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See detailLoss in risk-taking: Absence of optimal gain or reduction in one’s own resources?
Anselme, Patrick ULg

in Behavioural Brain Research (2012), 229(2), 443-446

Determining how living beings react to tasks that reflect realistic situations of risk has given rise to a vast literature. However, I argue that the methodologies traditionally used to test humans and ... [more ▼]

Determining how living beings react to tasks that reflect realistic situations of risk has given rise to a vast literature. However, I argue that the methodologies traditionally used to test humans and nonhumans relative to risk often fail to achieve their goal. When risk is modelled in laboratory, potential decision cost (or potential loss) typically denotes an absence of optimal gain. In contrast, when risk occurs in real-life situations, potential loss denotes the reduction in an individual’s limited resources – whether energetic, social, financial, etc. This conceptual difference about the nature of risk may have important implications for the understanding of the parameters that control risk-taking behaviour. [less ▲]

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See detailLoss of axin2 in murine aortic valves leads to myxomatous disease
Hulin, Alexia ULg; Alfieri, Christina M.; Yutzey, Katherine E.

Poster (2015)

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See detailLoss of Axin2 leads to Myxomatous Valve Disease
Hulin, Alexia ULg; Yutzey, Katherine

Poster (2016)

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See detailLoss of Axin2 results in impaired heart valve maturation and subsequent myxomatous valve disease.
Hulin, Alexia ULg; Moore, Vicky; James, Jeanne M. et al

in Cardiovascular Research (2017), 113(1), 40-51

AIMS: Myxomatous valve disease (MVD) is the most common aetiology of primary mitral regurgitation. Recent studies suggest that defects in heart valve development can lead to heart valve disease in adults ... [more ▼]

AIMS: Myxomatous valve disease (MVD) is the most common aetiology of primary mitral regurgitation. Recent studies suggest that defects in heart valve development can lead to heart valve disease in adults. Wnt/beta-catenin signalling is active during heart valve development and has been reported in human MVD. The consequences of increased Wnt/beta-catenin signalling due to Axin2 deficiency in postnatal valve remodelling and pathogenesis of MVD were determined. METHODS AND RESULTS: To investigate the role of Wnt/beta-catenin signalling, we analysed heart valves from mice deficient in Axin2 (KO), a negative regulator of Wnt/beta-catenin signalling. Axin2 KO mice display enlarged mitral and aortic valves (AoV) after birth with increased Wnt/beta-catenin signalling and cell proliferation, whereas Sox9 expression and collagen deposition are decreased. At 2 months in Axin2 KO mice, the valve extracellular matrix (ECM) is stratified but distal AoV leaflets remain thickened and develop aortic insufficiency. Progressive myxomatous degeneration is apparent at 4 months with extensive ECM remodelling and focal aggrecan-rich areas, along with increased BMP signalling. Infiltration of inflammatory cells is also observed in Axin2 KO AoV prior to ECM remodelling. Overall, these features are consistent with the progression of human MVD. Finally, Axin2 expression is decreased and Wnt/beta-catenin signalling is increased in myxomatous mitral valves in a murine model of Marfan syndrome, supporting the importance of Wnt/beta-catenin signalling in the development of MVD. CONCLUSIONS: Altogether, these data indicate that Axin2 limits Wnt/beta-catenin signalling after birth and allows proper heart valve maturation. Moreover, dysregulation of Wnt/beta-catenin signalling resulting from loss of Axin2 leads to progressive MVD. [less ▲]

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See detailLoss of beta-catenin promotes chondrogenic differentiation of aortic valve interstitial cells.
Fang, Ming; Alfieri, Christina M.; Hulin, Alexia ULg et al

in Arteriosclerosis, thrombosis, and vascular biology (2014), 34(12), 2601-8

OBJECTIVE: The Wnt/beta-catenin signaling pathway has been implicated in human heart valve disease and is required for early heart valve formation in mouse and zebrafish. However, the specific functions ... [more ▼]

OBJECTIVE: The Wnt/beta-catenin signaling pathway has been implicated in human heart valve disease and is required for early heart valve formation in mouse and zebrafish. However, the specific functions of Wnt/beta-catenin signaling activity in heart valve maturation and maintenance in adults have not been determined previously. APPROACH AND RESULTS: Here, we show that Wnt/beta-catenin signaling inhibits Sox9 nuclear localization and proteoglycan expression in cultured chicken embryo aortic valves. Loss of beta-catenin in vivo in mice, using Periostin(Postn)Cre-mediated tissue-restricted loss of beta-catenin (Ctnnb1) in valvular interstitial cells, leads to the formation of aberrant chondrogenic nodules and induction of chondrogenic gene expression in adult aortic valves. These nodular cells strongly express nuclear Sox9 and Sox9 downstream chondrogenic extracellular matrix genes, including Aggrecan, Col2a1, and Col10a1. Excessive chondrogenic proteoglycan accumulation and disruption of stratified extracellular matrix maintenance in the aortic valve leaflets are characteristics of myxomatous valve disease. Both in vitro and in vivo data demonstrate that the loss of Wnt/beta-catenin signaling leads to increased nuclear expression of Sox9 concomitant with induced expression of chondrogenic extracellular matrix proteins. CONCLUSIONS: beta-Catenin limits Sox9 nuclear localization and inhibits chondrogenic differentiation during valve development and in adult aortic valve homeostasis. [less ▲]

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See detailLoss of calcyphosin gene expression in mouse and other rodents
Clément, S.; Dumont, J.; Schurmans, Stéphane ULg

in Biochemical and Biophysical Research Communications (1997), 232

alcyphosine-for calcium binding and regulated by cyclic AMP through phosphorylation protein-is a target of both the cyclic AMP and the Ca(+2)-phophatidylinositol cascades first isolated from dog thyroid ... [more ▼]

alcyphosine-for calcium binding and regulated by cyclic AMP through phosphorylation protein-is a target of both the cyclic AMP and the Ca(+2)-phophatidylinositol cascades first isolated from dog thyroid, and then from rabbit and human brain. Although the exact function of this 24kD protein is unknown, calcyphosine could be implicated in the cross-signaling between these cascades to coordinate cellular proliferation and differentiation. Here, we report the sequence of a pseudogene which is the murine calcyphosine homologue, and demonstrate that it represents the unique sequence homologous to the dog calcyphosine gene in the murine genome. The lack of expression of this murine pseudogene in brain and thyroid-two major sites of dog calcyphosine expression-was extended to 5 other rodents, and suggest the existence of alternative pathway(s) to fill the function of calcyphosine in rodents [less ▲]

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See detailLoss of Elp3 Impairs the Acetylation and Distribution of Connexin-43 in the Developing Cerebral Cortex.
Laguesse, Sophie; Close, Pierre ULg; Van Hees, Laura ULg et al

in Frontiers in Cellular Neuroscience (2017), 11

The Elongator complex is required for proper development of the cerebral cortex. Interfering with its activity in vivo delays the migration of postmitotic projection neurons, at least through a defective ... [more ▼]

The Elongator complex is required for proper development of the cerebral cortex. Interfering with its activity in vivo delays the migration of postmitotic projection neurons, at least through a defective alpha-tubulin acetylation. However, this complex is already expressed by cortical progenitors where it may regulate the early steps of migration by targeting additional proteins. Here we report that connexin-43 (Cx43), which is strongly expressed by cortical progenitors and whose depletion impairs projection neuron migration, requires Elongator expression for its proper acetylation. Indeed, we show that Cx43 acetylation is reduced in the cortex of Elp3cKO embryos, as well as in a neuroblastoma cell line depleted of Elp1 expression, suggesting that Cx43 acetylation requires Elongator in different cellular contexts. Moreover, we show that histones deacetylase 6 (HDAC6) is a deacetylase of Cx43. Finally, we report that acetylation of Cx43 regulates its membrane distribution in apical progenitors of the cerebral cortex. [less ▲]

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See detailLoss of hip bone mineral density over time is associated with spine and hip fracture incidence in osteoporotic postmenopausal women.
Bruyère, Olivier ULg; Varela, A. R.; Adami, S. et al

in European journal of epidemiology (2009), 24

The objective of the study assess the relationship between bone mineral density (BMD) loss over time and fracture incidence in postmenopausal women. This is a posthoc analysis that includes women from the ... [more ▼]

The objective of the study assess the relationship between bone mineral density (BMD) loss over time and fracture incidence in postmenopausal women. This is a posthoc analysis that includes women from the placebo group of two large randomized controlled trials having assessed the efficacy of a new anti-osteoporotic drug. BMD was assessed every 6 months during 3 years at the lumbar spine, the femoral neck and the total proximal femur. Vertebral fractures were assessed using a semiquantitative method. Hip fractures were based on written documentation. All patients received calcium and vitamin D. In the present study that included 1,775 patients (with complete data at baseline and after 3 years), the logistic regression analysis, adjusted for covariates, showed that 3-year change in lumbar BMD was not statistically associated with the new vertebral fractures after 3 years. However, femoral neck and total proximal femur BMD changes was statistically correlated with the incidence of new vertebral fractures (P < 0.001). When considering change in BMD after the first year of follow-up, a decrease in total proximal femur BMD was statistically associated with an increase in the incidence of new vertebral fractures during the last 2 years of follow-up (P = 0.048). The 3-year change in femoral neck and total proximal BMD was statistically correlated with the incidence of hip and fragility fracture after 3 years (all P < 0.001). In this elderly osteoporotic population receiving calcium and vitamin D, a decrease in hip BMD after 1 or 3 year of follow-up, is associated with an increased risk of fracture incidence. However, spine BMD changes do not influence vertebral fracture incidence. [less ▲]

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See detailLoss of mitochondrial ATP synthase subunit beta (Atp2) alters mitochondrial and chloroplastic function and morphology in Chlamydomonas.
Lapaille, M.; Thiry, Marc ULg; Perez, E. et al

in Biochimica et Biophysica Acta-Bioenergetics (2010), 1797

Mitochondrial F(1)F(O) ATP synthase (Complex V) catalyses ATP synthesis from ADP and inorganic phosphate using the proton-motive force generated by the substrate-driven electron transfer chain. In this ... [more ▼]

Mitochondrial F(1)F(O) ATP synthase (Complex V) catalyses ATP synthesis from ADP and inorganic phosphate using the proton-motive force generated by the substrate-driven electron transfer chain. In this work, we investigated the impact of the loss of activity of the mitochondrial enzyme in a photosynthetic organism. In this purpose, we inactivated by RNA interference the expression of the ATP2 gene, coding for the catalytic subunit beta, in the green alga Chlamydomonas reinhardtii. We demonstrate that in the absence of beta subunit, complex V is not assembled, respiratory rate is decreased by half and ATP synthesis coupled to the respiratory activity is fully impaired. Lack of ATP synthase also affects the morphology of mitochondria which are deprived of cristae. We also show that mutants are obligate phototrophs and that rearrangements of the photosynthetic apparatus occur in the chloroplast as a response to ATP synthase deficiency in mitochondria. Altogether, our results contribute to the understanding of the yet poorly studied bioenergetic interactions between organelles in photosynthetic organisms. [less ▲]

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See detailLoss of nucleotide regulation of epithelial chloride transport in the jejunum of P2Y4-null mice
Robaye, B.; Ghanem, E.; Wilkin, F. et al

in Molecular Pharmacology (2003), 63(4), 777-783

The P2Y4 receptor is responsive to UTP in human and to ATP and UTP in rodents. With the aim of identifying its pharmacotherapeutic interest, we generated P2Y4-null mice by a classic gene targeting method ... [more ▼]

The P2Y4 receptor is responsive to UTP in human and to ATP and UTP in rodents. With the aim of identifying its pharmacotherapeutic interest, we generated P2Y4-null mice by a classic gene targeting method. The proportion of genotypes was consistent with X-linked Mendelian transmission. Gene inactivation was checked by the complete disappearance of P2Y4 receptor mRNA from liver, stomach, and intestine. The P2Y4-null mice had a grossly normal behavior, growth, and reproduction. Chloride secretion by the jejunal epithelium was assessed in Ussing chambers by the measurement of the short circuit current in the presence of phlorizin. We show here that the UTP- and ATPinduced chloride secretory responses observed in wild-type mice are abolished in P2Y4-null mice. This is the first clearcut demonstration of a biological role of the P2Y4 receptor [less ▲]

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See detailLoss of one Ha-rasl allele in some human colorectal tumours
Lambert, S. A.; Martial, Joseph ULg; Winkler, Rose ULg

in Leukemia Research (1986), 10

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See detailLoss of oocytes due to conditional ablation of Murine double minute 2 (Mdm2) gene is p53-dependent and results in female sterility.
Livera, Gabriel; Uzbekov, Rustem; Jarrier, Peggy et al

in FEBS Letters (2016), 590(16), 2566-74

Murine double minute 2 and 4 (Mdm2, Mdm4) are major p53-negative regulators, preventing thus uncontrolled apoptosis induction in numerous cell types, although their function in the female germ line has ... [more ▼]

Murine double minute 2 and 4 (Mdm2, Mdm4) are major p53-negative regulators, preventing thus uncontrolled apoptosis induction in numerous cell types, although their function in the female germ line has received little attention. In the present work, we have generated mice with specific invalidation of Mdm2 and Mdm4 genes in the mouse oocyte (Mdm2(Ocko) and Mdm4(Ocko) mice), to test their implication in survival of these germ cells. Most of the Mdm2(Ocko) but not Mdm4(Ocko) mice were sterile, with a dramatic reduction of the weight of ovaries and genital tract, a strong increase in follicle-stimulating hormone and luteinizing hormone serum levels, and a reduction of anti-mullerian hormone serum levels. Histological analyses revealed an obvious decrease of the number of growing follicles beyond the primary stage in Mdm2(Ocko) ovaries in comparison to controls, with a pronounced increase in the apparition of primary atretic follicles, most being devoid of oocyte. Similar phenotypes were observed with Mdm2(Ocko) Mdm4(Ocko) ovaries, with no worsening of the phenotype. However, we failed to detect any increase in p53 level in mutant oocytes, nor any other apoptotic marker, introgression of this targeted invalidation in p53-/- mice restored the fertility of females. This study is the first to show that Mdm2, but not Mdm4, has a critical role in oocyte survival and would be involved in premature ovarian insufficiency phenotype. [less ▲]

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See detailLoss of plant organogenic totipotency in the course of in vitro neoplastic progression
Gaspar, Thomas ULg; Kevers, Claire ULg; Bisbis, Badia et al

in In Vitro Cellular & Developmental Biology-Plant (2000), 36(3), 171-181

The aptitude for organogenesis from normal hormone-dependent cultures very commonly decreases as the tissues are serially subcultured. The reasons for the loss of regenerative ability may vary under ... [more ▼]

The aptitude for organogenesis from normal hormone-dependent cultures very commonly decreases as the tissues are serially subcultured. The reasons for the loss of regenerative ability may vary under different circumstances: genetic variation in the cell population, epigenetic changes, disappearance of an organogenesis-promoting substance, etc. The same reasons may be evoked for the progressive and eventually irreversible loss of organogenic totipotency in the course of neoplastic progressions from hormone-independent tumors and hyperhydric teratomas to cancers. As in animal cells, plant cells at the end of a neoplastic progression have probably undergone several independent genetic accidents with cumulative effects. They indeed are characterized by atypical biochemical cycles from which they are apparently unable to escape. The metabolic changes are probably not the primary defects that cause cancer, rather they may allow the cells to survive. How these changes, namely an oxidative stress, affect organogenesis is not known. The literature focuses on somatic mutations and epigenetic changes that cause aberrant regulation of cell cycle genes and their machinery. [less ▲]

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See detailLoss of Snail2 favors skin tumor progression by promoting the recruitment of myeloid progenitors
Villarejo, Ana; Molina Ortiz, Patricia ULg; Montenegro, Yenny et al

in Carcinogenesis (2015), 36(5), 585-597

Snail2 is a zinc finger transcription factor involved in driving epithelial to mesenchymal transitions. Snail2 null mice are viable, but display defects in melanogenesis, gametogenesis and hematopoiesis ... [more ▼]

Snail2 is a zinc finger transcription factor involved in driving epithelial to mesenchymal transitions. Snail2 null mice are viable, but display defects in melanogenesis, gametogenesis and hematopoiesis, and are markedly radiosensitive. Here, using mouse genetics, we have studied the contributions of Snail2 to epidermal homeostasis and skin carcinogenesis. Snail2 −/− mice presented a defective epidermal terminal differentiation and, unexpectedly, an increase in number, size and malignancy of tumor lesions when subjected to the two-stage mouse skin chemical carcinogenesis protocol, compared with controls. Additionally, tumor lesions from Snail2 −/− mice presented a high inflammatory component with an elevated percentage of myeloid precursors in tumor lesions that was further increased in the presence of the anti-inflammatory agent dexamethasone. In vitro studies in Snail2 null keratinocytes showed that loss of Snail2 leads to a decrease in proliferation indicating a non-cell autonomous role for Snail2 in the skin carcinogenic response observed in vivo. Bone marrow (BM) cross-reconstitution assays between Snail2 wild-type and null mice showed that Snail2 absence in the hematopoietic system fully reproduces the tumor behavior of the Snail2 null mice and triggers the accumulation of myeloid precursors in the BM, blood and tumor lesions. These results indicate a new role for Snail2 in preventing myeloid precursors recruitment impairing skin chemical carcinogenesis progression. [less ▲]

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See detailLoss of T cell microRNA provides systemic protection against autoimmune pathology in mice
Tian, L.; De Hertogh, G.; Fedeli, M. et al

in Journal of Autoimmunity (2012)

With an increasing number of studies demonstrating alterations in T cell microRNA expression during autoimmune disease, modulation of the T cell microRNA network is considered a potential therapeutic ... [more ▼]

With an increasing number of studies demonstrating alterations in T cell microRNA expression during autoimmune disease, modulation of the T cell microRNA network is considered a potential therapeutic strategy. Due to the complex and often opposing interactions of individual microRNA, prioritization of therapeutic targets first requires dissecting the dominant effects of the T cell microRNA network. Initial results utilizing a unidirectional screen suggested that the tolerogenic functions were dominanat, with spontaneous colitis resulting from T cell-specific excision of Dicer. Here we performed a bidirectional screen for microRNA function by removing Dicer from the T cells of both wildtype mice and Transforming Growth Factor β (TGFβ) receptor-deficient mice. This allowed the impact of microRNA loss on T cell activation, effector T cell differentiation and autoimmune pathology to be systematically assessed. This bidirectional screen revealed a dominant immunogenic functionfor T cell microRNA, with potent suppression of T cell activation, IFNγ production and autoimmune pathology in all targeted organs except the colon, where Dicer-dependent microRNA demonstrated a dominant tolerogenic function. These results reverse the original conclusions of microRNA function in T cells by revealing a systemic pro-autoimmune function. [less ▲]

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See detailThe loss of the chloride channel, ClC-5, delays apical iodide efflux and induces a euthyroid goiter in the mouse thyroid gland.
van den Hove, Marie-France; Croizet-Berger, Karine; JOURET, François ULg et al

in Endocrinology (2006), 147(3), 1287-96

Genetic inactivation of ClC-5, a voltage-gated chloride channel prominently expressed in the kidney, leads to proteinuria because of defective apical endocytosis in proximal tubular cells. Because thyroid ... [more ▼]

Genetic inactivation of ClC-5, a voltage-gated chloride channel prominently expressed in the kidney, leads to proteinuria because of defective apical endocytosis in proximal tubular cells. Because thyroid hormone secretion depends on apical endocytosis of thyroglobulin (Tg), we investigated whether ClC-5 is expressed in the thyroid and affects its function, using Clcn5-deficient knockout (KO) mice. We found that ClC-5 is highly expressed in wild-type mouse thyroid ( approximately 40% of mRNA kidney level). The protein was immunolocalized at the apical pole of thyrocytes. In Percoll gradients, ClC-5 overlapped with plasma membrane and early endosome markers, but best codistributed with the late endosomal marker, Rab7. ClC-5 KO mice were euthyroid (normal T4 and TSH serum levels) but developed a goiter with parallel iodine and Tg accumulation (i.e. normal Tg iodination level). When comparing ClC-5 KO with wild-type mice, thyroid 125I uptake after 1 h was doubled, incorporation into Tg was decreased by approximately 2-fold, so that trichloroacetic acid-soluble 125I increased approximately 4-fold. Enhanced 125I- efflux upon perchlorate and presence of 125I-Tg as autoradiographic rings at follicle periphery demonstrated delayed iodide organification. Endocytic trafficking of 125I-Tg toward lysosomes was not inhibited. Expression of pendrin, an I-/Cl- exchanger involved in apical iodide efflux, was selectively decreased by 60% in KO mice at mRNA and protein levels. Thus, ClC-5 is well expressed in the thyroid but is not critical for apical endocytosis, contrary to the kidney. Instead, the goiter associated with ClC-5 KO results from impaired rate of apical iodide efflux by down-regulation of pendrin expression. [less ▲]

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See detailLoss of the VHR dual-specific phosphatase causes cell-cycle arrest and senescence
Rahmouni, Souad ULg; Cerignoli, Fabio; Alonso, Andres et al

in Nature Cell Biology (2006), 8(5), 524-178

Protein tyrosine phosphatases regulate important processes in eukaryotic cells and have critical functions in many human diseases including diabetes to cancer(1-3). Here, we report that the human Vaccinia ... [more ▼]

Protein tyrosine phosphatases regulate important processes in eukaryotic cells and have critical functions in many human diseases including diabetes to cancer(1-3). Here, we report that the human Vaccinia H1-related (VHR) dual-specific protein tyrosine phosphatase regulates cell-cycle progression and is itself modulated during the cell cycle. Using RNA interference (RNAi), we demonstrate that cells lacking VHR arrest at the G1-S and G2-M transitions of the cell cycle and show the initial signs of senescence, such as flattening, spreading, appearance of autophagosomes, beta-galactosidase staining and decreased telomerase activity. In agreement with this notion, cells lacking VHR were found to upregulate p21(Cip-Waf1), whereas they downregulated the expression of genes for cell-cycle regulators, DNA replication, transcription and mRNA processing. Loss of VHR also caused a several-fold increase in serum-induced activation of its substrates, the mitogen-activated protein ( MAP) kinases Jnk and Erk. VHR-induced cell-cycle arrest was dependent on this hyperactivation of Jnk and Erk, and was reversed by Jnk and Erk inhibition or knock-down. We conclude that VHR is required for cell-cycle progression as it modulates MAP kinase activation in a cell-cycle phase-dependent manner. [less ▲]

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See detailLoss of the Y Chromosome in Bone Marrow Cells: Results on 1907 Consecutive Cases of Leukaemia and Preleukaemia
Herens, Christian ULg; Brasseur, Edmond ULg; Jamar, Michelle ULg et al

in Clinical & Laboratory Haematology (1999), 21(1), 17-20

Loss of the Y chromosome with a resulting 45, X0 karyotype is observed in normal bone marrow cells of elderly males but also in haematological malignancies. Whether Y loss in neoplastic cells is related ... [more ▼]

Loss of the Y chromosome with a resulting 45, X0 karyotype is observed in normal bone marrow cells of elderly males but also in haematological malignancies. Whether Y loss in neoplastic cells is related to the process seen in normal ageing or is part of the carcinogenic process is unknown. The present study concerns the cytogenetic data from 1907 consecutive leukaemic or preleukaemic male patients with special regard to the presence or absence of the Y chromosome. Sixty-five patients (3.4%) had a 45, X-Y clone in their bone marrow (BM) cells. Loss of Y was rare below the age of 50 but increased in older patients, reaching 25% of the men over 80. Sixteen patients (0.08%) had more than 90% X0 cells in their BM. A correlation between Y loss and leukaemia could be established in seven cases, three of which were acute myeloid leukaemia M2 subtype where -Y is known to be a secondary event. In three other cases, -Y was part of a complex karyotype. Only one patient exhibited a 45, X0 karyotype, with no other rearrangement, that could be positively correlated with the neoplastic process. [less ▲]

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