Interaction Between IGF1 Polymorphisms and the Risk of Acute Lymphoblastic Leukemia in Chinese Children

Lu, Lingling; Wang, Feng; He, Lulu; Xue, Yue; Wang, Yaping; Zhang, Heng; Rong, Liucheng; Wang, Meilin; Zhang, Zhengdong; Fang, Yongjun; Miao, Hongjun

doi:10.1159/000430301

Cited by 14 publications

(17 citation statements)

References 55 publications

(60 reference statements)

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“…In agreement with our results, Lu et al (2015) demonstrated that the trend in IGF-1 mRNA level was upward with the addition of variant A allele of rs6214 SNP, but the difference was not statistically significant.…”

Section: Discussionsupporting

confidence: 90%

Association of Insulin-Like Growth Factor-1 Gene Polymorphisms with Different Types of Myopia in Egyptian Patients

Zidan

Rezk

Fouda

et al. 2016

Genetic Testing and Molecular Biomarkers

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Section: Discussionsupporting

confidence: 90%

Association of Insulin-Like Growth Factor-1 Gene Polymorphisms with Different Types of Myopia in Egyptian Patients

Zidan

Rezk

Fouda

et al. 2016

Genetic Testing and Molecular Biomarkers

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“…New targets and therapy strategies against leukemia are still of intense interest [40-42]. Zinc plays dual roles in regulating cell proliferation and apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Zinc Depletion by TPEN Induces Apoptosis in Human Acute Promyelocytic NB4 Cells

Zhu

Wang

Zhou

et al. 2017

Cell Physiol Biochem

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Background/Aims: The effects of zinc signaling on proliferation or apoptosis of leukemia cells remain elusive. In the present study, we used N, N, N’, N’-tetrakis-(2-pyridylmethyl)-ethylene-diamine (TPEN), a membrane-permeable zinc chelator, to evaluate the effect of zinc depletion on survival and apoptosis of NB4 acute promyelocytic leukemia (APL) cells. Methods: The pro-apoptotic effects of TPEN on NB4 cells were examined by flow cytometry, and observed using an optical microscope. Intracellular labile zinc, nitric oxide (NO) or reactive oxygen species (ROS) changes caused by TPEN were measured by flow cytometry. We then explored possible roles of the crosstalk between intracellular labile zinc signaling and nitric oxide signaling in TPEN-triggered apoptosis. Results: we found that TPEN induced apoptosis in NB4 APL cells in a dosage-dependent manner. We further demonstrated that TPEN triggered apoptosis by attenuating intracellular zinc and nitric oxide signaling in NB4 cells. Both exogenous zinc supplement and the nitric donor sodium nitroprusside (SNP) pre-incubation reversed TPEN-mediated inhibition of intracellular NO and Zn²⁺ signaling, and rescued NB4 cells from apoptosis. Conclusion: These results suggest for the first time that crosstalk between zinc signaling and nitric oxide pathway is essential for the survival of NB4 cells. TPEN induces apoptosis in NB4 cells via negatively regulating intracellular NO and Zn²⁺ signaling. Our in vitro data suggest that zinc depletion by TPEN may be a potential therapeutic strategy for APL.

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“…Myelodysplastic syndrome (MDS) is used as a prime example of the veracity of the SMT by its proponents but we have learned that risk stratification is needed and that the evolution of risk for leukemia is "...less than 10% at 15 years for patients with low-risk MDS compared with more than 50% at 1 year for those with high-risk disease" [37]. Further acute lymphoblastic leukemia (ALL) is thought of as being caused by genetic factors, such as mutations or polymorphisms and environmental exposures; a minority of ALL in children was associated with polymorphisms of rs17251221, rs4946936 or rs6214 and rs6218 in the 3'UTR of insulin-like growth factor 1 (IGF1) [38][39][40]. Recently it was shown, that ALL cases are not inherited.…”

Section: Somatic Mutation Theorymentioning

confidence: 99%

Somatic Mutation Theory - Why it's Wrong for Most Cancers

Brücher¹,

Jamall

2016

Cell Physiol Biochem

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Hysteron proteron reverses both temporal and logical order and this syllogism occurs in carcinogenesis and the somatic mutation theory (SMT): the first (somatic mutation) occurs only after the second (onset of cancer) and, therefore, observed somatic mutations in most cancers appear well after the early cues of carcinogenesis are in place. It is no accident that mutations are increasingly being questioned as the causal event in the origin of the vast majority of cancers as clinical data show little support for this theory when compared against the metrics of patient outcomes. Ever since the discovery of the double helical structure of DNA, virtually all chronic diseases came to be viewed as causally linked to one degree or another to mutations, even though we now know that genes are not simply blueprints, but rather an assemblage of alphabets that can, under non-genetic influences, be used to assemble a business letter or a work of Shakespearean literature. A minority of all cancers is indeed caused by mutations but the SMT has been applied to all cancers, and even to chemical carcinogenesis, in the absence of hard evidence of causality. Herein, we review the 100 year story of SMT and aspects that show why genes are not just blueprints, how radiation and mutation are associated in a more nuanced view, the proposed risk of cancer and bad luck, and the in vitro and in vivo evidence for a new cancer paradigm. This paradigm is scientifically applicable for the majority of non-heritable cancers and consists of a six-step sequence for the origin of cancer. This new cancer paradigm proclaims that somatic mutations are epiphenomena or later events occurring after carcinogenesis is already underway. This serves not just as a plausible alternative to SMT and explains the origin of the majority of cancers, but also provides opportunities for early interventions and prevention of the onset of cancer as a disease.

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Interaction Between IGF1 Polymorphisms and the Risk of Acute Lymphoblastic Leukemia in Chinese Children

Cited by 14 publications

References 55 publications

Association of Insulin-Like Growth Factor-1 Gene Polymorphisms with Different Types of Myopia in Egyptian Patients

Association of Insulin-Like Growth Factor-1 Gene Polymorphisms with Different Types of Myopia in Egyptian Patients

Zinc Depletion by TPEN Induces Apoptosis in Human Acute Promyelocytic NB4 Cells

Somatic Mutation Theory - Why it's Wrong for Most Cancers

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