A hormone-receptor-positive (HR+) tumor is a tumor which consists of cells that express receptors for certain hormones. The term most commonly refers to estrogen receptor positive tumors (i.e. tumors that contain estrogen receptor positive cells), but can also include progesterone receptor positive tumors. Estrogen-receptor-positive tumors depend on the presence of estrogen for ongoing proliferation.

Classification

ER-positive is one of the Receptor statuses identified in the classification of breast cancer. Receptor status was traditionally considered by reviewing each individual receptor (ER, PR, her2) in turn, but newer approaches look at these together, along with the tumor grade, to categorize breast cancer into several conceptual molecular classes[1] that have different prognoses[2] and may have different responses to specific therapies.[3] DNA microarrays have assisted this approach.

Breast tumors that do not express ER, PR or Her2 are referred to as triple-negative breast cancers.[4]

Treatment

Endocrine treatment may be beneficial for patients with hormone receptor positive breast tumors.[5]

There are two ways for treating these kind of tumors:

  • Lowering systemic levels of estrogen, achieved by the use of drugs from the aromatase inhibitor category.[6][7] These drugs target one of the enzymes that takes part in the biosynthesis of estrogen.
  • Blockage of the estrogen receptors on the cancerous cells, thus preventing estrogen binding, leading to decreased proliferation. Drugs in this category are referred to as SERMs (selective estrogen receptor modulator) since they are able to block estrogen receptors in a selective manner.

See also

References

  1. ↑ Prat, A.; Perou, C. M. (2011). "Deconstructing the molecular portraits of breast cancer". Molecular Oncology. 5 (1): 5–23. doi:10.1016/j.molonc.2010.11.003. PMC 5528267. PMID 21147047.
  2. ↑ "National Comprehensive Cancer Network (NCCN) guidelines, Breast Cancer Version 2.2011" (PDF).
  3. ↑ Geyer, F. C.; Marchiò, C.; Reis-Filho, J. S. (2009). "The role of molecular analysis in breast cancer". Pathology. 41 (1): 77–88. doi:10.1080/00313020802563536. PMID 19089743. S2CID 39374813.
  4. ↑ Foulkes WD, Smith IE, Reis-Filho JS (November 2010). "Triple-negative breast cancer". The New England Journal of Medicine. 363 (20): 1938–48. doi:10.1056/Nejmra1001389. PMID 21067385. S2CID 205115843.
  5. ↑ DeVita, Vincent T.; Lawrence, Theodore S.; Rosenberg, Steven A.; Robert A. Weinberg; Ronald A. DePinho (2008-04-01). DeVita, Hellman, and Rosenberg's cancer: principles & practice of oncology. Lippincott Williams & Wilkins. pp. 1646–. ISBN 978-0-7817-7207-5. Retrieved 1 August 2011.
  6. ↑ Trunet PF, Vreeland F, Royce C, Chaudri HA, Cooper J, Bhatnagar AS (April 1997). "Clinical use of aromatase inhibitors in the treatment of advanced breast cancer". J. Steroid Biochem. Mol. Biol. 61 (3–6): 241–5. doi:10.1016/S0960-0760(97)80018-0. PMID 9365196. S2CID 24690564.
  7. ↑ Younus J, Vandenberg TA (April 2005). "A practical overview of aromatase inhibitors in postmenopausal women with hormone receptor-positive breast cancer". Bull Cancer. 92 (4): E39–44. PMID 15888383.
  8. ↑ Legha SS (August 1988). "Tamoxifen in the treatment of breast cancer". Ann. Intern. Med. 109 (3): 219–28. doi:10.7326/0003-4819-109-3-219. PMID 3291659.

Further reading

http://www.breastcancer.org/treatment/hormonal/what_is_it/hormone_role.jsp

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