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French Institute of Health, Medical Research, University Paris - Sud, Assistance Publique Hopitaux De Paris and University Paris Est Creteil | Date: 2015-06-24

The invention relates to a method for diagnosing, staging and/or monitoring a hemoglobin-related disorder such as -thalassemia or a treatment against said hemoglobin-related disorder in a subject in need thereof based on the detection and/or quantification the presence of free -Hb pool in a biological sample obtained from said subject.

Itzykson R.,French Institute of Health and Medical Research
Blood | Year: 2013

Genomic studies in chronic myeloid malignancies, including myeloproliferative neoplasms (MPN), myelodysplastic syndromes (MDS), and MPN/MDS, have identified common mutations in genes encoding signaling, epigenetic, transcription, and splicing factors. In the present study, we interrogated the clonal architecture by mutation-specific discrimination analysis of single-cell-derived colonies in 28 patients with chronic myelomonocytic leukemias (CMML), the most frequent MPN/MDS. This analysis reveals a linear acquisition of the studied mutations with limited branching through loss of heterozygosity. Serial analysis of untreated and treated samples demonstrates a dynamic architecture on which most current therapeutic approaches have limited effects. The main disease characteristics are early clonal dominance, arising at the CD34(+)/CD38(-) stage of hematopoiesis, and granulomonocytic differentiation skewing of multipotent and common myeloid progenitors. Comparison of clonal expansions of TET2 mutations in MDS, MPN, and CMML, together with functional invalidation of TET2 in sorted progenitors, suggests a causative link between early clonal dominance and skewed granulomonocytic differentiation. Altogether, early clonal dominance may distinguish CMML from other chronic myeloid neoplasms with similar gene mutations. Source

Vitale I.,French Institute of Health and Medical Research
Nature reviews. Molecular cell biology | Year: 2011

The improper distribution of chromosomes during mitosis compromises cellular functions and can reduce cellular fitness or contribute to malignant transformation. As a countermeasure, higher eukaryotes have developed strategies for eliminating mitosis-incompetent cells, one of which is mitotic catastrophe. Mitotic catastrophe is driven by a complex and poorly understood signalling cascade but, from a functional perspective, it can be defined as an oncosuppressive mechanism that precedes (and is distinct from) apoptosis, necrosis or senescence. Accordingly, the disruption of mitotic catastrophe precipitates tumorigenesis and cancer progression, and its induction constitutes a therapeutic endpoint. Source

French Institute of Health, Medical Research and University Paris - Sud | Date: 2015-04-21

The present disclosure relates to a Co-029 inhibitor for inhibiting the migration of cancer cells which express Co-029. The disclosure relates to a Co-029 inhibitor for the treatment of cancer and/or the prevention of cancer metastasis and pharmaceutical compositions comprising said inhibitor and provides Co-029 antibodies. The disclosure provides a method for predicting the response of a patient afflicted with or susceptible to be afflicted with cancer to a medical treatment with a Co-029 inhibitor, a method for diagnosing a cancer in a patient and a method for predicting the survival in a cancer patient.

Candidate compounds for use in neuro-protection and repair in neurological disorders involving Tau dysfunction (including Alzheimers disease) are identified from a direct interaction between proteins FKBP52 and Tau. The method for screening a drug for the prevention and treatment of neurological disorders involving Tau dysfunction includes determining the ability of a candidate compound, to modulate binding between a Tau polypeptide and a FKBP52 polypeptide, and selecting positively the candidate compound that modulates binding.

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