23 research outputs found
Association between mode of breast cancer detection and diagnosis delay
abstract We investigated the association between mode of breast cancer (Bca) detection and diagnosis delay in a case-series of primary, histologically confirmed Bca patients from Southern Italy. Nine hundred and fifty nine women diagnosed with incident, primary Bca were recruited in two southern Italian regions. We grouped the mode of detection into two categories: Self-Detection (S-D) and Mammography (MG). Diagnosis delay was defined as the time between detection and a histologically confirmed diagnosis of invasive Bca. 20.9% detected Bca with MG while 79.1% had S-D Bca. Women who detected Bca themselves (S-D) were more likely to delay breast cancer diagnosis than women who were diagnosed by a mammography (MG) (OR: 2.0; 95% CI: 1.39–2.87); when considering the model adjusted for health system-related characteristics, the risk increased (OR: 2.13; 95% CI: 1.47–3.09). Our study indicates a disadvantage in terms of diagnostic delay for women who were admitted and treated in community hospitals compared to women admitted and treated in breast health services
Nonrandom Distribution of Aberrant Promoter Methylation of Cancer-Related Genes in Sporadic Breast Tumors
Abstract
Purpose: In an effort to additionally determine the global patterns of CpG island hypermethylation in sporadic breast cancer, we searched for aberrant promoter methylation at 10 gene loci in 54 primary breast cancer and 10 breast benign lesions.
Experimental Design: Genomic DNA sodium bisulfate converted from benign and malignant tissues was used as template in methyl-specific PCR for BRCA1, p16, ESR1, GSTP1, TRβ1, RARβ2, HIC1, APC, CCND2, and CDH1 genes.
Results: The majority of the breast cancer (85%) showed aberrant methylation in at least 1 of the loci tested with half of them displaying 3 or more methylated genes. The highest frequency of aberrant promoter methylation was found for HIC1 (48%) followed by ESR1 (46%), and CDH1 (39%). Similar methylation frequencies were detected for breast benign lesions with the exception of the CDH1 gene (P = 0.02). The analysis of methylation distribution indicates a statistically significant association between methylation of the ESR1 promoter, and methylation at CDH1, TRβ1, GSTP1, and CCND2 loci (P < 0.03). Methylated status of the BRCA1 promoter was inversely correlated with methylation at the RARβ2 locus (P < 0.03).
Conclusions: Our results suggest a nonrandom distribution for promoter hypermethylation in sporadic breast cancer, with tumor subsets characterized by aberrant methylation of specific cancer-related genes. These breast cancer subgroups may represent separate biological entities with potential differences in sensitivity to therapy, occurrence of metastasis, and overall prognosis
Aging impacts transcriptomes but not genomes of hormone-dependent breast cancers
Age is one of the most important risk factors for human malignancies, including breast cancer; in addition, age-at-diagnosis has been shown to be an independent indicator of breast cancer prognosis. However, except for inherited forms of breast cancer, there is little genetic or epigenetic understanding of the biological basis linking aging with sporadic breast cancer incidence and its clinical behavior
More Children Means More Tumours? We Can Do More to Protect the Health of Our Kids—A Call for a New Epidemiology That Can Change the World
In encyclopaedic dictionaries published until 1955, the word “tumour” was defined as an “occupational disease suffered by the workers of chemical industries”, thus referring to a very specific cause [...
BRCA1 expression and molecular alterations in familial breast cancer
The aim of the study was to evaluate the
performance of immunohistochemical MS110
expression in a series of familial and sporadic breast
cancer patients. An immunohistochemical study was
performed on TMA samples from 93 sporadic and 94
familial breast cancer patients with (7/94) and without
BRCA1 germline mutations. BRCA1 protein expression
level was evaluated using the monoclonal MS110
antibody. Immunohistochemistry, performed on TMA
samples, showed positive nuclear staining for BRCA1 in
34 sporadic and 37 familial breast tumours, respectively.
All the tumours from patients carrying BRCA1
mutations showed complete loss of both BRCA1 and
ERa expression, regardless of the type of mutation. The
percentage of MS110 positive cases was significantly
lower in mutated versus wild type BRCA1 familial cases
(p=0.02) while the percentage of patients with higher
ERa expression was significantly lower in BRCA1-
mutated versus BRCA1-wild type familial patients
(p=0.05). Interestingly, the presence of the E1038G
polymorphism in BRCA1 exon 11 was significantly
associated with protein expression (p=0.029). The
frequency of MS110 negative cases also detected in
BRCA1-wild type tumours, points to the inability of the
BRCA1 IHC expression in discriminating between
familial and sporadic breast cancer
Breast cancer: biological characteristics in postmenopausal type 2 diabetic women. Identification of therapeutic targets
HYPOTHESIS: Epidemiological data have suggested a possible relationship between diabetes mellitus and cancer risk, particularly breast cancer. We set out to investigate the effect of diabetes mellitus on the expression of estrogen and progesteron receptors and on the proliferative activity of primary breast cancer. METHODS: We selected 77 diabetic women and 578 control patients all in post-menopause and diagnosed with primary breast cancer. All patients underwent surgical excision of the tumor and on the specimens were performed an assessment of estrogen receptor and progesteron receptor and proliferative activity assay by (3)H-Thymidine incorporation. RESULTS: Diabetic women showed a decreased proliferative activity, while having the same estrogen receptor and progesteron receptor status and mean cytoplasmic concentration of their receptors than control group. Insulin treated women had a lower proliferative activity than non-insulin treated ones. CONCLUSION: Hyperinsulinemia and hyperglicemia influence in negative way the proliferative activity of diabetic women, likely inducing the expression of transforming growth factor beta, despite the high serum levels of Insulin-like growth factor and estrogen