are evident in the stem-cell context, in which its expression is relatively high compared with terminally differentiated cells...
  33. ncbi request reprint Relief of p53-mediated telomerase suppression by p73
    Wen Hong Toh
    Laboratory of Molecular Carcinogenesis, Division of Cellular and Molecular Research, National Cancer Centre, 11, Hospital Drive, Singapore 169610, Singapore
    J Biol Chem 280:17329-38. 2005
    ..Together, our data indicate a plausible way by which p73, through HDM2, can oppose p53 tumor suppressor function, thereby possibly contributing to tumorigenesis...
  34. pmc The tumour-suppressor p53 is not required for pancreatic beta cell death during diabetes and upon irradiation
    Shin Yuen Nam
    Division of Cellular and Molecular Research, Humphrey Oei Institute of Cancer Research, National Cancer Centre, 11 Hospital Drive, Singapore 169610, Singapore
    J Physiol 586:407-17. 2008
    ..The results therefore demonstrate that p53 may not be causally involved in pancreatic beta cell death, and suggests that the classical cell death pathway dependent on p53 may not be operating in pancreatic beta cells...
  35. ncbi request reprint Transactivation-dependent and -independent regulation of p73 stability
    Iqbal Dulloo
    Laboratory of Molecular Carcinogenesis, Division of Cellular and Molecular Research, National Cancer Centre, 11 Hospital Drive, Singapore 169610
    J Biol Chem 280:28203-14. 2005
    ..Taken together, the data suggest that p73 turnover is tightly regulated in a transactivation-dependent and -independent manner, resulting in the controlled expression of the various p73 forms...
  36. ncbi request reprint The pro-inflammatory oxidant hypochlorous acid induces Bax-dependent mitochondrial permeabilisation and cell death through AIF-/EndoG-dependent pathways
    Matthew Whiteman
    Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, Republic of Singapore
    Cell Signal 19:705-14. 2007
    ..Our study provides a novel insight into the potential mechanisms of cell death in the inflamed human joint...
  37. ncbi request reprint Evaluation of the combined effect of p53 codon 72 polymorphism and hotspot mutations in response to anticancer drugs
    Faina Vikhanskaya
    Laboratory of Molecular Carcinogenesis, National Cancer Centre, Singapore, Department of Biochemistry, National University of Singapore, Singapore
    Clin Cancer Res 11:4348-56. 2005
    ..Together, the data show that the status of codon 72 polymorphism and p53 mutations can be used as a means for prediction of treatment response, although variables for each cancer type requires detailed evaluation...