RESUMO
BACKGROUND: KRAS mutations are common and clearly contribute to malignant progression. The frequency of NRAS mutations and their relationship to clinical, pathologic, and molecular features remains unclear. METHODS: We evaluated 130 colorectal tumors for mutations in KRAS and NRAS gene. We tested for mutations in codons 61 and 146 of KRAS and codons 12, 13, 59, 61 and 146 of NRAS. Mutation status was determined by targeted dideoxy sequencing. RESULTS: Among the analyzed primary tumors, 36.2% had KRAS mutation. Of the 83 KRAS codon 12 and 13 wild-type patients, 7.2% had KRAS codon 61, 146 or NRAS. 40.7% harbored any RAS mutation. CONCLUSION: The frequency of other RAS (NRAS and KRAS exon 3, 4) activating mutations in colorectal cancers is relatively low in Korean colorectal cancer patients.
Assuntos
Adenocarcinoma Mucinoso/genética , Adenocarcinoma/genética , Carcinoma de Células em Anel de Sinete/genética , Neoplasias Colorretais/genética , GTP Fosfo-Hidrolases/genética , Proteínas de Membrana/genética , Mutação/genética , Proteínas Proto-Oncogênicas p21(ras)/genética , Adenocarcinoma/secundário , Adenocarcinoma Mucinoso/secundário , Adulto , Idoso , Idoso de 80 Anos ou mais , Biomarcadores Tumorais/genética , Carcinoma de Células em Anel de Sinete/secundário , Neoplasias Colorretais/patologia , Feminino , Seguimentos , Humanos , Metástase Linfática , Masculino , Pessoa de Meia-Idade , Estadiamento de Neoplasias , Prognóstico , República da CoreiaRESUMO
This study aimed to investigate the potential association of TYK2 and STAT3 genes with the susceptibility to Crohn's disease (CD) among Malaysians. DNA samples were obtained from 80 CD patients and 100 healthy controls. Polymerase chain reaction-restriction fragment length polymorphism methods were employed for genotyping, followed by statistical analysis. In our current study, none of the single nucleotide polymorphisms of either TYK2 or STAT3 was statistically associated with the susceptibility to CD in our local population (P > 0.05). In contrast, there was a statistically significant association between the G/G homozygotes of the STAT3 rs2293152 and the healthy control group (χ(2) = 6.229, P < 0.05). In conclusion, our study does not support the role of the TYK2 and STAT3 genes influencing CD susceptibility.
Assuntos
Povo Asiático/genética , Doença de Crohn/genética , Fator de Transcrição STAT3/genética , TYK2 Quinase/genética , Frequência do Gene , Predisposição Genética para Doença , Genótipo , Heterozigoto , Homozigoto , Humanos , Malásia , Polimorfismo de Fragmento de Restrição , Polimorfismo de Nucleotídeo ÚnicoRESUMO
The protein product of the c-fos proto-oncogene was immunocytochemically localized in forebrain regions of adult male Lewis rats subjected to a physically aversive footshock stimulus or a Pavlovian-conditioned, non-aversive, auditory stimulus. Animals receiving the conditioned stimulus were first conditioned by repeatedly pairing electric footshock, the unconditioned stimulus (US), with an auditory cue, the conditioned stimulus (CS). These animals were later tested with the CS in the absence of the US, a procedure which, like footshock itself, suppresses immune function. In animals exposed to the conditioned or unconditioned stressor, c-Fos was strongly expressed in cells of the paraventricular nuclei (PVN) of the hypothalamus, some of which contain corticotropin-releasing hormone (CRH), and other forebrain areas directly associated with autonomic function, the ventral lateral septal nuclei (LSV), the medial amygdaloid nuclei (AME), the sensorimotor cortex, the basal ganglia and thalamic nuclei. Control animals exhibited very little or no c-Fos in the above areas. The identified forebrain nuclei can now be targeted for further study aimed at elucidating their role in stress-induced immune alteration.