scholarly journals Nuclear PDCD4 Expression Defines a Subset of Luminal B-Like Breast Cancers with Good Prognosis

2020 ◽  
Vol 11 (5-6) ◽  
pp. 218-239
Author(s):  
Santiago Madera ◽  
María F. Chervo ◽  
Violeta A. Chiauzzi ◽  
Matías G. Pereyra ◽  
Leandro Venturutti ◽  
...  
Keyword(s):  
Good Prognosis ◽  
Breast Cancers ◽  
Luminal B ◽  
Pdcd4 Expression

scholarly journals Surgery for Good Prognosis Breast Cancers

2021 ◽  
Author(s):  
Stuart A. McIntosh
Keyword(s):  
Surgical Treatment ◽  
Minimally Invasive ◽  
Good Prognosis ◽  
Surgical Approaches ◽  
Breast Cancers ◽  
Randomised Trials ◽  
High Quality ◽  
High Quality Evidence ◽  
Small Breast ◽  
Quality Evidence

Abstract Purpose of Review The introduction of mammographic screening programmes has resulted increasing numbers of women with small breast cancers with biologically favourable characteristics. Many of these cancers may represent overdiagnosis, with a resulting treatment burden for women and healthcare costs for providers. Here, current surgical approaches to the treatment of such tumours are reviewed, together with alternative approaches to their management. Recent Findings The surgical treatment of small, screen-detected breast cancers with biologically favourable characteristics has been extrapolated from the management of symptomatic breast cancers. There is no prospective randomised evidence for conventional open surgery compared with other approaches in this setting. A number of minimally invasive techniques, most notable vacuum-assisted excision, have been described for the management of these tumours, but at present, there is a lack of high-quality evidence to support their routine use. There are currently ongoing randomised trials evaluating risk-adapted surgical and minimally invasive approaches to the management of good prognosis disease. Summary It is possible that the surgical treatment of good prognosis screen-detected breast cancers may be de-escalated. However, high-quality evidence from ongoing prospective randomised trials will be required in order to change clinical practice.

Molecular profiles of genomically high risk ER+ HER2- breast cancer tumors classified as functionally basal or luminal B by the 80-gene signature.

2021 ◽  
Vol 39 (15_suppl) ◽  
pp. 563-563
Author(s):  
Joyce O'Shaughnessy ◽  
Virginia G. Kaklamani ◽  
Yuan Yuan ◽  
Julie Barone ◽  
Sami Diab ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
High Risk ◽  
Neoadjuvant Chemotherapy ◽  
Enrichment Analysis ◽  
Gene Signature ◽  
Breast Cancers ◽  
Luminal B ◽  
Estrogen Response ◽  
Luminal Type ◽  
Basal Type

563 Background: The 80-gene signature (BluePrint/BP) classifies early-stage breast cancers based on functional molecular pathways as luminal, HER2, or Basal-type. In the NBRST study, 13% of immunochemistry (IHC) defined ER+ HER2- cancers reclassified as Basal-type by the BP assay (ER+ Basal), and these had worse prognosis but responded better to neoadjuvant chemotherapy than ER+ HER2- cancers classified as genomically luminal-type. The 70-gene risk of recurrence signature (MammaPrint/MP) further stratifies luminal-type cancers into low risk luminal A or high risk (HR) luminal B. HR cancers can be further stratified into High 1 (H1) or High 2 (H2), and the I-SPY2 trial has shown higher pCR rates in ER+ cancers classified as H2. Here, we investigated biological differences among ER+ Basal, ER- Basal, H1 luminal B, and H2 luminal B cancers by full transcriptome analysis. Methods: From the FLEX Study (NCT03053193), 1501 breast cancers with known IHC ER status were classified by MP and BP: 103 ER+ Basal, 210 ER- Basal and 1188 luminal B (H1 n=1034, H2 n=154). Clinical factors were assessed by either the Chi-square or Fisher’s exact tests; ANOVA or t test were used to analyze age. Differentially expressed genes (DEGs) were detected using Limma and pathway analyses were performed with GSEA. DEGs with a fold change >2 and FDR < 0.05 were considered significant. Results: Basal-type cancers (ER+/ER-) were larger and higher grade than luminal B cancers. Clustering analysis showed similar transcriptional profiles between ER+ Basal and ER- Basal cancers, distinct from luminal B cancers. Few DEGs were detected between ER+ Basal and ER- Basal cancers, and significantly more DEGs were found between ER+ Basal and luminal B cancers. Only three upregulated genes were detected in ER+ Basal compared to ER- Basal cancers: ESR1 and two immune-related genes ( FDCSP and LTF). Enrichment analysis of DEGs indicated increased immune activation and cell proliferation in ER+ Basal and ER- Basal cancers, and decreased estrogen response between ER+ Basal and luminal B cancers. Enrichment analysis between luminal B H1 and H2 cancers showed H2 cancers had higher immune activation and cell proliferation and lower estrogen response. Conclusions: Reclassification by BP of IHC defined ER+ HER2- cancers identified a subgroup of ER+ cancers that are biologically closer to ER- Basal than luminal-type cancers. Significant differences in response to neoadjuvant chemotherapy that have been seen between ER+ Basal and luminal B breast cancers lend support to the clinical importance of these findings. These data explain the poor prognosis observed in patients with ER+ Basal cancers and suggest that optimized chemotherapy, such as that for triple negative cancer, might be of benefit. BP provides clinically actionable information beyond pathological subtyping, which may guide neoadjuvant treatment recommendations. Clinical trial information: NCT03053193.

Gene expression profiling of luminal B breast cancers reveals NHERF1 as a new marker of endocrine resistance

2011 ◽  
Vol 130 (2) ◽  
pp. 409-420 ◽  
Author(s):  
Thomas Karn ◽  
Eugen Ruckhäberle ◽  
Lars Hanker ◽  
Volkmar Müller ◽  
Marcus Schmidt ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gene Expression Profiling ◽  
Expression Profiling ◽  
Endocrine Resistance ◽  
Breast Cancers ◽  
Luminal B

Comparison of peritumoral stromal tissue stiffness obtained by shear wave elastography between benign and malignant breast lesions

2018 ◽  
Vol 59 (10) ◽  
pp. 1168-1175 ◽  
Author(s):  
Hye Sun Park ◽  
Hee Jung Shin ◽  
Ki Chang Shin ◽  
Joo Hee Cha ◽  
Eun Young Chae ◽  
...  
Keyword(s):  
Shear Wave ◽  
Malignant Tumors ◽  
Shear Wave Elastography ◽  
Breast Cancers ◽  
Tissue Stiffness ◽  
Linear Arrangement ◽  
Luminal B ◽  
Tumor Subtypes ◽  
Stromal Tissue ◽  
Malignant Breast

Background Aggressive breast cancers produce abnormal peritumoral stiff areas, which can differ between benign and malignant lesions and between different subtypes of breast cancer. Purpose To compare the tissue stiffness of the inner tumor, tumor border, and peritumoral stroma (PS) between benign and malignant breast masses by shear wave elastography (SWE). Material and Methods We enrolled 133 consecutive patients who underwent preoperative SWE. Using OsiriX commercial software, we generated multiple 2-mm regions of interest (ROIs) in a linear arrangement on the inner tumor, tumor border, and PS. We obtained the mean elasticity value (Emean) of each ROI, and compared the Emean between benign and malignant tumors. Odds ratios (ORs) for prediction of malignancy were calculated. Subgroup analyses were performed among tumor subtypes. Results There were 85 malignant and 48 benign masses. The Emean of the tumor border and PS were significantly different between benign and malignant masses ( P < 0.05 for all). ORs for malignancy were 1.06, 1.08, 1.05, and 1.04 for stiffness of the tumor border, proximal PS, middle PS, and distal PS, respectively ( P < 0.05 for all). Malignant masses with a stiff rim were significantly larger than malignant masses without a stiff rim, and were more commonly associated with the luminal B and triple negative subtypes. Conclusion Stiffness of the tumor border and PS obtained by SWE were significantly different between benign and malignant masses. Malignant masses with a stiff rim were larger in size and associated with more aggressive pathologic subtypes.

scholarly journals Ribavirin Treatment Effects on Breast Cancers Overexpressing eIF4E, a Biomarker with Prognostic Specificity for Luminal B-Type Breast Cancer

2011 ◽  
Vol 17 (9) ◽  
pp. 2874-2884 ◽  
Author(s):  
Filippa Pettersson ◽  
Christina Yau ◽  
Monica C. Dobocan ◽  
Biljana Culjkovic-Kraljacic ◽  
Hélène Retrouvay ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Treatment Effects ◽  
Breast Cancers ◽  
Luminal B

scholarly journals Ki67 index in intrinsic breast cancer subtypes and its association with prognostic parameters

2019 ◽  
Vol 12 (1) ◽  
Author(s):  
Atif Ali Hashmi ◽  
Kashif Ali Hashmi ◽  
Muhammad Irfan ◽  
Saadia Mehmood Khan ◽  
Muhammad Muzzammil Edhi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Ductal Carcinoma ◽  
Prognostic Significance ◽  
Breast Cancer Subtypes ◽  
Prognostic Parameters ◽  
Ki67 Index ◽  
Breast Cancers ◽  
Cancer Subtypes ◽  
Luminal B ◽  
Cancer Management

Abstract Objectives Ki67 is the most commonly used marker to evaluate proliferative index in breast cancer, however no cutoff values have been clearly defined for high ki67 index. Cancer management should be according to loco-regional profile; therefore, we aimed to determine ki67 index in 1951 cases of intrinsic breast cancer subtypes and its association with other prognostic parameters in our set up. Results Triple negative breast cancers showed highest ki67 index (mean 50.9 ± 23.7%) followed by Her2neu (mean 42.6 ± 21.6%) and luminal B cancers (mean 34.9 ± 20.05%). Metaplastic and medullary breast cancers significantly showed higher ki67 index as compared to ductal carcinoma, NOS. No significant association of ki67 index was noted with any of the histologic parameters in different subtypes of breast cancer expect for tumor grade. Although, ki67 index is a valuable biomarker in breast cancer, however no independent prognostic significance of ki67 could be established in our study.

Prognostic significance of the progesterone receptor status in Ki67-high and -low Luminal B-like HER2-negative breast cancers

Breast Cancer ◽  
2014 ◽  
Vol 23 (2) ◽  
pp. 310-317 ◽  
Author(s):  
Kaolu Sato ◽  
Minoru Miyashita ◽  
Takanori Ishida ◽  
Akihiko Suzuki ◽  
Hiroshi Tada ◽  
...  
Keyword(s):  
Progesterone Receptor ◽  
Prognostic Significance ◽  
Breast Cancers ◽  
Progesterone Receptor Status ◽  
Receptor Status ◽  
Luminal B

Basal-like Breast Cancer—Characteristics, Risks, and Associations

2012 ◽  
Vol 08 (01) ◽  
pp. 26
Author(s):  
Andrew Y Shuen ◽  
William D Foulkes ◽  
◽  
Keyword(s):  
Breast Cancer ◽  
Massively Parallel Sequencing ◽  
Target Identification ◽  
Response To Therapy ◽  
Breast Cancers ◽  
Luminal A ◽  
Luminal B ◽  
Predictors Of Response ◽  
Epidemiological Risk ◽  
Basal Like Breast Cancer

Breast cancer is a heterogeneous disease. Gene expression profiling has demonstrated the existence of at least five ‘intrinsic’ subtypes: luminal A, luminal B, human epidermal growth factor-2 receptor (HER2), normal-like, and basal-like. While the estrogen receptor (ER), progesterone receptor (PR), and HER2 remain the most important prognostic markers and predictors of response to therapy, interrogating thousands of genetic transcripts more accurately captures the biological complexity and clinical heterogeneity of this disease. Target identification through massively parallel sequencing is likely to bear fruit in the coming years. Attention to basal-like breast cancers has grown substantially due to their generally poor prognosis, lack of targeted therapies, and connection withBRCA1-related cancers. In this article, we discuss the basal-like subgroup with respect to its cellular origins, relationship toBRCA1, and associated epidemiological risk factors.

FGFR: Proof-of-concept study of AZD4547 in patients with FGFR1 or FGFR2 amplified tumours.

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. TPS2626-TPS2626 ◽  
Author(s):  
Elizabeth Catherine Smyth ◽  
Nicholas C. Turner ◽  
Sanjay Popat ◽  
Shethah Morgan ◽  
Kate Owen ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tyrosine Kinases ◽  
Research Network ◽  
Tumor Growth Inhibition ◽  
Breast Cancers ◽  
Open Label ◽  
Multi Centre Study ◽  
Lung Cancers ◽  
Luminal B ◽  
Royal Marsden Hospital

TPS2626 Background: Genetic modifications of the FGFR family of transmembrane tyrosine kinase growth factor receptors are described in a range of cancers. Amplification of FGFR2 is detected in up to 10% of oesophagogastric cancers where it is associated with poor prognosis. FGFR1 amplification has also been demonstrated in 10% of breast cancers, is more common in luminal B ER positive tumors, and is also associated with inferior survival outcomes. Finally, FGFR1 amplification has been described in up to 22% of squamous cell lung cancers. AZD4547 is a potent and selective inhibitor of FGFR-1, 2 and 3 receptor tyrosine kinases. Preclinically, AZD4547 potently inhibits growth in FGFR amplified gastric and lung cancer cell lines and induces dose dependent tumor growth inhibition and regression in FGFR amplified tumour xenograft and patient derived explant models. Methods: This is an open label, phase II non-randomised multi-centre study to assess the efficacy of AZD4547 monotherapy and resulting molecular changes in serial biopsies in pts with previously treated FGFR1 amplified advanced breast cancer, FGFR2 amplified advanced oesophagogastric cancer, or FGFR1 amplified advanced squamous lung cancer. Eligibility include centrally verified FGFR amplified tumour (ratio >2.2), PS=0-2, ability to comply with the collection of tumor biopsies (mandatory at baseline and on days 10-14), calcium and phosphate within normal limits, measurable disease (RECIST 1.1), and no history of significant eye disease. Pts may be prescreened for FGFR amplification on archival tissue while undergoing first line or adjuvant chemotherapy. Sixteen pts will be enrolled per cohort. All pts will receive AZD4547 80mg bd on a two week on, one week off schedule. The primary endpoint is correlation between change in pERK in pretreatment and day 10-14 biopsy and change in tumour diameter on week 8 CT. Secondary endpoints include ORR, DCR and PFS. Multiple exploratory translational endpoints are also planned. The study is currently open at the Royal Marsden Hospital and will open at 15 selected UK cancer centres. This study is sponsored by the Royal Marsden Hospital, funded by AstraZeneca and has been adopted to the UK National Cancer Research Network (NCRN) portfolio. Clinical trial information: 2011-003718-18.

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