Analysis of HFE and TFR2 gene mutations in patients with acute leukemia

Veneri, Dino; Franchini, Massimo; Krampera, Mauro; Matteis, Giovanna De; Solero, Pietro; Pizzolo, Giovanni

doi:10.1016/j.leukres.2005.01.001

Cited by 10 publications

(7 citation statements)

References 21 publications

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“…Veneri et al, 171 who administered H. pylori eradication therapy to 43 patients with H. pylori -positive ITP, reported the therapy to be successful in 41 of the 43 and recognized continuous improvement in 20 (48.8%) of these 41 patients on long-term observation. According to another report by the same authors, 172 the frequencies of HLA-DRB 111, HLA-DRB 114, and HLA-DQB 103 as host factors were high in H. pylori -positive ITP, while the frequency of HLA-DRB 103 as a host factor was higher in the H. pylori -negative ITP group than in the H. pylori -positive ITP group, and HLA-DQB 103 showed favorable platelet reactivity after eradication therapy in H. pylori -positive ITP. 172 Inaba et al 173 administered H. pylori eradication therapy to 35 patients with chronic ITP (25 H. pylori -positive ITP patients and 10 H. pylori -negative ITP patients), and succeeded in eradicating the bacteria in all of the patients with H. pylori -positive ITP.…”

Section: Future Prospectsmentioning

confidence: 95%

“…According to another report by the same authors, 172 the frequencies of HLA-DRB 111, HLA-DRB 114, and HLA-DQB 103 as host factors were high in H. pylori -positive ITP, while the frequency of HLA-DRB 103 as a host factor was higher in the H. pylori -negative ITP group than in the H. pylori -positive ITP group, and HLA-DQB 103 showed favorable platelet reactivity after eradication therapy in H. pylori -positive ITP. 172 Inaba et al 173 administered H. pylori eradication therapy to 35 patients with chronic ITP (25 H. pylori -positive ITP patients and 10 H. pylori -negative ITP patients), and succeeded in eradicating the bacteria in all of the patients with H. pylori -positive ITP. They reported that the platelet count was improved in 11 (44%) of the 25 patients, while the platelet count was unchanged in the 10 H. pylori -negative ITP patients.…”

Section: Future Prospectsmentioning

confidence: 95%

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Helicobacter pylori: present status and future prospects in Japan

2007

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The discovery of Helicobacter pylori has already changed the natural history of peptic ulcer disease, with most patients being cured at their fi rst presentation. Similarly, the incidence of gastric cancer and other diseases related to H. pylori are likely to be greatly reduced in the near future. Isolation of the spiral intragastric bacterium H. pylori totally reversed the false dogma that the stomach was sterile, and it taught us that chronic infectious disease can still exist in modern society. Helicobacter pylori's unique location, persistence, and evasion of the immune system offer important insights into the pathophysiology of the gut. Also, the fact that it was overlooked for so long encourages us to think "outside the box" when investigating other diseases with obscure etiologies. We should consider such provocative scientifi c ideas as bridges to the future disease control.

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Section: Future Prospectsmentioning

confidence: 95%

Section: Future Prospectsmentioning

confidence: 95%

Helicobacter pylori: present status and future prospects in Japan

2007

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“…However, there was no difference between patients positive or negative for the HFE mutations in terms of serum ferritin levels. The study therefore highlighted the presence of iron overload in many AML patients but did not support the evidence of an association between HFE mutations and iron overload in acute leukemia [33]. …”

Section: Discussionmentioning

confidence: 98%

“…Veneri et al studied the prevalence of 12 mutations of the HFE gene and its correlation with the iron status in 82 adult patients with acute leukemia of whom 58.5% were affected by acute myeloid leukemia (AML) [33]. 32.9% of the patients had at least one HFE gene mutation and mean serum ferritin levels were increased at diagnosis.…”

Section: Discussionmentioning

confidence: 99%

Highly Elevated Serum Hepcidin in Patients with Acute Myeloid Leukemia prior to and after Allogeneic Hematopoietic Cell Transplantation: Does This Protect from Excessive Parenchymal Iron Loading?

Eisfeld

Westerman

Krahl

et al. 2011

Advances in Hematology

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Hepcidin is upregulated by inflammation and iron. Inherited (HFE genotype) and treatment-related factors (blood units (BU), Iron overload) affecting hepcidin (measured by C-ELISA) were studied in 42 consecutive patients with AML prior to and after allogeneic hematopoietic cell transplantation (HCT). Results. Elevated serum ferritin pre- and post-HCT was present in all patients. Median hepcidin pre- and post-HCT of 358 and 398 ng/mL, respectively, were elevated compared to controls (median 52 ng/mL) (P < .0001). Liver and renal function, prior chemotherapies, and conditioning had no impact on hepcidin. Despite higher total BU after HCT compared to pretransplantation (P < .0005), pre- and posttransplant ferritin and hepcidin were similar. BU influenced ferritin (P = .001) and hepcidin (P = .001). No correlation of pre- or posttransplant hepcidin with pretransplant ferritin was found. HFE genotype did not influence hepcidin. Conclusions. Hepcidin is elevated in AML patients pre- and post-HCT due to transfusional iron-loading suggesting that hepcidin synthesis remains intact despite chemotherapy and HCT.

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“…70 Similarly, a 2005study did not find differences in HFE gene variant allele frequencies in adult acute leukemia cases compared with the general population ( n = 82). 71 However, HFE genotype (H63D and C282Y) has been found to be associated with increased risk of childhood ALL in females ( n = 163 ALL, 995 controls). 72 It must be noted that the childhood ALL risk finding for C282Y was considerably weakened when it was examined in a more detailed study of polymorphisms in that chromosomal region.…”

Section: Leukemiamentioning

confidence: 99%

Evidence for the Influence of the Iron Regulatory MHC Class I Molecule HFE on Tumor Progression in Experimental Models and Clinical Populations

Weston

Connor

2014

Translational Oncogenomics

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Proteins involved in iron regulation are modifiers of cancer risk and progression. Of these, the HFE protein (high iron gene and its protein product) is of particular interest because of its interaction with both iron handling and immune function and the high rate of genetic polymorphisms resulting in a mutant protein. Clinical studies suggest that HFE polymorphisms increase the risk of certain cancers, but the inconsistent outcomes suggest a more nuanced effect, possibly interacting with other genetic or environmental factors. Some basic science research has been conducted to begin to understand the implications of variant HFE genotype on cancer, but the story is far from complete. In particular, putative mechanisms exist for HFE to affect tumor progression through its role in iron handling and its major histocompatibility complex class I structural features. In this review, the current understanding of the role of HFE in cancer is described and models for future directions are identified.

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Analysis of HFE and TFR2 gene mutations in patients with acute leukemia

Cited by 10 publications

References 21 publications

Helicobacter pylori: present status and future prospects in Japan

Helicobacter pylori: present status and future prospects in Japan

Highly Elevated Serum Hepcidin in Patients with Acute Myeloid Leukemia prior to and after Allogeneic Hematopoietic Cell Transplantation: Does This Protect from Excessive Parenchymal Iron Loading?

Evidence for the Influence of the Iron Regulatory MHC Class I Molecule HFE on Tumor Progression in Experimental Models and Clinical Populations

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