Although this result is currently a matter of controversy, further studies must be independently repeated to be conclusive; -- another RFLP was found in c-mos proto-oncogene, which is detected only in patients with breast cancers or other types of tumors.
There was up to 5-fold enrichment of the targeted MSV in the bone marrow of mice bearing early or late stage MDA-MB-231 tumors and of mice with late stage, but not early stage, MCF-7 tumors.
How this process occurs and more importantly, why, has recently become the focus of several research groups, prompting this review in which we discuss two related phenomena that accompany the reversible polyploidy of tumor cells: the induction of meiosis genes such as MOS and the decrease in genomic instability observed during the reversion from polyploidy to para-diploidy.
Female transgenic mice lacking a functional c-mos proto-oncogene develop ovarian teratomas, indicating that c-mos may behave as a tumour-suppressor gene for this type of tumour.
In the present report, we examine, in a series of non-small cell lung carcinomas (NSCLCs), the status of K-ras and c-mos oncoproteins in correlation with the tumor neo-angiogenesis state and the major angiogenic factor, vascular endothelial growth factor (VEGF).
We carried out direct sequence analysis of human c-mos and human ENRB in a series of sporadic MTC and phaeochromocytomas to determine if somatic mutations in these two genes could account for some of the sporadic MEN 2-related tumours in which no RET mutations are detected.No somatic mutations were found.
Rhim et al. were first to show that superinfection of Ad12-SV40-infected immortalized human epidermal cells with an RNA tumor virus containing a ras oncogene, such as Ki-MSV, or their treatment with chemical carcinogens, leads to the ability of cells to both grow in anchorage-independent fashion and to form tumors in athymic nude mice.
The occurrence of rare hypervariable Ha-ras alleles or of a rare c-mos allele in white blood cell DNA is claimed to be associated with susceptibility to cancer.
To determine whether the c-mos oncogene has been translocated in AML-M2 with this translocation and to isolate DNA sequences and genes from these two chromosomes that may be important in malignancy, we constructed somatic cell hybrids between a Chinese hamster ovary cell (CHO) mutant defective in glycine metabolism and myeloblasts with an 8;21 translocation from a patient with AML.
The scores in all sleep dimensions of the MOS-sleep were higher in CPP (more disturbances) compared to pain free patients, and differences were observed among the three groups of PCP, with FM most severely affected.
At month 3, statistically significant improvements from baseline versus placebo were reported in PtGA, Pain, HAQ DI, all 8 SF-36 domains, FACIT-F, and MOS Sleep with tofacitinib 10 mg BID, and in PtGA, Pain, HAQ DI, 7 SF-36 domains, FACIT-F, and MOS Sleep with tofacitinib 5 mg BID.
Pain and Medical Outcomes Study Sleep questionnaire (MOS-Sleep) were assessed at baseline and 3 months after opioid titration in 231 opioid naïve CNCP patients.
This longitudinal mailed survey study examined Health Promoting Lifestyle Profile II (HPLP) scores and MOS SF 36 scores as predictors of PROMIS® Pain Interference, Pain Intensity, Fatigue, Sleep Disturbance, and Applied Cognition Abilities Scores among 260 adults with MS.
The Brief Pain Inventory (BPI), Hospital Anxiety and Depression Scale (HADS), and sleep scale developed for the MOS study (MOS-SQ) were used to measure pain features and psychosocial adjustment.
Another protooncogene, c-mos, is also retained at the conserved junction, suggesting that one or both of these genes may play a role in the pathogenesis of acute myelogenous leukemia.
We isolated the 21q+ chromosome of this translocation in a somatic cell hybrid and showed that the c-mos oncogene had not been translocated to chromosome 21, ruling out the possibility that translocation of c-mos to chromosome 21 is necessary for development of AML-M2.
The findings in the former patient suggest that either c-mos is not involved in the etiology of M2-ANLL or, alternatively, if c-mos is important in the pathogenesis of this disease, it must be activated by some mechanism other than transposition of this oncogene to an aberrant position.