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NCT Number: NCT07459816

Genomic of CONgenital Sideroblastic Anemias

Congenital sideroblastic anemias (CSA) are a group of rare disorders characterized by abnormal iron utilization during erythropoiesis, leading to mitochondrial iron overload, the formation of ring sideroblasts, and ineffective erythropoiesis resulting in anemia. Ring sideroblasts are erythroid precursors that contain non-heme iron deposits in their mitochondria, forming a distinctive ring-like pattern around the nucleus. Mitochondria are double membrane organelle provide a large amount of energy for cellular activities, by the process of oxidative phosphorylation (OXPHOS). The role of mitochondria has been well described in erythropoiesis. CSA exhibits clinical heterogeneity, affecting only the erythroid system in some cases, while in others presenting as part of broader syndromic conditions. Their molecular basis remains imperfectly known, although the development of next- generation sequencing technology brought tremendous advances in the understanding of their genetic features. More than 20 genes have been identified as causative of CSA, with all modes of inheritance observed: X-linked recessive, autosomal dominant, autosomal recessive, pseudo- dominant, and mitochondrial. These genes are typically involved in one of four key mitochondrial pathways: i) Heme biosynthesis (e.g., ALAS2, SLC25A38); ii) Iron-sulfur cluster biosynthesis and transport (e.g., GLRX5, HSPA9, HSCB); iii) tRNA synthesis and maturation (e.g., PUS1, YARS2, LARS2, IARS2, SARS2, MARS1, TRNT1); iv) Mitochondrial respiratory chain synthesis (e.g., NDUFB11).

However, in nearly 30% of cases within the French CSA cohort, the underlying genetic cause remains unknown. In these patients with molecularly unexplained whole genome or exome sequencing approaches focusing on genes involved in mitochondrial function and iron metabolism identified several possibly pathogenic variants in CSA patients. These genes were not clearly described as playing a role in erythropoiesis or heme or iron metabolism. We hope to confirm their role in CSA. However, in nearly 30% of cases within the French CSA cohort , the underlying genetic cause remains unknown. The investigators hope to confirm the role in CSA of gene identified with exome sequencing approaches.

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Key information

Sex eligibility

All sexes

Study type

Interventional

Phase

Not applicable

Primary location

Amiens University Hospital

Amiens, 80054, France

Location status: Recruiting

Who can participate

Healthy volunteers accepted: Yes

Only the study team can determine whether someone qualifies for participation.

Inclusion criteria

  • Patient with unexplained congenital sideroblastic anemia on the molecular side with the gene panels used routinely
  • Patients already identified by exome sequencing approach carrying bi-allelic variants of candidate genes of the mitochondrial respiratory pathway.
  • Patients meeting the same criteria who will be identified prospectively over the next 12 months

Exclusion criteria

  • NA

Treatment and study plan

blood redrawal

Biological

Peripheral blood mononuclear cells collected in EDTA (7 mL) and ACD tube (7 mL) during a routine sample collection for patients

Primary outcomes

  1. Identification of genetic variants in Congenital sideroblastic anemias

    Time frame: 1 year

    Variants potentially altering the splicing site

  2. Identification of nonsense and missense genetic variants in Congenital sideroblastic anemias

    Time frame: 1 year

    Nonsense and missense variants: study of protein expression or protein size by Western Blot or protein-protein interactions in blood mononuclear cells

Secondary outcomes

  1. level of mitochondrial membrane potential

    Time frame: 1 year

    Measurement of the level of mitochondrial membrane potential (TMRM in flow cytometry)

  2. Measurement of mitochondrial Ros production

    Time frame: 1 year

    Measurement of mitochondrial Ros production (Mitosox in flow cytometry)

  3. Measurement of mitochondrial mass

    Time frame: 1 year

    Measurement of mitochondrial mass (MitoTracker in flow cytometry)

  4. Measurement of erythroid differentiation

    Time frame: 1 year

    Measurement of erythroid differentiation

Study contacts

Contact information is provided by the study sponsor or research team.

Ophélie Evrard, MD

CONTACT

[email protected]

33+322835127

Sponsors and collaborators

Lead sponsor

Centre Hospitalier Universitaire, Amiens

Other

Registry information

Acronym: GASCON-2

Important dates

Study start
2025
Primary completion
2026
Study completion
2026
First posted
Mar 10, 2026
Registry last updated
Mar 11, 2026

OpenTrials presents study information sourced from ClinicalTrials.gov. The official registry record should be consulted for the latest information.

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This listing is for discovery and informational purposes only. It is not medical advice, does not guarantee that a study is recruiting, and does not determine eligibility. Contact the study team and a qualified healthcare professional when considering participation.

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