Steroidogenesis in Human Breast Cancer, Benign Breast Disease and Normal Breast Tissue

1973 ◽  
Vol 1 (3) ◽  
pp. 762-765
Author(s):  
WILLIAM R. MILLER ◽  
DAVID McDONALD ◽  
A. P. M. FORREST
Keyword(s):  
Breast Cancer ◽  
Human Breast Cancer ◽  
Breast Tissue ◽  
Benign Breast Disease ◽  
Normal Breast Tissue ◽  
Breast Disease ◽  
Normal Breast ◽  
Human Breast

Evaluation of the expression levels of nm23-h1 mRNA in primary breast cancer, benign breast disease, axillary lymph nodes and normal breast tissue

Pathology ◽  
1994 ◽  
Vol 26 (4) ◽  
pp. 423-428 ◽  
Author(s):  
Rebecca J. Goodall ◽  
Hugh J.S. Dawkins ◽  
Peter D. Robbins ◽  
Erika Hähnel ◽  
Mohinder Sarna ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Lymph Nodes ◽  
Primary Breast Cancer ◽  
Breast Tissue ◽  
Benign Breast Disease ◽  
Normal Breast Tissue ◽  
Breast Disease ◽  
Normal Breast ◽  
Axillary Lymph Nodes ◽  
Axillary Lymph

Prostate specific antigen in breast cancer, benign breast disease and normal breast tissue

1996 ◽  
Vol 40 (2) ◽  
pp. 171-178 ◽  
Author(s):  
He Yu ◽  
Eleftherios P. Diamandis ◽  
Michael Levesque ◽  
Maurizia Giai ◽  
Riccardo Roagna ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Prostate Specific Antigen ◽  
Breast Tissue ◽  
Benign Breast Disease ◽  
Normal Breast Tissue ◽  
Specific Antigen ◽  
Breast Disease ◽  
Normal Breast

Glycolytic Enzymes in Breast Cancer, Benign Breast Disease and Normal Breast Tissue

Tumor Biology ◽  
1987 ◽  
Vol 8 (5) ◽  
pp. 251-263 ◽  
Author(s):  
A. Hennipman ◽  
J. Smits ◽  
B. van Oirschot ◽  
J.C. van Houwelingen ◽  
G. Rijksen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Breast Tissue ◽  
Benign Breast Disease ◽  
Normal Breast Tissue ◽  
Breast Disease ◽  
Normal Breast ◽  
Glycolytic Enzymes

scholarly journals Targeted next-generation sequencing assays using triplet samples of normal breast tissue, primary breast cancer, and recurrent/metastatic lesions

2020 ◽  
Author(s):  
Toshiaki Akahane ◽  
Naoki Kanomata ◽  
Oi Harada ◽  
Tetsumasa Yamashita ◽  
Junichi Kurebayashi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Primary Tumor ◽  
Primary Breast Cancer ◽  
Breast Tissue ◽  
Normal Breast Tissue ◽  
Metastatic Breast ◽  
Normal Breast ◽  
Human Breast ◽  
Metastatic Lesions ◽  
Generation Sequencing

Abstract Background: Next-generation sequencing (NGS) has shown that recurrent/metastatic breast cancer lesions may have additional genetic changes compared with the primary tumor. These additional changes may be related to tumor progression and/or drug resistance. However, breast cancer-targeted NGS is not still widely used in clinical practice to compare the genomic profiles of primary breast cancer and recurrent/metastatic lesions.Methods: Triplet samples of genomic DNA were extracted from each patient’s normal breast tissue, primary breast cancer, and recurrent/metastatic lesion(s). A DNA library was constructed using the QIAseq Human Breast Cancer Panel (93 genes, Qiagen) and then sequenced using MiSeq (Illumina). The Qiagen web portal was utilized for data analysis.Results: Successful results for three or four samples (normal breast tissue, primary tumor, and at least one metastatic/recurrent lesion) were obtained for 11 of 35 breast cancer patients with recurrence/metastases (36 samples). We detected shared somatic mutations in all but one patient, who had a germline mutation in TP53. Additional mutations that were detected in recurrent/metastatic lesions compared with primary tumor were in genes including TP53 (three patients) and one case each of ATR, BLM, CBFB, EP300, ERBB2, MUC16, PBRM1, and PIK3CA. Actionable mutations and/or copy number variations (CNVs) were detected in 73% (8/11) of recurrent/metastatic breast cancer lesions.Conclusions: The QIAseq Human Breast Cancer Panel assay showed that recurrent/metastatic breast cancers sometimes acquired additional mutations and CNV. Such additional genomic changes could provide therapeutic target.

Loss of ALX4 expression in epithelial cells and adjacent stromal cells in breast cancer

2009 ◽  
Vol 62 (10) ◽  
pp. 908-914 ◽  
Author(s):  
H Chang ◽  
N Mohabir ◽  
S Done ◽  
P A Hamel
Keyword(s):  
Breast Cancer ◽  
Epithelial Cells ◽  
Tissue Microarray ◽  
Stromal Cells ◽  
Breast Tissue ◽  
Normal Breast Tissue ◽  
Normal Breast ◽  
Human Breast ◽  
Duct Carcinoma ◽  
Normal Human Breast

Background:Loss of the stromally-restricted homeodomain transcription factor, Alx4, causes defective mouse mammary epithelial morphogenesis.Aims:To begin to define the role of ALX4 in the human breast and in breast cancer, the expression pattern of ALX4 in the normal human breast and changes in expression in breast cancer were determined.Methods:Cells expressing ALX4 in the human breast were identified by co-immunofluorescence using α-ALX4 antibodies and markers of specific mammary cell types. ALX4 expression in breast cancer was then determined by immunohistochemistry on tumour sections that also harboured regions of normal breast tissue. Using criteria that required ALX4 staining in both stromal and epithelial cells, changes in ALX4 expression in tumours on a tissue microarray were determined.Results:ALX4 was expressed in both stromal and luminal epithelial cells in the human breast. Scoring tissue sections of duct carcinoma in situ (DCIS) or invasive ductal carcinoma (IDC) that also harboured regions of normal breast tissue, a loss of ALX4 (p<0.001) in stromal and epithelial cells in breast tumours was observed. Analysis of ALX4 expression in 123 sections on a tissue microarray confirmed a highly significant loss (p<0.001) of ALX4 in breast cancer in the tumours themselves and in adjacent stromal cells.Conclusions:These data show a distinct pattern of expression of ALX4 in the human breast relative to the murine mammary gland. Furthermore, characterisation of ALX4 in breast cancer showed that loss of ALX4 in tumours and the surrounding untransformed stroma is a basic characteristic of DCIS and IDC.

scholarly journals Targeted next-generation sequencing assays using triplet samples of normal breast tissue, primary breast cancer, and recurrent/metastatic lesions

BMC Cancer ◽  
2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Toshiaki Akahane ◽  
Naoki Kanomata ◽  
Oi Harada ◽  
Tetsumasa Yamashita ◽  
Junichi Kurebayashi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Primary Tumor ◽  
Primary Breast Cancer ◽  
Breast Tissue ◽  
Normal Breast Tissue ◽  
Metastatic Breast ◽  
Normal Breast ◽  
Human Breast ◽  
Metastatic Lesions ◽  
Generation Sequencing

Abstract Background Next-generation sequencing (NGS) has shown that recurrent/metastatic breast cancer lesions may have additional genetic changes compared with the primary tumor. These additional changes may be related to tumor progression and/or drug resistance. However, breast cancer-targeted NGS is not still widely used in clinical practice to compare the genomic profiles of primary breast cancer and recurrent/metastatic lesions. Methods Triplet samples of genomic DNA were extracted from each patient’s normal breast tissue, primary breast cancer, and recurrent/metastatic lesion(s). A DNA library was constructed using the QIAseq Human Breast Cancer Panel (93 genes, Qiagen) and then sequenced using MiSeq (Illumina). The Qiagen web portal was utilized for data analysis. Results Successful results for three or four samples (normal breast tissue, primary tumor, and at least one metastatic/recurrent lesion) were obtained for 11 of 35 breast cancer patients with recurrence/metastases (36 samples). We detected shared somatic mutations in all but one patient, who had a germline mutation in TP53. Additional mutations that were detected in recurrent/metastatic lesions compared with primary tumor were in genes including TP53 (three patients) and one case each of ATR, BLM, CBFB, EP300, ERBB2, MUC16, PBRM1, and PIK3CA. Actionable mutations and/or copy number variations (CNVs) were detected in 73% (8/11) of recurrent/metastatic breast cancer lesions. Conclusions The QIAseq Human Breast Cancer Panel assay showed that recurrent/metastatic breast cancers sometimes acquired additional mutations and CNV. Such additional genomic changes could provide therapeutic target.

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