|
Primary malignant neoplasm
|
0.050 |
GeneticVariation
|
group |
BEFREE |
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.
|
3352917 |
1988 |
|
Leukemia, Myelocytic, Acute
|
0.050 |
Biomarker
|
disease |
BEFREE |
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.
|
3466666 |
1987 |
|
Primary malignant neoplasm
|
0.050 |
GeneticVariation
|
group |
BEFREE |
A single point mutation responsible for c-mos polymorphism in cancer patients.
|
2894001 |
1987 |
|
Leukemia, Myelocytic, Acute
|
0.050 |
Biomarker
|
disease |
BEFREE |
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.
|
3021321 |
1986 |
|
Leukemia, Myelocytic, Acute
|
0.050 |
GeneticVariation
|
disease |
BEFREE |
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.
|
2982159 |
1985 |
|
Leukemia, Myelocytic, Acute
|
0.050 |
GeneticVariation
|
disease |
BEFREE |
The role of the c-mos gene in the 8;21 translocation in human acute myeloblastic leukemia.
|
3860954 |
1985 |
|
Primary malignant neoplasm
|
0.050 |
GeneticVariation
|
group |
BEFREE |
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.
|
2982159 |
1985 |
|
Mixed Salivary Gland Tumor
|
0.030 |
GeneticVariation
|
disease |
BEFREE |
Subsequent FISH analyses of pleomorphic adenomas using YACs as well as cosmids revealed that all but two of the 8q12 breakpoints in the primary tumors tested mapped within a 300-kb interval between the MOS proto-oncogene and STS EM156.
|
9268638 |
1997 |
|
Mixed Salivary Gland Tumor
|
0.030 |
Biomarker
|
disease |
BEFREE |
Collectively, our cytogenetic and molecular data suggest involvement of the c-mos gene in the pathogenesis of pleomorphic adenomas.
|
1677749 |
1991 |
|
Mixed Salivary Gland Tumor
|
0.030 |
Biomarker
|
disease |
BEFREE |
No rearrangement of c-mos in salivary gland pleomorphic adenomas with 8q12 aberrations.
|
1976432 |
1990 |
|
Malignant neoplasm of breast
|
0.030 |
GeneticVariation
|
disease |
BEFREE |
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.
|
2564734 |
1989 |
|
Malignant neoplasm of breast
|
0.030 |
Biomarker
|
disease |
BEFREE |
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.
|
2905174 |
1988 |
|
Malignant neoplasm of breast
|
0.030 |
Biomarker
|
disease |
BEFREE |
In the case of Ha-MSV-containing constructs stably integrated in the two human breast cancer lines, however, CAT expression was more than two orders of magnitude greater than that transiently expressed in these cells.
|
2825673 |
1987 |
|
leukemia
|
0.030 |
Biomarker
|
disease |
BEFREE |
Localization of the human c-mos gene by in situ hybridization in two cases of acute nonlymphocytic leukemia type M2.
|
3466666 |
1987 |
|
leukemia
|
0.030 |
GeneticVariation
|
disease |
BEFREE |
A rare EcoRI restriction fragment length polymorphism (RFLP) in the 3' end of the human c-mos locus has been identified in DNA from patients with breast tumors, esophageal carcinomas and leukemias.
|
2894001 |
1987 |
|
leukemia
|
0.030 |
Biomarker
|
disease |
BEFREE |
As neoplastic cells produce high levels of plasminogen activator, it is of interest that aberrations of chromosome 8 have been linked to various leukemias and lymphomas and that two human oncogenes, c-mos and c-myc, have also been mapped to chromosome 8.
|
3840278 |
1985 |
|
Malignant neoplasm of stomach
|
0.020 |
Biomarker
|
disease |
BEFREE |
Among these genes, MOS was found to be a possible surrogate marker for GC development.
|
30828872 |
2019 |
|
Stomach Carcinoma
|
0.020 |
Biomarker
|
disease |
BEFREE |
Among these genes, MOS was found to be a possible surrogate marker for GC development.
|
30828872 |
2019 |
|
Bodily Pain
|
0.020 |
Biomarker
|
phenotype |
BEFREE |
The MOS 36-item Short-Form Health Survey was completed at baseline and 6, 12, and 24 months after surgery; the bodily pain, physical functioning, and role-physical subscales were used for this analysis (higher scores = less disability).
|
31201809 |
2019 |
|
Bodily Pain
|
0.020 |
Biomarker
|
phenotype |
BEFREE |
Convergent validity was demonstrated with PAL-I total score and Roland-Morris Disability Questionnaire (Pearson correlation 0.82), MOS-36 Physical Functioning (-0.71), and MOS-36 Bodily Pain (-0.71).
|
29889120 |
2018 |
|
Malignant neoplasm of stomach
|
0.020 |
AlteredExpression
|
disease |
BEFREE |
Methylation levels in MOS in non-neoplastic gastric mucosae increased in the presence of GC, regardless of H. pylori infection status (p < 0.01).
|
22252584 |
2012 |
|
Stomach Carcinoma
|
0.020 |
AlteredExpression
|
disease |
BEFREE |
Methylation levels in MOS in non-neoplastic gastric mucosae increased in the presence of GC, regardless of H. pylori infection status (p < 0.01).
|
22252584 |
2012 |
|
Tumor Progression
|
0.020 |
Biomarker
|
phenotype |
BEFREE |
Increases of MOS, MYC, EXT1, and PTK2 (located on 8q) were detected exclusively in moderately and poorly differentiated tumors, suggesting that these alterations contribute to tumor progression.
|
15133472 |
2004 |
|
Carcinoma
|
0.020 |
GeneticVariation
|
group |
BEFREE |
The carcinomas with concomitant alterations of c-mos and p53 [c-mos(P)/p53 positive] had significantly lower AI values (P < 0.001) and were more frequently associated with aneuploidy (P = 0.015) than the c-mos(N)/p53 negative tumors but not the c-mos(N)/p53 positive tumors, which suggests that p53 status is the main determinant of ploidy status and apoptosis in our series.
|
11212247 |
2001 |
|
Non-Small Cell Lung Carcinoma
|
0.020 |
Biomarker
|
disease |
BEFREE |
In view of the apparent link between c-mos and p53, we investigated in a series of 56 non-small cell lung carcinomas: a) the status of c-mos; b) its relationship to genomic instability (aneuploidy) and two kinetic parameters of the tumors, proliferation and apoptotic indexes (AI); and c) its association with p53 alterations and their concomitant relationship with the above parameters.
|
11212247 |
2001 |