Overview of Breast Cancer

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Each year, over 40,000 women and almost 500 men in the United States succumb to breast cancer1. While survival rates for breast cancer patients have been increasing, from 61% for patients diagnosed in 1973 to 83% for patients diagnosed in 1992, there is still a long way to go in understanding how to treat this complex disease2. Indeed, breast cancer can be categorized into several subtypes based on the expression of the receptors for hormones estrogen and progesterone, and expression of HER2. Whether or not a tumor expresses receptors for the hormones estrogen and/or progesterone, or HER2, has implications for both available treatments and prognosis. Expression of these molecules has been shown in epidemiologic studies to differ based on ethnicity, with triple-negative breast cancers, the subtype with the worst prognosis, having the highest incidence in African American women. Hormone receptor (HR) positive/HER2 negative breast cancer is the most common subtype across ethnicities and is the most treatable. HR-positive, HER2-negative breast cancer is often diagnosed by mammography and is therefore frequently detected before it is able to metastasize3.

 

Many groups are investigating novel pathways driving breast cancer formation and progression that may lead to the development of new treatment options for this disease. Some of these pathways, including hepatocyte growth factor (HGF)/c-MET4, Notch, Wnt, and Sonic hedgehog, as well as the activity of a class of proteins called cyclin dependent kinases, signal in the breast cancer cells themselves and drive processes such as cell cycle progression and cell proliferation5. Breast cancer cells may also undergo epigenetic changes, including changes to DNA methylation status6. In HER2+ breast cancer, several genes that are differentially methylated when compared to normal breast tissue are involved in the PI3K and Wnt signaling pathways, already implicated in breast cancer pathogenesis7. Indeed, the more HER2 amplification in a particular case of breast cancer, the higher the frequency of aberrant methylation at sites across the genome8.

 

Other avenues of breast cancer research include investigating the advancement of treatment options for this disease. As in many types of cancer, immunotherapies have shown some promise in breast cancer. Blockade of the PD-1/PD-L1 pathway may be a targetable pathway in triple-negative breast cancer, which currently has no useful treatment options available9. Other ongoing immunotherapy clinical trials include tumor antigen-derived vaccination strategies targeting molecules including WT-1, HER2, and NY-ESO-1, and adoptive T cell therapy10. Clinical applications of immunotherapies are in addition existing targeted therapies for certain types of breast cancer. These include trastuzumab, an anti-HER2 monoclonal antibody11, and therapies that deplete the hormones driving HR+ breast cancer progression, including aromatase inhibitors and estrogen receptor modulators12.

 

>Detection of human Chk1, Phospho (S317) in FFPE breast carcinoma by IHC

Detection of human Chk1, Phospho (S317) in FFPE breast carcinoma by IHC. Antibody: Rabbit anti-Chk1, Phospho (S317) (A304-673A). Secondary: HRP-conjugated goat anti-rabbit IgG (A120-501P). Substrate: DAB.

Detection of human MEK1 in FFPE breast carcinoma by IHC

Detection of human MEK1 in FFPE breast carcinoma by IHC. Antibody: Rabbit anti-MEK1 (IHC-00619). Secondary: HRP-conjugated goat anti-rabbit IgG (A120-501P). Substrate: DAB.

Detection of human TPR in FFPE breast carcinoma by IHC.

Detection of human TPR in FFPE breast carcinoma by IHC. Antibody: Rabbit anti-TPR (IHC-00099). Secondary: HRP-conjugated goat anti-rabbit IgG (A120-501P). Substrate: DAB.

 

Below is the entire list of targets involved in Breast Cancer research. Can’t find what you are looking for? Bethyl offers a custom antibody service.

 

References

1. CDC - Breast Cancer Statistics [Internet]. (2017) [cited 2018 Apr 23].

2. Iqbal J, Ginsburg O, Rochon PA, Sun P, Narod SA. (2015) Differences in Breast Cancer Stage at Diagnosis and Cancer-Specific Survival by Race and Ethnicity in the United States. JAMA. American Medical Association; 313:165.

3. Kohler BA, Sherman RL, Howlader N, Jemal A, Ryerson AB, Henry KA, et al. Annual Report to the Nation on the Status of Cancer, 1975-2011, Featuring Incidence of Breast Cancer Subtypes by Race/Ethnicity, Poverty, and State. (2015) J Natl Cancer Inst. Oxford University Press; 107:djv048.

4. Ho-Yen CM, Jones JL, Kermorgant S. (2015) The clinical and functional significance of c-Met in breast cancer: a review. Breast Cancer Res. 17:52.

5. Nwabo Kamdje AH, Seke Etet PF, Vecchio L, Muller JM, Krampera M, Lukong KE. (2014) Signaling pathways in breast cancer: Therapeutic targeting of the microenvironment. Cell Signal. Pergamon;26:2843–56.

6. Pinto R, De Summa S, Pilato B, Tommasi S. (2014) DNA methylation and miRNAs regulation in hereditary breast cancer: epigenetic changes, players in transcriptional and post- transcriptional regulation in hereditary breast cancer. Curr Mol Med. 14:45–57.

7. Lindqvist BM, Wingren S, Motlagh PB, Nilsson TK. (2014) Whole genome DNA methylation signature of HER2-positive breast cancer. Epigenetics. Taylor & Francis;9:1149–62.

8. Terada K, Okochi-Takada E, Akashi-Tanaka S, Miyamoto K, Taniyama K, Tsuda H, et al. (2009) Association between frequent CpG island methylation and HER2 amplification in human breast cancers. Carcinogenesis. 30:466–71.

9. Cimino-Mathews A, Foote JB, Emens LA. (2015) Immune targeting in breast cancer. Oncology (Williston Park). 29:375–85.

10. Criscitiello C, Curigliano G. (2015) Immunotherapy of Breast Cancer. Prog tumor Res. 42:30–43.

11. Dokmanovic M, Wu WJ. (2015) Monitoring Trastuzumab Resistance and Cardiotoxicity. Adv Clin Chem. page 95–130.

12. Dalmau E, Armengol-Alonso A, Muñoz M, Seguí-Palmer MÁ. (2014) Current status of hormone therapy in patients with hormone receptor positive (HR+) advanced breast cancer. The Breast. 23:710–20.