Latency today : considerations on children in psychotherapy

A latência é o período do desenvolvimento menos abordado pela literatura psicanalítica e menos compreendido, apesar de corresponder à idade na qual ocorre a maior procura por atendimento psicológico. Além disso, questiona-se um possível encurtamento do período da latência em nossa cultura. Partindo desses apontamentos, este estudo tem como objetivo descrever os conflitos e as defesas de crianças que buscaram atendimento psicoterápico em um serviço-escola, verificando se estas apresentariam as características típicas da latência. Foi realizado um estudo de caso coletivo com oito crianças com idade entre 7 e 9 anos, o qual consistia em um encontro de testagem para a aplicação dos testes psicológicos CBCL, Teste de Bender, Desenho da Figura Humana e Teste das Fábulas. Como resultado, foi possível identificar que algumas crianças apresentaram características típicas da latência, demonstrando intenso uso de mecanismos de defesa a fim de lidar com os conflitos advindos do Complexo de Édipo.The latency period is the least developed on psychoanalytic literature and also the least comprehended, although is the age which constitutes the largest proportion of psychological demand care in childhood. Moreover, the issue about a possible shortening of the latency period in our culture is being thought. Based on these ideas, the present study aims to describe the conflicts and the defenses of children who sought psychotherapy at a service-school, verifying if such children would present the characteristics of a work of latency. This was a collective case study with eight children aged between 7 and 9 years, which consisted on a testing date for application of psychological tests CBCL, Teste de Bender, Desenho da Figura Humana e Teste das Fábulas. As a result, it was possible to identify some children who had typical features of this period, showing intense use of defense mechanisms to deal with conflicts derivated from the Oedipus complex

BRCA2 polymorphic stop codon K3326X and the risk of breast, prostate, and ovarian cancers

Background: The K3326X variant in BRCA2 (BRCA2*c.9976A>T; p.Lys3326*; rs11571833) has been found to be associated with small increased risks of breast cancer. However, it is not clear to what extent linkage disequilibrium with fully pathogenic mutations might account for this association. There is scant information about the effect of K3326X in other hormone-related cancers. Methods: Using weighted logistic regression, we analyzed data from the large iCOGS study including 76 637 cancer case patients and 83 796 control patients to estimate odds ratios (ORw) and 95% confidence intervals (CIs) for K3326X variant carriers in relation to breast, ovarian, and prostate cancer risks, with weights defined as probability of not having a pathogenic BRCA2 variant. Using Cox proportional hazards modeling, we also examined the associations of K3326X with breast and ovarian cancer risks among 7183 BRCA1 variant carriers. All statistical tests were two-sided. Results: The K3326X variant was associated with breast (ORw = 1.28, 95% CI = 1.17 to 1.40, P = 5.9x10- 6) and invasive ovarian cancer (ORw = 1.26, 95% CI = 1.10 to 1.43, P = 3.8x10-3). These associations were stronger for serous ovarian cancer and for estrogen receptor–negative breast cancer (ORw = 1.46, 95% CI = 1.2 to 1.70, P = 3.4x10-5 and ORw = 1.50, 95% CI = 1.28 to 1.76, P = 4.1x10-5, respectively). For BRCA1 mutation carriers, there was a statistically significant inverse association of the K3326X variant with risk of ovarian cancer (HR = 0.43, 95% CI = 0.22 to 0.84, P = .013) but no association with breast cancer. No association with prostate cancer was observed. Conclusions: Our study provides evidence that the K3326X variant is associated with risk of developing breast and ovarian cancers independent of other pathogenic variants in BRCA2. Further studies are needed to determine the biological mechanism of action responsible for these associations

Functional mechanisms underlying pleiotropic risk alleles at the 19p13.1 breast-ovarian cancer susceptibility locus

A locus at 19p13 is associated with breast cancer (BC) and ovarian cancer (OC) risk. Here we analyse 438 SNPs in this region in 46,451 BC and 15,438 OC cases, 15,252 BRCA1 mutation carriers and 73,444 controls and identify 13 candidate causal SNPs associated with serous OC (P=9.2 × 10-20), ER-negative BC (P=1.1 × 10-13), BRCA1-associated BC (P=7.7 × 10-16) and triple negative BC (P-diff=2 × 10-5). Genotype-gene expression associations are identified for candidate target genes ANKLE1 (P=2 × 10-3) and ABHD8 (P<2 × 10-3). Chromosome conformation capture identifies interactions between four candidate SNPs and ABHD8, and luciferase assays indicate six risk alleles increased transactivation of the ADHD8 promoter. Targeted deletion of a region containing risk SNP rs56069439 in a putative enhancer induces ANKLE1 downregulation; and mRNA stability assays indicate functional effects for an ANKLE1 3′-UTR SNP. Altogether, these data suggest that multiple SNPs at 19p13 regulate ABHD8 and perhaps ANKLE1 expression, and indicate common mechanisms underlying breast and ovarian cancer risk

Functional mechanisms underlying pleiotropic risk alleles at the 19p13.1 breast-ovarian cancer susceptibility locus

A locus at 19p13 is associated with breast cancer (BC) and ovarian cancer (OC) risk. Here we analyse 438 SNPs in this region in 46,451 BC and 15,438 OC cases, 15,252 BRCA1 mutation carriers and 73,444 controls and identify 13 candidate causal SNPs associated with serous OC (P = 9.2 x 10(-20)), ER-negative BC (P = 1.1 x 10(-13)), BRCA1-associated BC (P = 7.7 x 10(-16)) and triple negative BC (P-diff = 2 x 10(-5)). Genotype-gene expression associations are identified for candidate target genes ANKLE1 (P = 2 x 10(-3)) and ABHD8 (PPeer reviewe

BRCA2 Polymorphic Stop Codon K3326X and the Risk of Breast, Prostate, and Ovarian Cancers

To access publisher's full text version of this article click on the hyperlink at the bottom of the pageGovernment of Canada through Genome Canada Canadian Institutes of Health Research Ministere de l'Economie, de l'Innovation et des Exportations du Quebec through Genome Quebec National Health and Medical Research Council (NHMRC) Senior Research Fellowship Australian NHMRC Project 1010719 National Institutes of Health (NIH) CA128978 CA116167 NIH specialized program of research excellence in breast cancer P50 CA116201 Breast Cancer Research Foundation Consortium of Investigators of Modifiers of BRCA1/2 (CIMBA) data management and analysis through Cancer Research-UK grant C12292/A11174 Cancer Research UK C1287/A10118 C1287/A12014 C1287/A 10710 C12292/ A11174 C1281/A12014 C5047/A8384 C5047/A15007 C5047/ A10692 C8197/A16565 European Community's Seventh Framework Programme 223175 (HEALTH-F2-2009-223175) European Union COST programme BM0606 Ovarian Cancer Research Fund PPD/RPCI.07 US National Cancer Institute Genetic Associations and Mechanisms in Oncology (GAME-ON) Post-Genome Wide Association Study (GWAS) Initiative U19-CA148112 Wellcome Trust 076113 European Community's Seventh Framework Programme (COGS) 223175 (HEALTH-F2-2009-223175) National Institutes of Health CA128978 Post-Cancer GWAS initiative (GAME-ON initiative) 1U19 CA148537 1U19 CA148065 1U19 CA148112 Department of Defence W81XWH-10-1-0341 Canadian Institutes of Health Research (CIHR) for the CIHR Team in Familial Risks of Breast Cancer, Komen Foundation for the Cure Breast Cancer Research Foundation, Ovarian Cancer Research Fundinfo:eu-repo/grantAgreement/EC/FP7/22317

BRCA2 Polymorphic Stop Codon K3326X and the Risk of Breast, Prostate, and Ovarian Cancers

Background: The K3326X variant in BRCA2 (BRCA2∗c.9976A>T p.Lys3326∗rs11571833) has been found to be associated with small increased risks of breast cancer. However, it is not clear to what extent linkage disequilibrium with fully pathogenic mutations might account for this association. There is scant information about the effect of K3326X in other hormonerelated cancers. Methods: Using weighted logistic regression, we analyzed data from the large iCOGS study including 76637 cancer case patients and 83796 control patients to estimate odds ratios (ORw) and 95% confidence intervals (CIs) for K3326X variant carriers in relation to breast, ovarian, and prostate cancer risks, with weights defined as probability of not having a pathogenic BRCA2 variant. Using Cox proportional hazards modeling, we also examined the associations of K3326X with breast and ovarian cancer risks among 7183 BRCA1 variant carriers. All statistical tests were two-sided. Results: The K3326X variant was associated with breast (ORw = 1.28, 95% CI = 1.17 to 1.40, P = 5.9×10-6) and invasive ovarian cancer (ORw = 1.26, 95% CI = 1.10 to 1.43, P = 3.8×10-3). These associations were stronger for serous ovarian cancer and for estrogen receptor-negative breast cancer (ORw = 1.46, 95% CI = 1.2 to 1.70, P = 3.4×10-5 and ORw = 1.50, 95% CI = 1.28 t

Functional mechanisms underlying pleiotropic risk alleles at the 19p13.1 breast-ovarian cancer susceptibility locus

10.1038/ncomms12675NATURE COMMUNICATIONS7