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Intravenous Ferric Carboxymaltose vs. Oral Iron Substitution in Patients With Metastatic Colorectal Cancer (CRC) and Iron Deficiency Anemia: a Randomized Multicenter Treatment Optimization Study.

ABSTRACT: Iron deficiency has a high prevalence in colorectal cancer patients ranging at ca. 60%. About 70% of these patients suffer from iron deficiency anemia (IDA) which adds both physical and cognitive impediments to an already straining chemotherapy. Moreover, a chronic disease like cancer often results in a reduced availability of iron for the body. In clinical practice iron substitution is usually administered orally. Due to low resorption rates, frequent gastric side effects and thus poor patient compliance a parenteral substitution seems to be a better option in terms of efficacy. In the framework of a randomized multicenter clinical trial (‘FerInject’) a comparison of efficacy parameters of parenteral vs. oral iron substitution will now be conducted in order to identify the best treatment form for clinical practice in oncology. Furthermore detailed quality of life-data (QoL) will be collected in both treatment arms for effect comparison.

DISEASE(S): Metastatic Colorectal Cancer,Iron Deficiencies,Anemia,Colorectal Neoplasms,Anemia, Iron-deficiency

PROVIDER: 2191960 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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Iron deficiency anemia in mice involves alterations in mitophagy and gene expression in erythroblasts

Project description:Since iron deficiency anemia (IDA) is one of the most common diseases in worldwide, it is an essential issue to prevent and to treat the IDA in public healthcare system. However, the precise adaptive responses and their mechanisms of the hematopoietic system induced by iron deficient state are not fully understood. In this study, low iron diet conditions which induce sever iron deficiency anemia in mice were established. Transcriptome analyses in erythroblasts under normal or iron deficient states were performed to describe the pathological details of IDA. Under iron deficient state, extensive gene expression changes and mitophagy disorder were induced during the terminal maturation of erythroblasts. These findings provide a new insight into pathophysiology and molecular biology of IDA and the function of iron as a coordinator of gene expression networks in erythrocyte maturation.

2016-12-14 | GSE77694 | GEO

Helicobacter pylori sabA gene is associated with iron deficiency anemia (IDA) in childhood and adolescence

Project description:Background Gastric Helicobacter pylori colonization leads to iron deficiency anemia (IDA), especially in children and adolescents. However the pathogenesis is poorly understood. Objective We sought to identify specific H. pylori genes involved in IDA development, by comparing bacterial genome-wide expression profiling in patients affected or not. Methods H. pylori were isolated from four children with IDA and four from matched controls without IDA. Based on these isolates, cDNA microarrays under iron-replete or depleted conditions were systematically performed to compare gene expression profiles at the whole genome level. Real-time reverse-transcription (RT-) PCR and protein assays were performed for further assessing the profile differentiation of the identified H. pylori IDA-associated genes. Results We identified 29 and 11 genes with significantly higher or lower expression in the IDA isolates compared to non-IDA isolates, respectively. Especially notable were higher expression of sabA gene encoding sialic acid-binding adhesin in the IDA isolates, which was confirmed by real-time RT-PCR study. Moreover, iron-depletion in vitro led to up-regulation of fecA1 and frpB1 genes and down-regulation of pfr, as predicted. Known iron-regulated genes such as fur, pfr, fecA, and feoB did not significantly differ between both groups. The IDA isolates had significantly higher expression of vacuolating cytotoxin gene vacA than non-IDA isolates, consistent with the results of VacA protein assays. There were no significant differences in bacterial growth value between IDA and non-IDA isolates. Conclusions It is likely that H. pylori carrying high expression of sabA causes IDA, especially in children and adolescents who have increased daily iron demand. In addition, it is possible that several host-interactive genes, including vacA, may play a synergistic role for sabA in IDA development.

2017-07-25 | GSE101807 | GEO

A strong anti-inflammatory signature revealed by liver transcription profiling of Tmprss6-/- mice

Project description:Tmprss6 is the master inhibitor of hepcidin and its inactivation causes iron refractory iron deficiency anemia both in human and in mice. Mice with iron deficiency anemia (IDA)-low hepcidin show a pro-inflammatory response that is blunted in iron deficienct-high hepcidin Tmprss6 null mice. We investigated the transcriptional response associated with chronic hepcidin overexpression by comparing whole genome transcription profiling of the liver of Tmprss6 KO mice and IDA animals, irrespective of iron deficiency.

2013-10-09 | GSE46287 | GEO

A strong anti-inflammatory signature revealed by liver transcription profiling of Tmprss6-/- mice

2013-10-09 | E-GEOD-46287 | biostudies-arrayexpress

Multiomic profiling of iron-deficient infant monkeys reveals alterations in neurologically important biochemicals in serum and cerebrospinal fluid before the onset of anemia

Project description:The effects of iron deficiency (ID) during infancy extend beyond the hematologic compartment and include short- and long-term adverse effects on many tissues including the brain. However, sensitive biomarkers of iron-dependent brain health are lacking in humans. To determine whether serum and cerebrospinal fluid (CSF) biomarkers of ID-induced metabolic dysfunction are concordant in the pre/early anemic stage of ID before anemia in a nonhuman primate model of infantile iron deficiency anemia (IDA). ID (n = 7), rhesus infants at 4 mo (pre-anemic period) and 6 mo of age (anemic) were examined. Hematological, metabolomic and proteomic profiles were generated via HPLC/MS at both time points to discriminate serum biomarkers of ID-induced brain metabolic dysfunction. We identified 227 metabolites and 205 proteins in serum. Abnormalities indicating altered liver function, lipid dysregulation and increased acute phase reactants were present in ID. In CSF, we measured 210 metabolites and 1560 proteins with changes in ID infants indicative of metabolomic and proteomic differences indexing disrupted synaptogenesis. Systemic and CSF proteomic and metabolomic changes were present and concurrent in the pre-anemic and anemic periods. Multiomic serum and CSF profiling uncovered pathways disrupted by ID in both the pre-anemic and anemic stages of infantile IDA, including evidence for hepatic dysfunction and activation of acute phase response. Parallel changes observed in serum and CSF potentially provide measurable serum biomarkers of ID that reflect at-risk brain processes prior to progression to clinical anemia. Data availability:The proteomics data have been deposited into the ProteomeXchange Consortium via the PRIDE partner repository with the data set identifier <a href='https://www.ebi.ac.uk/pride/archive/projects/PXD028275' rel='noopener noreferrer' target='_blank'>PXD028275</a>.

2022-07-12 | MTBLS3388 | MetaboLights

Multiomic Profiling of Iron Deficient Infant Monkeys Reveals Alterations in Neurologically Important Biochemicals in Serum and CSF Prior to the Onset of Anemia

Project description:Background: The effects of iron deficiency anemia (IDA) during infancy extend beyond the hematologic compartment and include short- and long-term adverse effects on many tissues including the brain. However, biomarkers of iron-dependent brain health are lacking in humans. Prior analyses in rhesus infants indicated abnormal serum and cerebral spinal fluid (CSF) multiomic profiles both prior to and during IDA, characterized by alterations suggestive of hepatic and brain metabolic dysfunction, and impaired energy metabolism. Objective: To determine whether serum and CSF biomarkers of iron deficiency (ID)-induced metabolic dysfunction are concordant in the pre/early anemic stage of ID in a nonhuman primate model of infantile IDA. Methods: Paired serum and CSF specimens were collected from iron-sufficient (IS; n = 12) and ID (n = 7) rhesus infants at 4-months (preanemic period) and 6-months (anemic period) of age. Hematological, metabolomic, and proteomic profiles were generated via HPLC/MS at both timepoints to discover serum biomarkers of ID-induced brain metabolic dysfunction. Results: We identified and quantified 227 metabolites and 205 proteins in serum. Abnormalities indicating altered liver function, lipid dysregulation, and increased acute phase proteins were present in ID. In CSF, we measured 210 metabolites and 1,560 proteins with ID infants displaying metabolomic and proteomic changes indicating disrupted synaptogenesis. Concurrent systemic and CSF proteomic and metabolomic changes were present in the preanemic and anemic periods. Conclusions: Multiomic serum and CSF profiling uncovered pathways disrupted by ID in both the preanemic and anemic stages of infantile IDA, including evidence for liver metabolic dysfunction and acute phase responses. Parallel changes observed in serum and CSF potentially provide measurable serum biomarkers that reflect at-risk brain processes early during ID.

2022-03-18 | PXD028275 | Pride

Comparison of transcriptomic responses to individual and combinatorial copper and iron deficiencies in Arabidopsis thaliana rosettes.

Project description:Purpose: plants exposed to multiple simultaneous adverse growth conditions trigger molecular responses that differ from the sum of those to individual stressors. Copper and iron are fundamental elements required for proper photosynthesis, energy production, DNA metabolism and hormone sensing, among all. Therefore, copper and iron deprivation limits plant yield. In natural environments, simultaneous deficiency to copper and iron can occur. As part of a multiple high-throughput study to identify combinatorial responses to both copper and iron deficiency, RNA-Seq profiling of Arabidopsis thaliana rosette leaves exposed to copper and/or iron deficiencies have been conducted. Methods: RNA-Seq libraries were prepared from total RNA of whole rosettes of 20-d-old plants treated for control conditions, copper deficiency, iron deficiency or simultaneous deficiency to both copper and iron for 10 d and sequenced using Illumina protocols. 2 independent plants were RNA-Seq-sequenced per treatment. Adaptor sequences were removed with Trimmomatic and the resulting reads mapped to the Arabidopsis genome (Araport11) with Tophat 2.1.1. Read counts and differential expression analysis were conducted with Cufflinks/Cuffdiff. Results: for RNA-Seq analysis a Tophat/Cuffdiff pipeline was designed. Each sample provided app. 9 million reads. After applying a cut-off of absolute log2(FC) ≥ 1 to controls and a FDR ≤ 0.05, copper deficiency led to 83 differentially expressed genes, followed by 1708 during iron deficiency, while the combinatorial treatment altered 2056 transcripts. Comparison of differential expressed genes among treatments indicated that double deficiency led to app. 45% rewiring of all detected transcriptional changes. Conclusions: our data support that combinatorial copper and iron deficiency treatments in plants triggers transcriptional responses that differ from those to single deficiencies.

2020-06-11 | GSE125894 | GEO

Iron-Heme-Bach1 Axis Is Involved In Erythroblast Adaptation To Iron Deficiency

Project description:Iron plays the central role in the oxygen transport by the erythrocyte as a constituent of heme and hemoglobin. The importance of iron and heme also resides in their regulatory roles during erythroblast maturation. The transcription factor Bach1 may be involved in their regulatory roles since it is inactivated by direct binding of heme. To address whether Bach1 is involved in the responses of erythroblasts to iron status, low iron conditions that induced severe iron deficiency in mice were established. Under iron deficiency, extensive gene expression changes and mitophagy disorder were induced during maturation of erythroblasts. Bach1 mice showed more severe iron deficiency anemia in the developmental phase of mice and a retarded recovery once iron was replenished when compared with wild-type mice. In the absence of Bach1, the expression of globin genes and Hmox1 (encoding heme oxygenase-1) was de-repressed in erythroblasts under iron deficiency, suggesting that Bach1 represses these genes in erythroblasts under iron deficiency to balance the levels of heme and globin. Moreover, an increase in genome-wide DNA methylation was observed in erythroblasts of Bach1–/– mice under iron deficiency. These findings reveal the principle role of iron as a regulator of gene expression in erythroblast maturation and suggest that the iron-heme-Bach1 axis is important for a proper adaptation of erythroblast to iron deficiency to avoid toxic aggregates of non-heme globin.

2016-12-14 | GSE78955 | GEO

Iron Therapy in Colo-Rectal Neoplasm and Iron Deficiency Anemia: Intravenous Iron Sucrose Versus Oral Ferrous Sulphate.

Project description:The main objective of this study is to evaluate the efficacy of intravenous iron sucrose in increasing preoperative haemoglobin values in patients with colo-rectal neoplasm and iron deficiency anemia, compared to the standard treatment with oral iron. It will also determine whether intravenous iron sucrose administration improves outcomes such as postoperative haemoglobin values, serum ferritin values, transfusional needs, postoperative complications, or length of hospital stay.

| 2019445 | ecrin-mdr-crc

Iron Chelators Treatment on MCF-7 Human Breast Cancer Cell

Project description:Iron-deficiency affects 500 million people, yet the molecular role of iron in gene expression remains poorly characterized. Moreover, the alterations in global gene expression after iron chelation remains unclear and are important to assess for understanding the molecular pathology of iron-deficiency and the biological effects of iron chelators. We assessed the effect on whole genome gene expression of two iron chelators (desferrioxamine and 2-hydroxy-1-napthylaldehyde isonicotinoyl hydrazone) that have markedly different permeability properties. Sixteen genes were significantly regulated by both chelators, while a further 50 genes were regulated by either ligand. Most of the genes identified in this study have not been previously described to be iron-regulated and are important for understanding the molecular and cellular effects of iron-deficiency.

2010-02-28 | GSE17832 | GEO

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