1: Cancer Res. 1999 Jul 15;59(14):3365-8. 

Expression of B-myb in neuroblastoma tumors is a poor prognostic factor
independent from MYCN amplification.

Raschella G, Cesi V, Amendola R, Negroni A, Tanno B, Altavista P, Tonini GP, De
Bernardi B, Calabretta B.

ENEA CR Casaccia, Section of Toxicology and Biomedical Sciences, Rome, Italy.

The transcription factors of the Myb family are expressed in several tissues and
play an important role in cell proliferation, differentiation, and survival In
this study, the expression of A-myb, B-myb, and c-myb was investigated in a
group of 64 neuroblastomas at different dinical stages by a sensitive reverse
transcription-PCR tchnique and correlated with patients' survival. All of the
myb genes were frequently expressed in neuroblastoma tumors. Interestingly, the
expression of B-myb, which was detected in 33 cases, was associated with an
increased risk of death (P = 0.027 in a univariate analysis), whereas there was
no correlation with A-myb and c-myb expression. In addition, in a multivariate
Cox regression analysis that included myb gene expression, MYCN status, age at
diagnosis, and tumor staging, MYCN amplification and B-myb expression were
independently associated to an increased risk (P < 0.01 and P = 0.015,
respectively). In overall survival curves obtained by stratifying the
neuroblastoma cases on the basis of MYCN status and B-myb expression, the group
of patients without MYCN amplification and positive for B-myb expression had
worse survival probability than that without MYCN amplification and
nonexpressing B-myb (P < 0.01). In summary, these findings provide the first
demonstration that B-myb expression can be a useful prognostic marker in human
neuroblastoma. Moreover, B-myb expression has a prognostic value complementary
to MYCN amplification and can identify a group of high-risk patients that would
not be predicted on the basis of the MYCN status only.

PMID: 10416595 [PubMed - indexed for MEDLINE]


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2: Cytogenet Cell Genet. 1993;62(4):217-9. 

Novel RFLPs at protooncogene and cancer-related gene loci on mouse chromosomes.

Santos J, Pellicer A.

Department of Pathology and Kaplan Cancer Center, New York University School of
Medicine, NY 10016.

DNA probes for the NRAS, HRAS, KRAS2, LCK, RAF1, MET, MYCL1, MYCN, MYB, ERBB2,
FOS, CSF1R, and SRC protooncogene loci; the retinoblastoma gene locus (RB1); the
tumor virus integration sites INT2, PVT1, and MLV12; and the locus of the
tumor-specific antigen T1A were used to screen mouse genomic DNAs from RF/J,
CAST/Ei, MOLF/Ei, Mus musculus musculus, M. m. poschiavinus, and M. spretus.
Polymorphic DNA fragments for the 18 DNA probes have been identified using
Southern blot hybridization and restriction fragment length polymorphism (RFLP)
analysis.

PMID: 8095010 [PubMed - indexed for MEDLINE]


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3: Br J Cancer. 1991 Jun;63(6):851-8. 

Oncogenes in human testicular cancer: DNA and RNA studies.

Peltomaki P, Alfthan O, de la Chapelle A.

Department of Medical Genetics, University of Helsinki, Finland.

Oncogene dosage and expression were studied in 16 testicular neoplasms, 14 of
germ cell and two of non-germ cell origin. In comparison with normal DNA, tumour
DNA of a total of eight patients (seven with germ cell neoplasm and one with
testicular lymphoma) showed increased dosages of KRAS2, PDGFA, EGFR, MET and
PDGFB. The most frequent (occurring in six tumours) and prominent (up to
3-4-fold) increases were detected in the dosages of KRAS2 (on chromosome 12p)
and PDGFA (chromosome 7p), relative to a reference locus from chromosome 2.
Importantly, there was a similar increase in 12p dosage in general in these
tumours, suggesting the presence of the characteristic isochromosome 12p marker.
On the contrary, possible 7p polysomy (assessed by molecular methods) did not
explain the PDGFA (or EGFR) changes in all cases. NRAS, MYCN, CSFIR, MYB, MYC,
ABL, HRASI, TP53, and ERBB2 did not reveal any consistent alterations in tumour
DNA. In RNA dot blot assays the expression of KRAS2, PDGFA, EGFR, or MYC was
generally not increased in the tumour samples when compared to that in normal
testicular tissue of the same patients although there was interindividual
variation in mRNA levels. It thus appears that while oncogene dosage changes
occur in a proportion of testis cancers, they are often part of changes in large
chromosomal regions or whole arms and are seldom accompanied by altered
expression.

PMID: 1829952 [PubMed - indexed for MEDLINE]


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4: Prog Clin Biol Res. 1991;366:151-6. 

Patterns of regulation of nuclear proto-oncogenes MYCN and MYB in retinoic acid
treated neuroblastoma cells.

Thiele CJ.

Molecular Genetics Section, National Cancer Institute, Bethesda, MD 20892.

PMID: 2068135 [PubMed - indexed for MEDLINE]


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