Epidemiology of basal-like breast cancer

Millikan, Robert C.; Newman, Beth; Tse, Chiu Kit; Moorman, Patricia G.; Dorsey, Kathleen C; Dressler, Lynn G.; Smith, Lisa von Huth; Labbok, Miriam H.; Geradts, Joseph; Bensen, Jeannette T.; Jackson, Susan; Nyante, Sarah J.; Livasy, Chad; Carey, Lisa A.; Earp, H. Shelton; Perou, Charles M.

doi:10.1007/s10549-007-9790-6

Cited by 206 publications

(373 citation statements)

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“…However, these and other published data provide a strong clinical rationale for further scientific and epidemiologic research to directly evaluate any pathogenetic role for progenitor cells retained after cessation or weaning. 7,8 We observed a linear relationship between duration of breastfeeding per child and triple-negative BC phenotype (Fig. 2), without an obvious inflection point that would identify an optimal prevention target for breastfeeding duration.…”

Section: Discussionmentioning

confidence: 78%

“…[3][4][5] Undifferentiated BC phenotype is more prevalent in carriers of BRCA1 germ-line mutation, and among premenopausal African American women. [4][5][6][7] There is also a reported association with shorter lifetime duration of breastfeeding. [7][8][9] However, both parity and breastfeeding duration might contribute in combination to risk by altering the population of progenitor cells that are retained within breast parenchyma, a cell type that known to have enhanced survival potential under physiological or pathologic stress.…”

mentioning

confidence: 99%

“…[4][5][6][7] There is also a reported association with shorter lifetime duration of breastfeeding. [7][8][9] However, both parity and breastfeeding duration might contribute in combination to risk by altering the population of progenitor cells that are retained within breast parenchyma, a cell type that known to have enhanced survival potential under physiological or pathologic stress. 8,[10][11][12][13][14][15] Indeed, recruitment and expansion of progenitor cells within breast terminal ducts sustains epithelial expansion during pregnancy and lactation, and this is followed by epithelial differentiation or apoptosis during the course of weaning.…”

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confidence: 99%

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Higher parity and shorter breastfeeding duration

Shinde

Forman

Kuerer

et al. 2010

Cancer

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BACKGROUND:The combination of increased parity and shorter breastfeeding duration might increase the odds of the least differentiated triple-negative breast cancer (BC) phenotype, theoretically because an expanded progenitor cell population from each pregnancy would incompletely differentiate postpartum. METHODS: Subjects consisted of a consecutive case series of 2473 women treated for invasive breast cancer between 2001 and 2006. Breast cancer phenotype (triple-negative BC, vs non-triple-negative BC) was compared with reproductive and demographic information. Odds ratios (OR) with 95% confidence intervals (CIs) for the association of breastfeeding duration (months per child) and parity with triple-negative BC were calculated after adjusting for ethnicity, age at menarche, family history, and age at diagnosis. RESULTS: Compared with non-triple-negative BC, triple-negative BC was associated with shorter duration of breastfeeding per child (OR, 0.93; 95% CI, 0.90-0.97) and with higher parity (OR, 1.12; 95% CI, 1.06-1.20). By using multivariate logistic regression, triple-negative BC was independently associated with higher parity ( 40 years vs >60 years). CONCLUSIONS: Among women with invasive breast cancer, higher parity and the absence or short duration of breastfeeding were independently associated with triple-negative BC. Any duration of breastfeeding was found to be associated with lower probability of triple-negative BC, and the odds of this phenotype decreased with increasing duration of breastfeeding. Cancer 2010;116:4933-43.

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Section: Discussionmentioning

confidence: 78%

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confidence: 99%

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confidence: 99%

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Higher parity and shorter breastfeeding duration

Shinde

Forman

Kuerer

et al. 2010

Cancer

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“…Maybe a large part of the racial difference in the distribution of BLBC may be attributable to different distribution of specific risk factors. The use of oral contraceptives in women <40 years old, younger age at diagnosis, hispanic ethnicity, lower socio-economic status, with abdominal adiposity and metabolic syndrome were also shown to significantly increase risk of BLBC [50,52] (Table 3). Interestingly, as shown on Table 3, some of the principal risk factors of BLBC are opposite to those observed for BC (Luminal A).…”

Section: Clinicopathological Features Of Blbcmentioning

confidence: 99%

Molecular insights on basal-like breast cancer

Dominguez‐Valentin

Silva

Privat

et al. 2012

Breast Cancer Res Treat

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Molecular classification of breast cancer (BC) identified diverse subgroups that encompass distinct biological behaviour and clinical implications, in particular in relation to prognosis, spread, and incidence of recurrence. Basal like breast cancers (BLBC) compose up to 15% of BC and are characterized by lack of estrogen receptor (ER), progesterone receptor (PR), and HER-2 amplification with expression of basal cytokeratins 5/6, 14, 17, epidermal growth factor receptor (EGFR), and/or c-KIT. There is an overlap in definition between triple-negative BC and BLBC due to the triple-negative profile of BLBC. Also, most BRCA1-associated BCs are BLBC, triple negative, and express basal cytokeratins (5/6, 14, 17) and EGFR.There is a link between sporadic BLBC (occurring in women without germline BRCA1 mutations) with dysfunction of the BRCA1 pathway. Despite the molecular and clinical similarities, these subtypes respond differently to neoadjuvant therapy. BLBCs are associated with an aggressive phenotype, high histological grade, poor clinical behavior, and high rates of recurrences and/or metastasis. Their molecular features render these tumors especially refractory to anti-hormonal-based therapies and the overall prognosis of this subset remains poor. In this article the molecular profile, genomic and epigenetic characteristics as well as BRCA1 pathway dysfunction, clinicopathological behavior, and therapeutic options in BLBC are presented, with emphasis on the discordant findings in current literature.

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“…1,[7][8][9][10][11][12] Of particular relevance to patient management, the 'basallike' subtype comprises B15% of all invasive breast cancers and is responsible for a disproportionately high number of metastatic breast cancer cases and breast cancer-related deaths. 13,14 This aggressive subtype is also associated with early age of onset, [15][16][17][18] BRCA-related hereditary cancers [19][20][21][22] and has a particularly high incidence in women of African ethnicity. [23][24][25] Despite its characteristically poor prognosis and resistance to established molecularly targeted therapies (eg, tamoxifen, aromatase inhibitors and trastuzumab), basal-like breast cancer is usually a diagnosis of exclusion in the clinical setting, based on lack of expression of hormone receptors and HER2.…”

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confidence: 99%

A survey of immunohistochemical biomarkers for basal-like breast cancer against a gene expression profile gold standard

et al. 2013

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Gene expression profiling of breast cancer delineates a particularly aggressive subtype referred to as 'basallike', which comprises B15% of all breast cancers, afflicts younger women and is refractory to endocrine and anti-HER2 therapies. Immunohistochemical surrogate definitions for basal-like breast cancer, such as the clinical ER/PR/HER2 triple-negative phenotype and models incorporating positive expression for CK5 (CK5/6) and/or EGFR are heavily cited. However, many additional biomarkers for basal-like breast cancer have been described in the literature. A parallel comparison of 46 proposed immunohistochemical biomarkers of basal-like breast cancer was performed against a gene expression profile gold standard on a tissue microarray containing 42 basal-like and 80 non-basal-like breast cancer cases. Ki67 and PPH3 were the most sensitive biomarkers (both 92%) positively expressed in the basal-like subtype, whereas CK14, IMP3 and NGFR were the most specific (100%). Among biomarkers surveyed, loss of INPP4B (a negative regulator of phosphatidylinositol signaling) was 61% sensitive and 99% specific with the highest odds ratio (OR) at 108, indicating the strongest association with basal-like breast cancer. Expression of nestin, a common marker of neural progenitor cells that is also associated with the triple-negative/basal-like phenotype and poor breast cancer prognosis, possessed the second highest OR at 29 among the 46 biomarkers surveyed, as well as 54% sensitivity and 96% specificity. As a positively expressed biomarker, nestin possesses technical advantages over INPP4B that make it a more ideal biomarker for identification of basal-like breast cancer. The comprehensive immunohistochemical biomarker survey presented in this study is a necessary step for determining an optimized surrogate immunopanel that best defines basal-like breast cancer in a practical and clinically accessible way.

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Epidemiology of basal-like breast cancer

Cited by 206 publications

References 0 publications

Higher parity and shorter breastfeeding duration

Higher parity and shorter breastfeeding duration

Molecular insights on basal-like breast cancer

A survey of immunohistochemical biomarkers for basal-like breast cancer against a gene expression profile gold standard

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