Related Experiment Video
Updated: May 14, 2026

11:42
Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
Published on: April 7, 2017
Molecular alterations in metaplastic breast carcinoma
Caroline Louise Cooper1, Rooshdiya Z Karim, Christina Selinger
1Department of Tissue Pathology and Diagnostic Oncology, Royal Prince Alfred Hospital, Camperdown, New South Wales, Australia. caroline.cooper@sswahs.nsw.gov.au
Journal of Clinical Pathology
|February 2, 2013
Summary
Metaplastic breast carcinoma is a rare cancer with poor prognosis and limited treatment options. Research is exploring its genetic basis to find new therapeutic targets for this challenging malignancy.
Area of Science:
- Oncology
- Genetics
- Pathology
Background:
- Metaplastic carcinoma of the breast (MCB) is a rare, heterogeneous breast cancer subtype.
- MCB typically presents as larger tumors with less nodal metastasis than invasive ductal carcinoma.
- MCB often lacks hormone and HER2 receptor expression, limiting standard treatment efficacy.
Purpose of the Study:
- To review the pathogenesis theories of metaplastic breast carcinoma.
- To highlight known genetic alterations in MCB.
- To identify potential therapeutic targets for improved treatment strategies.
Main Methods:
- Literature review of metaplastic breast carcinoma.
- Analysis of genetic changes in MCB subsets.
- Discussion of molecular alterations and therapeutic targets.
Main Results:
- MCB exhibits distinct clinical and morphological characteristics.
- Some actionable genetic alterations have been identified in subsets of MCB.
- Further characterization of the genetic basis is crucial for new treatment development.
Conclusions:
- Metaplastic breast carcinoma has a generally poor outcome and few therapeutic options.
- Understanding the genetic landscape of MCB is essential for identifying novel therapeutic targets.
- Continued research into MCB pathogenesis and molecular alterations is needed.
Related Concept Videos
Cellular Adaptation IV: Dysplasia and Metaplasia
DysplasiaDysplasia refers to abnormal changes in the size, shape, and organization of mature cells, characterized by pleomorphism, nuclear abnormalities, and increased mitotic activity. It commonly affects epithelial tissues, including the cervix, gastrointestinal tract, respiratory mucosa, and endometrium. Although it may occur alongside hyperplasia, dysplasia is not a true adaptive response but a preneoplastic change with potential to progress to cancer.When confined above the basement...
Tumor Progression
Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
Metastasis
Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
