Disease relevance of FES

• FES was observed in the nuclear, granular and plasma membrane fractions of primary human neutrophils and the myeloid leukemia cell line, HL-60 [1].
• Conversely, FES and KDR gene expression was lost in most advanced primary and metastatic melanomas [2].
• The human germ-line positions of the oncogenes ABL, SIS, and FES, the cellular counterparts of the v-onc genes of Abelson murine leukemia virus, simian sarcoma virus, and feline sarcoma virus, respectively, have been determined by in situ molecular hybridization of 3H-labeled v-onc gene probes to meiotic pachytene chromosomes [3].
• DNA copy number changes and evaluation of MYC, IGF1R, and FES amplification in xenografts of pancreatic adenocarcinoma [4].
• In order to understand the structural features that might lead to an estrogen receptor (ER) based breast tumor imaging agent with improved uptake characteristics, we have synthesized several new analogs of 16 beta-fluoroestradiol (beta FES) and studied their tissue distribution in immature rats [5].

Psychiatry related information on FES

• This paper aimed to examine the relationship between the trichotomous symptom structure of psychopathology and neuropsychological functioning in young people with first episode schizophrenia (FES), most of whom were receiving atypical antipsychotic medication [6].
• Finally, correlation analyses showed that for FES participants both executive and language tests significantly correlated with ANWLG total responses, while the correlation between ANWLG and only 1 language test was significant for LTLE participants [7].
• Forty-three adolescents with anorexia nervosa and 85 controls were administered the EAT, EDI, and FES [8].
• A total of 316 adolescents completed the self-administered questionnaire: The DSD, Somatic Symptom Scale, SAFE-C, FES, Coping, and Rosenberg's Self-Esteem Scale [9].
• Although ample research has documented the utility of the FES in predicting important cognitive and behavioral outcomes, psychometric data on the scale are lacking [10].

High impact information on FES

• Expression of the 93-kd tyrosine kinase encoded by the human c-fes proto-oncogene (also known as FES) is restricted to mature hematopoietic cells of the granulocytic and monocytic lineages, suggestive of a function essential to normal myeloid differentiation [11].
• Therefore, BLM, the gene that when mutated gives rise to Bloom syndrome, is tightly linked to FES, a gene whose chromosome position is known to be 15q26 [12].
• The locus mutated in BS, BLM, maps to chromosome subband 15q26.1, tightly linked to the proto-oncogene FES [13].
• A striking association of the C3 allele at FES with blm (delta = .422; p = 5.52 x 10(-7)) and of the 145-bp and 147-bp alleles at D15S127 with blm (delta = .392 and delta = .483, respectively; p = 2.8 x 10(-5) and p = 5.4 x 10(-7), respectively) was detected in Ashkenazi Jews with BS [13].
• We demonstrate herein that IL-4 stimulation induced rapid association of FES or a related protein with PI3 kinase in mouse T-cell lines [14].

Chemical compound and disease context of FES

• The positron-emitting estrogenic steroid 16 alpha-[18F]fluoro-17 beta-estradiol (FES) has been shown to exhibit selective uptake in primary breast carcinomas; the uptake of tracer by positron emission tomography (PET) is strongly correlated with the tumor estrogen-receptor concentration [15].
• Eleven postmenopausal women with biopsy-proved estrogen receptor-positive (ER+) metastatic breast cancer were studied by PET with FDG and 16alpha[18F]fluoro-17beta-estradiol (FES) before and 7-10 days after initiation of tamoxifen therapy [16].
• Ten persons with quadriplegia (C5 to C7) and eight with paraplegia (T4 to T11) performed FES-LCE training on an ERGYS I ergometer 10 to 30 minutes per day, 2 or 3 days per week for 12 to 16 weeks (36 total sessions) [17].
• OBJECTIVES: Evaluation of a FES (Functional Electrical Stimulation) device for the relief of postural hypertension and augmentation of cough in a C3 ventilator-dependent tetraplegic [18].

Biological context of FES

• We also show an association of human FES (hFES) with the src homology 2 (SH2) domain of PI3 kinase in a COS7 cell expression system [14].
• Co-expression with BCR induces activation of the FES tyrosine kinase and phosphorylation of specific N-terminal BCR tyrosine residues [19].
• Tetranucleotide repeat polymorphism at the human c-fes/fps proto-oncogene (FES) [20].
• To better understand the role played by FES in normal and neoplastic hematopoiesis, we used cell fractionation techniques to examine the subcellular localization of FES in myeloid cells and cell lines [1].
• Interestingly, however, when these genes were assigned to bovine syntenic groups utilizing a panel of bovine: hamster hybrid somatic cells, IGH genes were shown to be syntenic with the FES oncogene rather than FOS [21].

Anatomical context of FES

• FES is a non-receptor protein tyrosine kinase expressed in hematopoietic progenitors and differentiated myeloid cells [1].
• Localization of the cellular oncogenes ABL, SIS, and FES on human germ-line chromosomes [3].
• The FES oncogene was previously localized to human chromosome 15 by analysis of mouse x human somatic cell hybrids and to 15q26 by in situ hybridization of a radioactively labeled probe [22].
• The FES patients exhibited widespread GM reductions in the frontal, parietal, and temporal cortices and cerebellum in the baseline condition, as well as more circumscribed regions of GM increase, particularly in the occipital lobe [23].
• In airway mucosa, two layers of FES are discernible: one superficial network, attached to the basement membrane, and a deeper network, lying close to the airway smooth muscle [24].

Associations of FES with chemical compounds

• Furthermore, tyrosine phosphorylated FES or the closely related protein is found associated with the IL-4R [25].
• This result, along with the prior assignment of the loci for mitochondrial isocitrate dehydrogenase and FES to human chromosome 15 and mouse chromosome 7, suggest a conserved autosomal synteny group on the distal long arm of HSA15 and in the center of MMU7 [26].
• This linkage disequilibrium constitutes strong support for a founder-effect hypothesis: the chromosome in the hypothetical founder who carried blm also carried the C3 allele at FES and either the 145-bp or the 147-bp allele at D15S127 [13].
• We also wanted to establish the dose level of the anti-estrogen tamoxifen required to block target tissue uptake of FES [27].
• We have measured in vivo the uptake of 16 alpha-[18F]estradiol (FES) by target tissues in the immature rat at increasing dose levels (obtained by dilution of [18F]FES with unlabeled estradiol) [27].
• FES is phosphorylated on tyrosine residues in cells that carry KIT(D816V) mutation, and this phosphorylation is KIT dependent [28].

Physical interactions of FES

• Through a deletion analysis of the IL-4R we have identified a putative FES-binding site in the cytoplasmic domain of the IL-4R [25].

Regulatory relationships of FES

• The FER gene is evolutionarily conserved and encodes a widely expressed member of the FPS/FES protein-tyrosine kinase family [29].

Other interactions of FES

• Previous work in our laboratory has established that BCR is a substrate for c-FES, a non-receptor tyrosine kinase linked to myeloid growth and differentiation [19].
• The relationship between her genotype and phenotype are discussed in light of genes, including IGF1R and FES, mapped to the aneusomic segment [30].
• FES at 15q26.1 is also distal to the breakpoint in chromosome 15 in the translocation commonly seen in acute promyelocytic leukemia, t(15;17) (q24;q22) [3].
• LOMs (STRs: CD4, FES, F13B, TH01) are characterised by a number of repeats between 5-15 and a stable repeat sequence [31].
• Comparing the genomic structure of CSK with the exon/intron organisation of both, it is obvious that the exon/intron boundaries are in common either with those of the SRC-type or the FES boundaries [32].

Analytical, diagnostic and therapeutic context of FES

• Confirmation of 15q26.1 as the site of the FES protooncogene by fluorescence in situ hybridization [22].
• Forty-one patients with FES and 47 matched healthy controls underwent a T1-weighted structural MRI scan [23].
• Detrusor activity was inhibited by FES (functional electrical stimulation) applied to the anal sphincter causing decreased bladder spasticity and increased bladder capacity [33].
• Data on the incomes of families with a severely disabled child were obtained by replicating the Family Expenditure Survey. These data were compared with income data from a control group of families with children, drawn from the FES for the same period [34].
• Effects of joint motion constraints on the gait of normal subjects and their implications on the further development of hybrid FES orthosis for paraplegic persons [35].

References