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NCI CANCERLIT® Search: Breast Cancer, Hereditary - January 2002
National Cancer Institute®
Last Modified: January 1, 2002
Table of Contents
1
UI - 11191790
AU - Devilee P; Tollenaar RA; Cornelisse CJ
TI -
[From gene to disease; from BRCA1 or BRCA2 to breast cancer]
SO - Ned Tijdschr Geneeskd 2000 Dec 30;144(53):2549-51
AD - Afd. Antropogenetica, Leids Universitair Medisch Centrum, Postbus 9600,
2300 RC Leiden.
Hereditary breast cancer is a heterogeneous syndrome, both
phenotypically and genetically. It affects about 5% of all breast cancer
patients. The presence of ovarian cancer or breast cancer in males
defines important subtypes. BRCA1 and BRCA2 are involved in all
hereditary breast cancer syndromes in varying degrees. Both genes confer
strongly elevated breast and ovarian cancer risks in mutation carriers,
but these risks may be subject to modifying effects by other factors
(genetic and/or environmental) at the individual level. In the
Netherlands, DNA testing is offered under the national health insurance
programme and has led to the identification of over 500 families with
either a BRCA1 or BRCA2 mutation. The results of the test are being used
widely by Dutch women in the decision for or against prophylactic
surgery.
2
UI - 11011299
AU - Nixon RM; Pharoah P; Tabar L; Krusemo UB; Duffy SW; Prevost TC; Chen HH
TI -
Mammographic screening in women with a family history of breast cancer:
some results from the Swedish two-county trial.
SO - Rev Epidemiol Sante Publique 2000 Aug;48(4):325-31
AD - MRC Biostatistics Unit, Institute of Public Health, University Forvie
Site, Cambridge, CB2 2SR, UK. richard.nixon@mrc-bsu.cam.ac.uk.
BACKGROUND: The objective of this study is to compare the effectiveness
of mammographic screening in women with a family history of breast
cancer to those without. In the invited arm of a randomised trial of
breast cancer screening, data on family history of breast cancer were
available on 29.179 women aged 40-74 attending for screening. Among
those women, 358 were diagnosed with breast cancer during the trial.
METHODS: Those with and without a family history were compared with
respect to mammographic parenchymal pattern, interval cancer rates, mean
sojourn time and sensitivity of screening. In the 358 cancers, the
effect of family history was estimated on survival, incidence of
advanced cancers and their relationship to screen detection. RESULTS: A
significantly higher proportion of high risk mammographic patterns was
observed in association with family history among women aged 40-49.
Interval cancer rates were higher in women with a family history, and in
older women at least, mean sojourn time was shortened in women with a
family history (1.89 years compared to 2.70). Survival was better
(although not significantly so) in cancers in women with a family
history (relative hazard=0.52) independently of detection mode and was
significantly poorer in interval cancers then screen detected cancers
(relative hazard=2.72) independently of family history. Similarly,
interval cancers tended to be larger, and worse malignancy grade in
those with and without a family history of breast cancer. CONCLUSIONS:
These results suggest that the policy often adopted of annual screening
for woman aged 40-49, with a family history of breast cancer, is a
reasonable one, and that it may also be necessary to shorten the
inter-screening interval to one year in women aged over 50 but with a
positive family history.
3
UI - 11221545
AU - Hou MF; Tsai KB; Fan HM; Wang CY; Lin WC; Liu CS; Lin HJ; Chai CY; Fu
TI -
OY; Li SS; Chang YY; Huang TJ
Familial breast cancer in southern Taiwan.
SO - Kaohsiung J Med Sci 2000 Aug;16(8):414-21
AD - Department of Surgery, Kaohsiung Medical University, No. 100, Shih-Chuan
1st Road, Kaohsiung, Taiwan.
The purpose of this study is to evaluate whether there are pathobiologic
differences and differences in overall rates survival between familial
and non-familial breast cancer patients in Taiwan. A retrospective study
was performed evaluating 76 familial breast cancer patients in 69
families, which included two BRCA1 related cases and six BRCA2 related
cases. Patients were compared with 425 non-familial sporadic cases.
Familial breast cancer patients had similar ages and stages as
non-familial patients (mean, 46.6 years vs 48.9 years, p = 0.306).
However, the familial breast cancer patients with BRCA1 and BRCA2
related cases presented at lower stages (p = 0.034) and younger ages
than non-familial patients (mean, 45.1 years vs 48.9 years P = 0.042).
The occurrence of infiltrating ductal carcinoma and lobular carcinoma in
situ was not significantly different in the two groups. Mucinous
carcinoma was represented with 6.7% (4/76) and 1.3% (1/76) medullary
carcinoma. The overall grade of familial breast cancer, including BRCA1
and BRCA2 related cases in 8 infiltrating ductal carcinoma, was
significantly higher than that of controls. The mean follow up was 4.5
years for familial breast cancers. Five- and 10-year overall survival
rates were 69% and 61% for those with a family history, compared with
86% and 64% for those in the control group (p = 0.644). There were no
statistically significant differences in disease-free survival rates
between the two groups at 5 or 10 years (69% vs 78% in 5 years; 48% vs
58% in 10 years) (p = 0.862). Despite the younger ages and earlier
stages at presentation in familial breast cancer patients with BRCA1 and
BRCA2 related cases, the familial breast cancer patients had higher
grade patholobiologic characteristics, but similar prognoses when
compared with sporadic breast cancer patients. Owing to the limited
number of familial cases in this study, more cases and longer follow up
are needed.
4
UI - 11248061
AU - Levy-Lahad E; Lahad A; Eisenberg S; Dagan E; Paperna T; Kasinetz L;
TI -
Catane R; Kaufman B; Beller U; Renbaum P; Gershoni-Baruch R
A single nucleotide polymorphism in the RAD51 gene modifies cancer risk
in BRCA2 but not BRCA1 carriers.
SO - Proc Natl Acad Sci U S A 2001 Mar 13;98(6):3232-6
AD - Medical Genetics Unit, Shaare Zedek Medical Center and Hebrew
University/Hadassah Medical School, P.O. Box 3235, Jerusalem 91031,
Israel. lahad@szmc.org.il
BRCA1 and BRCA2 carriers are at increased risk for both breast and
ovarian cancer, but estimates of lifetime risk vary widely, suggesting
their penetrance is modified by other genetic and/or environmental
factors. The BRCA1 and BRCA2 proteins function in DNA repair in
conjunction with RAD51. A preliminary report suggested that a single
nucleotide polymorphism in the 5' untranslated region of RAD51 (135C/G)
increases breast cancer risk in BRCA1 and BRCA2 carriers. To investigate
this effect we studied 257 female Ashkenazi Jewish carriers of one of
the common BRCA1 (185delAG, 5382insC) or BRCA2 (6174delT) mutations. Of
this group, 164 were affected with breast and/or ovarian cancer and 93
were unaffected. RAD51 genotyping was performed on all subjects. Among
BRCA1 carriers, RAD51-135C frequency was similar in healthy and affected
women [6.1% (3 of 49) and 9.9% (12 of 121), respectively], and RAD-135C
did not influence age of cancer diagnosis [Hazard ratio (HR) = 1.18 for
disease in RAD51-135C heterozygotes, not significant]. However, in BRCA2
carriers, RAD51-135C heterozygote frequency in affected women was 17.4%
(8 of 46) compared with 4.9% (2 of 41) in unaffected women (P = 0.07).
Survival analysis in BRCA2 carriers showed RAD51-135C increased risk of
breast and/or ovarian cancer with an HR of 4.0 [95% confidence interval
1.6-9.8, P = 0.003]. This effect was largely due to increased breast
cancer risk with an HR of 3.46 (95% confidence interval 1.3-9.2, P =
0.01) for breast cancer in BRCA2 carriers who were RAD51-135C
heterozygotes. RAD51 status did not affect ovarian cancer risk. These
results show RAD51-135C is a clinically significant modifier of BRCA2
penetrance, specifically in raising breast cancer risk at younger ages.
5
UI - 11385712
AU - Caluseriu O; Cordisco EL; Viel A; Majore S; Nascimbeni R; Pucciarelli S;
TI -
Genuardi M
Four novel MSH2 and MLH1 frameshift mutations and occurrence of a breast
cancer phenocopy in hereditary nonpolyposis colorectal cancer.
SO - Hum Mutat 2001 Jun;17(6):521
AD - Istituto di Genetica Medica, Universita Cattolica del S. Cuore, Rome.
Hereditary nonpolyposis colorectal cancer (HNPCC) is caused by mutations
of genes encoding for proteins of the mismatch repair (MMR) machinery.
The majority of mutations occur in the MLH1 and MSH2 genes, and consist
of splice-site, frameshift and nonsense changes, leading to loss of
protein function. In this study, we screened 7 HNPCC families for
MLH1/MSH2 mutations. Sequence changes were identified in 5 families.
Four alterations were novel 1- or 2-bp deletions or insertions causing a
frameshift and appearance of premature stop codons (MLH1:
c.597-598delGA, c.1520-1521insT; MSH2: c.1444delA, c.119delG). The four
small insertions/ deletions were located within stretches of simple
repeated sequences. By reviewing the HNPCC mutation database, we found
that the majority of 1-2 bp frameshift mutations similarly affects
simple repetitive stretches, pointing to DNA polymerase slippage during
replication as the most likely source of such errors. We also evaluated
microsatellite instability (MSI) in a breast carcinoma (BC) from an MLH1
mutation carrier. While a colon cancer from the same individual showed
MSI, the BC specimen was MSI-negative, indicating that development of
the latter tumor was unrelated to MMR impairment, despite presence of a
constitutional MLH1 mutation. Hum Mutat 17:521, 2001. Copyright 2001
Wiley-Liss, Inc.
6
UI - 11394499
AU - Di Modugno F; Buglioni S; Mottolese M; Bello DD; Cascioli S; Chersi A;
TI -
Santoni A; Nistico P
Polyclonal antibodies against gp185HER2 peptides: their putative role in
the identification of a particular HER2 status in patients with breast
cancer.
SO - J Immunother 2001 May-Jun;24(3):221-31
AD - Laboratory of Pathophysiology, CRS Regina Elena Cancer Institute, Rome,
Italy.
The HER2 oncogene and its relative oncoprotein, gp185HER2, a
transmembrane glycoprotein belonging to the epidermal growth factor
receptor family, are overexpressed in a wide range of solid tumors
including breast and ovarian cancer. In patients with breast cancer,
both humoral and cell-mediated HER2 immune responses have been found as
well as in some patients with gp185HER2 nonoverexpressing tumors. To
establish whether peptide sequences identified as HLA-A2-restricted
T-cell epitopes are expressed in breast tumor cell lines and tissues, we
produced and characterized by different methodologic approaches
polyclonal antibodies raised against four gp185HER2 peptides. Two of the
antibodies recognized peptides eluted from the HLA-A2 groove of the
mDAmB231 breast cancer cell line expressing a basal level of gp185HER2.
Paraffin-embedded primary and metastatic breast tumors were specifically
immunostained by all four reagents, thereby showing an overlapping
reactivity. When this immunoreactivity was compared with that obtained
using two different monoclonal antibodies, in 105 breast primary tumors
and 36 corresponding lymph node metastases, we identified a subset of
tumors that were negative with anti-gp185HER2 monoclonal antibodies and
positive with the four antipeptide antibodies. Our novel observations
provide in vivo evidence of the complexity involved in evaluating HER2
expression, and open a new path for understanding the biologic
significance of HER2 status in breast tumors.
7
UI - 11432618
AU - Cardoso F; Di Leo A; Larsimont D; Gancberg D; Rouas G; Dolci S; Ferreira
TI -
F; Paesmans M; Piccart M
Evaluation of HER2, p53, bcl-2, topoisomerase II-alpha, heat shock
proteins 27 and 70 in primary breast cancer and metastatic ipsilateral
axillary lymph nodes.
SO - Ann Oncol 2001 May;12(5):615-20
AD - Jules Bordet Institute, Brussels, Belgium.
BACKGROUND: Breast cancer is a heterogeneous disease. Predictive
biological markers (BM) of responsiveness to therapy need to be
identified. Evaluation of BM is mainly done at the primary site.
However, in the adjuvant therapy of breast cancer, the main goal is
control of micrometastases. It is still unknown whether heterogeneity in
the expression of BM between the primary site and its micrometastases
exists. OBJECTIVE: To evaluate the expression of some BM with potential
predictive value from the primary breast cancer site and metastatic
ipsilateral axillary lymph nodes. PATIENTS AND METHODS: Focality
(percentage of positive cells) and intensity staining scores were
evaluated for each marker. Freshly cut sections (4 microm) from embedded
blocks of breast cancer fixed in formalin or bouin were put onto
superfrost slides (Menzel-Glaser). Protein expression was evaluated
immunohistochemically (IHC) using monoclonal antibodies against: topo
II-alpha (clone KiS1, 1 microg/ml, Roche) with a trypsine pre-treatment
(P); HSP27 (clone G3.1, 1/60, Biogenex), HSP70 (clone BRM.22, 1/80,
Biogenex) and HER2 (clone CB11, 1/40, Novocastra; without P); p53 (clone
D07, 1/750, Dako) and bcl-2 (clone 124, 1/60, Dako) with citrate buffer
as P. RESULTS: Overall, the percentage of discordant marker status in
the primary tumour and its metastatic lymph nodes was 2% for HER2, 6%
for p53, 15% for bcl-2, 19% for topoisomerase II-alpha, 24% for HSP27
and 30% for HSP70. For the subgroup of patients with positive BM in the
primary tumour, the percentage of discordance was 6% for HER2, 7% for
p53, 14% for bcl-2, 19% for HSP70, 21% for topoisomerase II-alpha and
36% for HSP27. For the subgroup of patients with positive BM in the
lymph nodes, the percentage of discordance was 9% for bcl-2, 15% for
HER2 and p53, 21% for topoisomerase II-alpha, 22% for HSP27 and 25% for
HSP70. CONCLUSIONS: 1) No biological marker had 100% concordant results.
2) Although some discordant cases might be explained by the limitations
of the IHC technique, future studies aiming to evaluate the predictive
value of BM in the adjuvant therapy of breast cancer should take into
account a possible difference in BM expression between the primary and
the metastatic sites.
8
UI - 11434504
AU - Yim DS; Parkb SK; Yoo KY; Yoon KS; Chung HH; Kang HL; Ahn SH; Noh DY;
TI -
Choe KJ; Jang IJ; Shin SG; Strickland PT; Hirvonen A; Kang D
Relationship between the Val158Met polymorphism of catechol O-methyl
transferase and breast cancer.
SO - Pharmacogenetics 2001 Jun;11(4):279-86
AD - Department of Pharmacology, Gachon Medical School, Inchon, Korea.
A case-control study was performed to assess the potential influence of
catechol O-methyl transferase (COMT) genotype on the risk of breast
cancer in Korean women. One hundred and sixty-three histologically
confirmed incident breast cancer cases and 163 age- and menopausal
status-matched control individuals with no present or previous history
of cancer were selected as study subjects. COMT genetic polymorphism was
determined by gel electrophoresis after NlaIII enzyme digestion of
amplified DNA. Odds ratios and 95% confidence intervals were estimated
by unconditional logistic regression after adjustment for known or
suspected risk factors of breast cancer. Women with at least one COMT
lower enzyme activity associated allele (COMT-L) were at elevated risk
for breast cancer (OR = 1.7, 95% CI = 1.04-2.78) compared with those
homozygous for high enzyme activity associated COMT-H alleles. Among
women with low (> or = 23.1) body mass index the COMT-L allele
containing genotypes posed a marginally significant increased risk of
breast cancer compared to the COMT-HH genotype (OR = 1.8, 95% CI =
0.95-3.48). Women with at least one COMT-L allele who had experienced a
full-term pregnancy when aged over 30 years or were nulliparous had
2.7-fold increased risk; however, this increase did not reach
statistical significance (OR = 2.7, 95% CI = 0.64-11.35). Furthermore,
never-drinking and never-smoking women with at least one COMT-L allele
were at increased risk of breast cancer compared to those with COMT-HH
genotype with ORs of 2.0 (95% CI = 1.23-3.38) and 1.7 (95% CI =
1.04-2.62), respectively. These results are consistent with studies
showing that COMT genotype of lower enzyme activity might be related to
increase in risk of breast cancer, and extend this finding to Korean
women.
9
UI - 11434389
AU - Campos B; Diez O; Cortes J; Domenech M; Pericay C; Alonso C; Baiget M
TI -
Conditions for single-strand conformation polymorphism (SSCP) analysis
of BRCA1 gene using an automated electrophoresis unit.
SO - Clin Chem Lab Med 2001 May;39(5):401-4
AD - Servei de Genetica, Hospital de la Santa Creu i Sant Pau, Barcelona,
Spain.
The single-strand conformation polymorphism procedure has been applied
in routine testing for hereditary diseases and cancer. However,
temperature, running time, gel composition, fragment length, etc. can
influence its sensitivity. Mutation detection in the clinical setting
depends on the development of automated technology, especially for large
genes such as the breast cancer gene BRCA1. We analysed DNA samples with
BRCA1 mutations in an automated system (GenePhor System;
Amersham-Pharmacia Biotech, Uppsala, Sweden). The concentrations of DNA
template and PCR primers, the effect of chilling after denaturation, and
the temperature and time of the electrophoresis were investigated. All
band-shifts were detected by electrophoresis at 5 degrees C for 2 h 15
min. Concentrations of DNA and samples used in the PCR did not affect
the SSCP pattern, but chilling the PCR product in ice after denaturation
was required. The type and position of mutation in the fragments did not
influence the probability of a mobility shift, although SSCP analysis
was more sensitive for fragments shorter than 350 bp. This automated
SSCP method meets the requirements of fast turnaround and sensitivity
and can be readily adapted to the screening of large genes such as
BRCA1.
10
UI - 11437066
AU - Carter RF
TI -
BRCA1, BRCA2 and breast cancer: a concise clinical review.
SO - Clin Invest Med 2001 Jun;24(3):147-57
AD - Department of Pathology & Molecular Medicine, McMaster University,
Hamilton, Ont.
Less than 5% of breast cancers are hereditary, but over 90% of
hereditary breast cancers are caused by a mutation of either BRCA1 or
BRCA2. The mutation may be inherited from either the maternal or the
paternal side of the family. Clinicians should consider specific
criteria in the family history to determine when a patient may benefit
from counselling and appropriate testing. Testing is generally offered
only to patients who are at high risk and is currently estimated to have
a sensitivity of about 85%. Test protocols are primarily oriented to
detecting frameshift and nonsense mutations that cause premature protein
truncations. Missense mutations also occur, but they are less common and
sometimes not clearly of clinical significance. Laboratory results need
to be correlated with the clinical picture, and genetic counselling is a
critical component in maximizing the benefits of testing. In the future,
application of more refined clinical criteria, as well as expected
improvements in laboratory techniques, will undoubtedly lead to
significantly better outcomes and options in surveillance and management
for hereditary breast and ovarian cancer syndromes caused by mutations
of BRCA1 and BRCA2.
11
UI - 11474658
AU - Mahavni V; Kim SC; Benda TA; Sanders L; Buller RE
TI -
The androgen receptor and DXS15-134 markers show a high rate of
discordance for germline X chromosome inactivation.
SO - J Med Genet 2001 Jul;38(7):474-8
12
UI - 11453492
AU - Setoguchi A; Okuda M; Nishida E; Yazawa M; Ishizaka T; Hong SH; Hisasue
TI -
M; Nishimura R; Sasaki N; Yoshikawa Y; Masuda K; Ohno K; Tsujimoto H
Results of hyperamplification of centrosomes in naturally developing
tumors of dogs.
SO - Am J Vet Res 2001 Jul;62(7):1134-41
AD - Department of Veterinary Internal Medicine, Graduate School of
Agricultural and Life Sciences, University of Tokyo, Japan.
OBJECTIVE: To evaluate results of centrosome hyperamplification in
naturally developing tumors of dogs. SAMPLE POPULATION: Tumor specimens
from 9 dogs with tumors (rhabdomyosarcoma, osteosarcoma, chondrosarcoma,
myxosarcoma, and mammary gland tumor) and 2 canine osteosarcoma cell
lines. PROCEDURE: 3 antibodies for centrosome proteins (ie,
anti-gamma-tubulin, anti-BRCA1, and anti-pericentrin) were used for
immunohistochemical analysis. Double immunostaining for centrosomes was
used to confirm the specificity of these antibodies for centrosomes.
Mutational analysis of the canine p53 gene was carried out by polymerase
chain reaction-single-strand conformation polymorphism analysis, and
expression of canine MDM2 protein was evaluated by use of
immunohistochemical analysis, using anti-MDM2 antibody. RESULTS:
Immunohistochemical analysis of dog osteosarcoma cell lines with
apparent aneuploidy revealed frequent hyperamplification of centrosomes
in the osteosarcoma cell lines. Similar hyperamplified centrosomes were
detected in the tumor tissues from all of the 9 tumors. The frequency of
cells with hyperamplified centrosomes (3 to 20/cell) in each tumor
tissue ranged from 9.50 to 48.1%, whereas centrosome hyperamplification
was not observed in normal lymph nodes from these dogs. In 8 of the 9
tumors, mutation of p53 gene or overexpression of MDM2, or both, was
detected. CONCLUSIONS AND CLINICAL RELEVANCE: Various types of naturally
developing tumors in dogs often have hyperamplification of centrosomes
associated with chromosome instability. Hyperamplification of
centrosomes is a novel tumor marker for use in cytologic and histologic
examinations of clinical specimens obtained from dogs.
13
UI - 11445874
AU - Naidu R; Wahab NA; Yadav M; Kutty MK; Nair S
TI -
Detection of amplified int-2/FGF-3 gene in primary breast carcinomas
using differential polymerase chain reaction.
SO - Int J Mol Med 2001 Aug;8(2):193-8
AD - International Medical University, Sesama Centre, Plaza Komenwel, Bukit
Jalil, 57000 Kuala Lumpur, Malaysia. kdrakeshna@hotmail.com
Amplification of int-2/FGF-3 gene was investigated by differential
polymerase chain reaction (dPCR) in 440 archival primary breast
carcinoma tissues. Of these, 23 were comedo ductal carcinoma in situ
(DCIS), 18 were non-comedo DCIS, 41 were comedo DCIS with adjacent
invasive ductal carcinomas, 19 were non-comedo DCIS with adjacent
invasive ductal carcinomas, 270 were invasive ductal carcinomas, 33 were
invasive lobular carcinomas, 21 were colloid carcinomas and 15 were
medullary carcinomas. Int-2 was amplified in 22% (96/440) of the primary
breast carcinomas. It was shown that int-2 was amplified in 13% (3/23)
of the comedo DCIS, 17% (7/41) of the comedo DCIS and 29% (12/41) of the
adjacent invasive ductal carcinomas, 26% (71/270) of the invasive ductal
carcinomas, 18% (6/33) of the invasive lobular carcinomas, 10% (2/21) of
the colloid carcinomas and 13% (2/15) of the medullary carcinomas. In
contrast, int-2 was not amplified in non-comedo DCIS and invasive ductal
carcinomas with adjacent non-comedo DCIS lesions. A significant
association was observed between int-2 amplification in the in situ
components and adjacent invasive lesion (P<0.05). All tumors with int-2
amplification in the in situ lesions (7/7) also demonstrated same degree
of amplification in the adjacent invasive components. However, 9% (5/53)
of the tumors with no amplified int-2 gene in the in situ components
showed int-2 amplification in the adjacent invasive lesions. A
significant relationship was noted between amplification of int-2 and
lymph node metastases (P<0.05) and poorly differentiated tumors (P<0.05)
but not with estrogen receptor status (P>0.05) and proliferation index
(Ki-67 and PCNA) (P>0.05). In Malaysia, majority of the patients belong
to younger age group (<50 years old) but a comparison of the age groups
showed that the amplification of int-2 was not statistically associated
with patient age (P>0.05). These observations indicate that
amplification of int-2 tends to strengthen the view that int-2 may have
the potential to be an indicator of poor prognosis regardless of the age
of the patient. Moreover, the presence of int-2 amplification in
preinvasive, preinvasive and adjacent invasive lesions, and invasive
carcinomas suggest that int-2 could be a marker of genetic instability
occurring in early and late stages of tumor development.
14
UI - 11456268
AU - Shibata A; Hayashi Y; Imai T; Funahashi H; Nakao A; Seo H
TI -
Somatic gene alteration of AIB1 gene in patients with breast cancer.
SO - Endocr J 2001 Apr;48(2):199-204
AD - Department of Endocrinology and Metabolism, Research Institute of
Environmental Medicine, Nagoya University, Japan.
AIB1 (amplified in breast cancer 1) is a coactivator which stimulates
the transcriptional activity of the liganded-estrogen receptor (ER). It
has been reported that AIBI gene is amplified and overexpressed in some
breast cancer cell lines. AIB1 contains a stretch of homopolymeric
glutamines (poly-Q). We reported that the poly-Q shows polymorphism,
which provides an opportunity to study somatic gene alteration such as
loss of heterozygosity (LOH). In the present study, we aimed to
investigate the frequency of somatic gene alteration in Japanese
patients with breast cancer. Amplification of AIB1 gene was detected
only in 1 (2.6%) of 39 breast cancer tissues by DNA dot blot analysis.
On the other hand, LOH was found in 2 (8%) breast cancer tissues out of
25 patients showing heterozygosity in peripheral blood mononuclear cells
(PBMC). Taken together, both LOH and amplification of AIB1 gene were
identified in breast cancer patients, raising the possibility that AIB1
have oncogenic as well as antioncogenic potential for the pathogenesis
of breast cancer.
15
UI - 11467450
AU - Callahan R; Raafat A
TI -
Notch signaling in mammary gland tumorigenesis.
SO - J Mammary Gland Biol Neoplasia 2001 Jan;6(1):23-36
AD - Laboratory of Tumor Immunology and Biology, National Cancer Institute,
Bethesda, Maryland 20892, USA. rc54d@nih.gov
The Notch receptor protein and its signaling pathway have been well
conserved throughout evolution and appear to be pivotal components in
cell fate decisions during development. Recent studies suggest that,
depending on the cellular and developmental context, Notch signaling may
also affect cell proliferation and programmed cell death. Mammals have
four related Notch genes. One of these, designated Notch-4, was found to
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