Disease relevance of MOS

• RESULTS: The principal meiotic regulator MOS was found to be significantly post-transcriptionally up-regulated after irradiation in p53 mutated but not p53 wild-type lymphoma cells [1].
• The c-mos proto-oncogene is the cellular counterpart of the viral oncogene v-mos isolated from Moloney murine sarcoma virus [2].
• The 5-kb allele of the MOS oncogene, previously proposed to be associated with breast cancer, was absent in these families, suggesting that polymorphism at this locus is not associated with inherited susceptibility [3].
• PURPOSE: To estimate the duration of survival (S) of patients with metastatic osteosarcoma (MOS) at diagnosis treated with a multiagent, ifosfamide-containing chemotherapeutic and surgical regimen and to evaluate the toxicity of this regimen [4].
• Hormone levels, quality of life (MOS Short-Form Health Survey), sexual function (International Index of Erectile Function), benign prostate hyperplasia severity (American Urological Association Symptom Index Score), prostate-specific antigen, and measures of safety were compared among groups [5].

Psychiatry related information on MOS

• Functional status was assessed by questionnaires characterizing walking ability (Walking Impairment Questionnaire, WIQ), habitual physical activity level (Physical Activity Recall, PAR), and physical, social, and role functioning, well-being, and overall health (Medical Outcomes Study SF-20, MOS) [6].
• The subscale, Mental Health, from the MOS SF-20 was used to assess affective well-being [7].
• CONCLUSIONS: In general, the 5 translations of the MOS HIV had similar psychometric properties to those reported in the validation study for the original US English version of the MOS HIV [8].
• Patient's self-assessment of QL was measured with the 36-item MOS Short Form (SF-36) [9].
• In this last group, among patients with similar levels of symptom severity, organic perceived causes were related to a lower physical health sum score on the MOS Short Form, and psychosocial perceived causes were related to less severe depressive symptoms, assessed with the Hospital Anxiety and Depression Scale at 6 months [10].

High impact information on MOS

• Mo-MSV DNA synthesized in vitro was found to induce morphological transformation of NIH-3T3 mouse fibroblasts upon transfection [11].
• The genome of MSV was shown to retain approximately 0.13 kb from the 5' end of the MuLV env region, including sequences which span the point in the MuLV env mRNA [12].
• When transformants derived by transfection with 5.8 kbp dsDNA were infected with Moloney murine leukemia virus (Mo-MLV) helper virus, Mo-MSV was rescued from a small portion of these cells, suggesting the establishment of the complete viral genome in these cells [11].
• The foci had a morphology indistinguishable from that of Mo-MSV-induced foci, and the induced transformed phenotype was stable [11].
• This DNA species has been purified by sedimentation of total in vitro synthesized Mo-MSV DNA through neutral sucrose gradients [11].

Chemical compound and disease context of MOS

• RESULTS: The MOS/ADR1 and MOS/IR1 cells were sevenfold and fivefold more resistant to doxorubicin than the parental murine osteosarcoma cells [13].
• METHODS: A total of 47 PD patients completed the Kidney Disease Quality of Life (KD-QOL) scale encompassing the Medical Outcomes Study Short-Form (MOS SF-36) self-administered questionnaire, the Multidimensional Health Locus of Control scale and the Ways of Coping Check-List (WCCL) scale [14].
• The presence of sleep disorders and the characteristics of the BDZ used were not associated with any score in the MOS SF-36 questionnaire, whereas the Prime diagnosis was the most important predictor, since subjects with depression and/or anxiety had a lower mean score on each scale than subjects without disorders [15].
• Other endpoints included evaluation over 3 months of low back pain intensity scale, Roland-Morris Disability Questionnaire (RMDQ), low back pain bothersomeness scale, patient- and investigator-global assessments, Patient Health Survey (MOS SF-12), rescue acetaminophen use, and discontinuation due to lack of efficacy [16].
• 9-(2-Phosphonylmethoxyethyl)adenine (PMEA) is a potent and selective inhibitor of the in vitro replication of a number of retroviruses, including HIV-1 and HIV-2, simian immunodeficiency virus (SIV), simian AIDS-related virus (SRV), feline immunodeficiency virus (FIV) and Moloney murine sarcoma virus (MSV) [17].

Biological context of MOS

• The maximum expression of MOS coincided with the maximal fraction of metaphase arrested cells and was directly proportional to both the extent of the arrest and the number of endopolyploid cells that subsequently emerged [1].
• Furthermore, we suggest that the coordinated expression of MOS and REC8 regulate the extent of arrested mitoses and polyploidy [1].
• By both in situ hybridization and molecular hydridization to sorted chromosome DNA (using a c-mos probe) we have localized the c-mos gene to band 8q11 [2].
• Human proto-oncogene c-mos maps to 8q11 [2].
• The c-mos gene locus has previously been assigned to human chromosome 8 [2].

Anatomical context of MOS

• Oocyte maturation is triggered by steroids in a transcription-independent fashion that involves an unusual positive feedback loop whereby MOS (a germ cell-specific Raf) activates MEK1, which in turn activates ERK2 [18].
• Cell cycle genes c-mos and cyclin-B1 are expressed in a specific pattern in human oocytes and preimplantation embryos [19].
• The proto-oncogene c-mos was expressed in an oocyte-specific manner and no mRNA for c-mos could be detected in the granulosa cells [19].
• Morphologically, the MOS/ADR1 cell line was composed of polygonal cells, whereas the MOS/IR1 cell line consisted of plump spindle cells with long cytoplasmic processes [13].
• Permeabilization of the plasma membrane by saponin increased both the accumulation of doxorubicin (p < 0.05) and the cytotoxic activity of this drug in all lines, but the effects were most pronounced in the MOS/IR1 cells [13].

Associations of MOS with chemical compounds

• The organic solvent was then evaporated to dryness and the residue reconstituted in 100 microliters of mobile phase prior to injecting a 20 microliters aliquot onto a Hypersil 5 MOS column, which was eluted with acetonitrile/acetate buffer (pH 5.5) 36:64 vol/vol [20].
• Ratings of current health and health free of angina using a verbal rating scale in which 0 = death and 100 = perfect health, the MOS SF-36, the Index of Coexistent Disease (a validated measure of comorbidity), and a question on the severity of anginal symptoms [21].
• The MOS/ADR1 cells were found to exhibit cross-resistance only to substrates for P-glycoprotein (such as doxorubicin, vincristine, and etoposide), whereas the MOS/IR1 cells were resistant to all of the drugs studied (including cisplatin and methotrexate) [13].
• The addition of a P-glycoprotein antagonist, verapamil, or the depletion of cellular adenosine triphosphate resulted in a marked increase in the accumulation of doxorubicin in the MOS/ADR1 cells (p < 0.05) but not in the MOS/ IR1 cells [13].
• At baseline and follow-up (20 weeks), subjects completed a questionnaire that included the 20 item MOS Short-Form Health Survey, Multidimensional Health Locus of Control Scale, and Philadelphia Geriatric Center Morale Scale, and bone density was measured by dual energy X-ray absorptiometry [22].

Other interactions of MOS

• ERK2 then acts back on MOS to enhance its expression and amplify the kinase signaling cascade [18].
• Detailed signaling studies reveal that Paxillin is acting early in the kinase cascade, because it is required for accumulation of MOS protein and complete activation of downstream kinase signaling in response to steroids [18].
• METHODS: We analysed the HRQL evolution over 5 years for 1,000 patients initiating a protease inhibitor (PI)-containing therapy, using MOS SF-36 physical (PCS) and mental (MCS) scores [23].
• The transient expression of c-mos and high levels of cyclin-B1 mRNA suggest that mechanisms similar to those found in lower organisms govern the growth and development of the human oocyte and preimplantation embryo [19].
• Since the long arm of chromosome 8 is frequently the site of increased gene copy number (ICN) in breast cancer, we screened 442 breast tumor DNAs for gains of E2F5, MOS, and MYC genes [24].

Analytical, diagnostic and therapeutic context of MOS

• Mortality was registered and MOS 36 Short-Form Health Survey answered at baseline and after 3, 6 and 12 months [25].
• A cross-sectional study was performed on the association between general health status, as determined by the MOS, with sleepiness, assessed using a standardized questionnaire [the Epworth sleepiness scale (ESS)] and the multiple sleep latency test (MSLT) [26].
• The MOS 36 item short form health survey questionnaire (SF-36) is widely acknowledged as the gold standard generic measure of health status; few studies however have evaluated its use for clinical trials in multiple sclerosis [27].
• RESULTS: TMLR patients scored significantly better compared to controls in the MOS SF-24 social functioning, energy, general health, and bodily pain domains, in the EuroQol usual activity domain and the EuroQol Visual Analogue Scale, and in the SAQ physical limitation, angina frequency and disease perception domains [28].
• The MOS short-form general health survey. Reliability and validity in a patient population [29].

References