Luminal A Breast Cancer and Molecular Assays: A Review

Gao, Jennifer; Swain, Sandra M.

doi:10.1634/theoncologist.2017-0535

Cited by 171 publications

(133 citation statements)

References 69 publications

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“…According to the last update of St. Gallen in 2013, the immunohistochemical profile of this subtype was defined as: ER+ (≥ 1%), high expression of PR (≥ 20%), HER2-(≤ 10%), and low levels of Ki-67 (< 14%) 42 . In addition, these tumors have characteristics of luminal epithelial cells of the breast, such as the high expression of cytokeratin's 7/8/18/19 43 . They include a wide range of low histological grade variants, such as IDC-NST, tubular, cribriform, mucinous, and classic ILC 6,43 .…”

Section: Luminal Amentioning

confidence: 99%

“…In addition, these tumors have characteristics of luminal epithelial cells of the breast, such as the high expression of cytokeratin's 7/8/18/19 43 . They include a wide range of low histological grade variants, such as IDC-NST, tubular, cribriform, mucinous, and classic ILC 6,43 . This subtype has been associated with a highly favorable prognosis, with a more indolent clinical course, and generally shows less lymph node involvement 44 .…”

Section: Luminal Amentioning

confidence: 99%

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Histological and molecular classification of breast cancer: what do we know?

Nascimento

Otoni²

2020

Mastology

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Breast cancer is the neoplasm most diagnosed malignancy and the leading cause of mortality among women on a global scale. A profound increase in the understanding and clinical management of breast cancer has occurred over the past two decades, which has led to significant progress in prevention, early detection, and personalized breast cancer therapy. However, the biggest obstacle still faced in clinical practice is the complete understanding of intertumoral and intratumoral heterogeneity, in addition to the mechanisms of multiple drug resistance in the systemic treatment of the disease. In view of this, many studies focus on analyzing morphological and, mainly, molecular patterns of breast cancer, with the purpose of grouping these tumors into classes or entities to assist in clinical management, in the elaboration of epidemiological and functional studies, and in the performance of clinical trials. The most common special histological types of breast cancer include: medullary carcinoma, metaplastic carcinoma, apocrine carcinoma, mucinous carcinoma, cribriform carcinoma, tubular carcinoma, neuroendocrine carcinoma, classic lobular carcinoma, and pleomorphic lobular carcinoma, in addition to the non-specific type of invasive ductal carcinoma, which constitutes the majority of newly diagnosed cases. As to their molecular aspect, intrinsic subtypes were identified based on global studies of gene expression profiles. Today, four molecular subgroups are widely reproduced and well established in the clinical routine, namely: Luminal A, Luminal B, HER2 +, and Triple Negative. Thus, the present article aims to briefly address the histological and molecular classification of breast cancer.

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Section: Luminal Amentioning

confidence: 99%

Section: Luminal Amentioning

confidence: 99%

Histological and molecular classification of breast cancer: what do we know?

Nascimento

Otoni²

2020

Mastology

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show abstract

“… 6 Each subtype might have different treatment strategies, and the predictive factors may not be the same. For example, the best treatment regimen for breast cancer with luminal A subtype, which is clinically acceptable, is endocrine therapy alone without chemotherapy, 17 whereas for luminal B subtype, the optimal combination of chemotherapy and endocrine therapy is necessary. Recently, the PAMELA study showed that breast cancer patients with the HER2+ subtype are more likely to benefit from the dual HER2 blockade treatment.…”

Section: Pathological Featuresmentioning

confidence: 99%

Predicting the response to neoadjuvant therapy for early-stage breast cancer: tumor-, blood-, and imaging-related biomarkers

Tan¹,

Yang²,

Yang³

et al. 2018

CMAR

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Neoadjuvant therapy (NAT) has been used increasingly in patients with locally advanced or early-stage breast cancer. However, the accurate evaluation and prediction of response to NAT remain the great challenge. Biomarkers could prove useful to identify responders or nonresponders, or even to distinguish between early and delayed responses. These biomarkers could include markers from the tumor itself, such as versatile proteins, genes, and ribonucleic acids, various biological factors or peripheral blood cells, and clinical and pathological features. Possible predictive markers could also include multiple features from functional imaging, such as standard uptake values in positron emission tomography, apparent diffusion coefficient in magnetic resonance, or radiomics imaging biomarkers. In addition, cells that indirectly present the immune status of tumor cells and/or their host could also potentially be used as biomarkers, eg, tumor-infiltrating lymphocytes, tumor-associated macrophages, and myeloid-derived suppressor cells. Though numerous biomarkers have been widely investigated, only estrogen and/or progesterone receptors and human epidermal growth factor receptor have been proven to be reliable biomarkers to predict the response to NAT. They are the only biomarkers recommended in several international guidelines. The other aforementioned biomarkers warrant further validation studies. Some multigene profiling assays that are commercially available, eg, Oncotype DX and MammaPrint, should be used with caution when extrapolated to NAT settings. A panel of combined multilevel biomarkers might be able to predict the response to NAT more robustly than individual biomarkers. To establish such a panel and its prediction model, reliable methods and extensive clinical validation are warranted.

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“…Moreover, tumor molecular subtypes enable to inform clinical outcomes and treatments. For example, treatment options can be made based on either Her2+, luminal or basal subtypes of breast cancer ( 1, 2, 3, 4 ). However, the enormous complexity of cancer subtypes, tumor microenvironment, subclones, and somatic genomic alteration landscapes has been reported.…”

Section: Introductionmentioning

confidence: 99%

Inherited defects in natural killer cells shape tumor immune microenvironment, clinical outcome and immunotherapy response

Xu¹,

Zou

et al. 2018

Preprint

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27Tumor immune microenvironment (TIME) plays an important role in metastasis and 28 immunotherapy. However, it has been not much known how to classify TIMEs and how TIMEs are 29 genetically regulated. Here we showed that tumors were classified into TIME-rich, -intermediate and -30 poor subtypes which had significant differences in clinical outcomes, abundances of tumor-infiltrating 31 lymphocytes (TILs), degree of key immune programs' activation, and immunotherapy response across 32 13 common cancer types (n= ~6,000). Furthermore, TIME-intermediate/-poor patients had significantly 33 more inherited genetic defects (i.e., functional germline variants) in natural killer (NK) cells, antigen 34 processing and presentation (APP) and Wnt signaling pathways than TIME-rich patients, and so did 35 cancer patients than non-cancer individuals (n=4,500). These results suggested that individuals who 36 had more inherited defects in NK cells, APP and Wnt pathways had higher risk of developing 37 cancers. Moreover, in the 13 common cancers the number of inheritably defected genes of NK 38 cells was significantly negative-correlated with patients' survival, TILs' abundance in TIMEs and 39 immunotherapy response, suggesting that inherited defects in NK cells alone were sufficient to shape 40 TILs' recruitment, clinical outcome and immunotherapy response, highlighting that NK cell activation 41 was required in the 13 cancer types to drive the recruitment of immune troops into TIMEs. Thus, we 42proposed that cancer was a disease of NK cell inherited deficiencies. These results had implications in 43 identifying of high-risk individuals based on germline genomes, implementing precision cancer 44 prevention by adoptive transfer of healthy NK cells, and improving existing immunotherapies by 45 combining of adoptive NK cell transfer (i.e., converting TIME-intermediate/-poor tumors into TIME-46 rich tumors) in and anti-PD-1 or CAR-T therapy. 47 48 49

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Luminal A Breast Cancer and Molecular Assays: A Review

Cited by 171 publications

References 69 publications

Histological and molecular classification of breast cancer: what do we know?

Histological and molecular classification of breast cancer: what do we know?

Predicting the response to neoadjuvant therapy for early-stage breast cancer: tumor-, blood-, and imaging-related biomarkers

Inherited defects in natural killer cells shape tumor immune microenvironment, clinical outcome and immunotherapy response

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