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What Is Hormone Receptor Positive

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Testing For Hormone Receptor

Hormone Receptor-Positive and HER2-Positive Breast Cancer: A Medical Update

After a breast cancer , the removed sample of breast is sent to a lab for testing. If the tissue is confirmed to have cancer cells, the tests help your care team learn more about the cancer and how to treat it. Your doctor will share the test results with you in a document called a pathology report.

One test performed on breast cancer cells is called an immunohistochemical staining , or IHC test. This test checks the hormone receptor status of the cancer cells. IHC tests show whether the cancer cells have estrogen receptors, progesterone receptors, or both.

D Extended Adjuvant Endocrine Therapy Recommendations

Recommendations for extended endocrine therapy are summarized in Figure 1 and Figure 2. In patients who are pre- or peri-menopausal at diagnosis and who do not receive OFS as part of their treatment paradigm, current ASCO guidelines recommend treatment with 5 years of adjuvant tamoxifen. After 5 years of tamoxifen, women who remain pre-menopausal are candidates for extended endocrine therapy with an additional 5 years of tamoxifen. Women who become post-menopausal during the first 5 years of tamoxifen in whom extended therapy is planned may either continue tamoxifen for an additional 5 years, or receive 5 years of an AI . NCCN guidelines recommend that women who are pre-menopausal at diagnosis, and who do not undergo treatment with OFS should consider tamoxifen for up to 10 years. Women who are pre-menopausal at diagnosis and who are treated with 5 years of tamoxifen-OFS or AI-OFS may consider an additional 5 years of tamoxifen if they remain pre-menopausal. Women who were pre-menopausal at diagnosis who become post-menopausal, may consider extended endocrine therapy with an AI for a further 5 years following tamoxifen .

What Is Metastatic Hormone Receptor

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If you have breast cancer, your medical oncologist and the other members of your care team will use certain key information to help gauge your prognosis and determine the most appropriate treatment. One of these data points is whether the cancer is confined to the breast or has spread to another part of the body. Breast cancer that has moved beyond its point of origin is called metastatic breast cancer.

Another important piece of information is whether the cancer depends on hormones estrogen and/or progesterone to grow. If it does, its known as hormone receptor-positive breast cancer. Around 70% of breast cancers are hormone receptor-positive, according to the American Cancer Society. Metastatic hormone receptor-positive breast cancer is breast cancer that grows with the help of one or both of the female hormones and affects an area of the body beyond the breast.

Currently, metastatic breast cancer, including hormone receptor-positive disease, has no cure. However, modern medicine continues to improve and patients are living longer with each advancement. Cancer specialists use hormone therapy and other treatments to reduce symptoms and help patients enjoy the best quality of life possible.

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Treatment Of Hormone Receptor

At Dignity Health hospitals, our cancer care team is committed to providing comprehensive treatment options for hormone receptor-positive breast cancer. In most cases, surgery will be the primary treatment option. Lumpectomy removes the tumor and some normal tissue surrounding it. Radiation therapy is usually necessary after lumpectomy. Mastectomy removes the entire breast. The stage of breast cancer will determine the type of surgery you need.

Other treatments include:

  • Hormone therapy works two ways to slow the growth of cancer cells.
  • Chemotherapy kills cancer cells or stop them from growing
  • Targeted therapy uses markers on cancer cells to identify and destroy those specific cells.

Your Dignity Health doctor will explain the options for your unique case and support you at every stage of treatment.

Hormone Receptor Status Explained

Challenges in Treating Estrogen Receptor

All breast cells and some breast cancer cells have proteins called estrogen or progesterone receptors. These receptors bond with their namesake hormones in the blood because they help the cells grow.

Breast cancer is hormone receptor-positive if it has estrogen and/or progesterone receptors, and its further classified based on which type of receptor it has. The cancer is known as ER-positive if it has estrogen receptors, and PR-positive if it has progesterone receptors.

Some breast cancers are hormone receptor-negative, meaning they dont have hormone receptors. Still other breast cancers may be triple-negative they dont have hormone receptors and arent affected by HER2, a protein that helps breast cancer grow and spread quickly.

Your cancer team will use a sample of the tumor to test for hormone receptors following a biopsy or surgery to remove the cancer. If you have hormone receptor-positive breast cancer, you have a treatment option available to you that patients with hormone receptor-negative disease dont hormone therapy.

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Hormone Receptor Positive Breast Cancer Has A More Favorable Outlook Following Diagnosis

About 70% of all invasive breast cancers demonstrate positive ER expression. Estrogen functions as a transcription factor and is an essential element in the tumorigenesis, differentiation, and growth of breast cancer tumors. Nonetheless, women with ER and PR positive breast tumors do have a lower mortality risk following diagnosis as compared to women with either ER- PR+, or ER- PR- breast tumors. Furthermore, women with ER and PR receptor negative tumors also tend to show HER-2 overexpression, which has also been shown to exert a negative influence on breast cancer outlook.

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Why Do I Need An Er/pr Test

You may need this test if you’ve been diagnosed with breast cancer. Knowing your hormone receptor status will help your health care provider decide how to treat it. If you have ER-positive, PR-positive, or HR-positive cancer, drugs that lower hormone levels or stop the hormones from fueling cancer growth can be very effective. If you have HR-negative cancer, these types of drugs won’t work for you.

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Receptors For Breast Cancer

Some breast cancer cells have hormone or protein receptors that affect how the cancer grows.

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Breast cancer cells may have receptors that hormones or a protein called HER2 can attach to and encourage the cells to grow. A pathologist tests the cancer cells that were taken during the biopsy or surgery for these receptors.

The results help you and your doctor decide on the most effective treatment for you.

Treating Metastatic Hormone Receptor

Understanding Estrogen Receptor-Positive (ER+) Metastatic Breast Cancer (MBC)

Typically, cancer specialists use medications that travel through the blood, a type of treatment known as systemic therapy, to treat metastatic breast cancer. In some cases, treatment may also involve surgery and/or radiation therapy.

Systemic therapy options include chemotherapy, targeted therapy, immunotherapy, and, for metastatic breast cancer that is hormone receptor-positive, hormone therapy. You may receive one type of systemic therapy at a time, or multiple therapies at once.

Hormone therapy plays a major role in treatment for people with metastatic hormone receptor-positive breast cancer. On the other hand, its not effective for hormone receptor-negative cancers. According to the National Cancer Institute, the goal of hormone therapy is to slow or halt cancers growth by disrupting its fuel estrogen and/or progesterone. Different types of medication accomplish this in different ways.

  • Aromatase inhibitors disrupt the aromatase enzyme, which contributes to estrogen production.
  • Ovarian suppression therapy uses medications or removal of the ovaries to reduce estrogen production. Sometimes, an ovarian suppression medication may be taken with an aromatase inhibitor.
  • Selective estrogen receptor downregulators prevent estrogen-to-receptor attachment. One of the most common SERDs is fulvestrant.
  • Selective estrogen receptor modulators attach to estrogen receptors and block the hormone from joining with the receptor. Tamoxifen is a common SERM.

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Is Stomach Cancer Hereditary

Stomach cancer is the second leading cause of cancer related deaths worldwide and in India, the fourth in the list of the most common cancers. As per the US National Institutes of Health close to ten percent of stomach cancer cases have a familial origin. Having a first degree relative such as father, mother, brother or sister with stomach cancer increases the risk of developing stomach cancer.

While gene mutations have been linked to stomach cancer in some people, the exact genetic factors are not fully understood. Scientists believe a combination of environmental and genetic factors could be responsible for familial stomach cancer.

Some of the inherited conditions that increase stomach cancer risk include:

Hereditary diffuse gastric cancer :

This is an inherited, rare condition that increases risk of stomach cancer caused by a mutation in a gene known as CDH1.

Diffuse gastric cancer also known as or linitis plastica orsignet ring cell gastric cancer affects almost the entire stomach rather than any one specific area in the stomach. According to the NIH, diffuse gastric cancers account for 20 percent of stomach cancers and HDGC is responsible for a small amount of these cancers. Women diagnosed with HDGC are at an increased risk of developing breast cancer.

Diagnosis of HDGC is made if any one criteria listed below are met apart from recommending CDH1 genetic testing:

Lynch syndrome:

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Will I Need To Do Anything To Prepare For The Test

You won’t need any special preparations if you are getting local anesthesia . If you are getting general anesthesia, you will probably need to fast for several hours before surgery. Your surgeon will give you more specific instructions. Also, if you are getting a sedative or general anesthesia, be sure to arrange for someone to drive you home. You may be groggy and confused after you wake up from the procedure.

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Combination Of Endocrine Therapies

As the available anti-endocrine drugs have different mechanisms of action, combination of agents is a logical approach to improve the effectiveness of ET. Conflicting results have been reported from the comparison of the combination of fulvestrant with anastrozole versus anastrozole as single agent. The FACT trial reported no clinical advantage with the combination , while the SWOG S0226 trial reported advantages in PFS and OS favoring the combination in 694 ABC patients . Subgroup analysis of this trial suggested that the benefits were largely restricted to women who had not received adjuvant tamoxifen and differences in the population included probably explain the conflicting results in the two studies. Furthermore, results of the second-line SoFEA trial showed that combining fulvestrant to anastrozole is not more effective that fulvestrant alone or exemestane alone in HR+ ABC that has progressed during therapy with a nonsteroidal AI. A subgroup analysis suggested those patients with tumors with both ER and PR positivity, favoring a more endocrine-sensitive phenotype, may obtain greater benefit . Based on these data, it could be hypothesized that patients with ET-naïve ABC and those with highly endocrine-sensitive tumors could derive the largest benefit from combination ET. However, in our opinion, we should wait for further evidence before considering the combination of AIs and fulvestrant in routine clinical practice . First-line ET trials are summarized in .

Chemically Induced Rodent Models And Genetically Engineered Mouse Models


Chemically induced rodent mammary carcinoma models developed in the 1980s have been widely used to investigate hormone-dependent BC. Tumors are induced in rats by a single dose of oral 7,12-dimethylbenzanthracene or intravenous or subcutaneous N-methylnitrosurea they form with a latency between 8 and 12 weeks and a nearly 100% incidence . Both NMU and DMBA-induced tumors express ER and PR . Administration of medroxyprogesterone acetate decreases latency and increases the incidence of DMBA-induced tumors . Importantly, these tumors faithfully recapitulate various aspects of the human disease. Their growth if hormone-dependent and pregnancy before carcinogen exposure reduces tumor incidence . However, these models were not readily amenable to mechanistic studies because genetic engineering of rat models has long proven challenging. Only recently with the advent of TALEN and CRISPR , technology pace has picked up . To date, most research efforts have focused on mouse models instead, which can be readily genetically manipulated. GEMMs represent an elegant tool to recapitulate in vivo carcinogenesis. They offer the advantage that tumors develop in the tissue of origin, in the presence of an intact immune system and organ microenvironment with stromal remodeling, inflammation and angiogenesis.

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Her2 Status In Breast Cancer

If your cancer appears to be aggressive and fast-growing, you might have higher levels of a protein called human epidermal growth factor receptor 2, or HER2 for short. Some genes, like HER2, and the proteins they make, do more than play a role in the development of breast cancer. They can also influence how your breast cancer behaves as well as how it may respond to specific cancer treatments.

Usually, HER2 receptors help control how a healthy breast cell grows, divides, and repairs itself. However, if the HER2 gene doesnt work correctly and produces too many copies of itself, it leads to the uncontrolled growth of breast cancer cells.

A Extended Tamoxifen Therapy

The role of extended tamoxifen therapy has been evaluated in several studies and the largest of those are discussed here in more detail. In the Adjuvant Tamoxifen: Longer Against Shorter trial, > 12,000 patients who were treated with tamoxifen for 5 years were randomized to either stopping therapy or continuing tamoxifen for 5 additional years. Ten years of tamoxifen resulted in reductions in the risk of breast cancer recurrence, breast cancer mortality and overall mortality. The risk of recurrence in years 5-14 was reduced by 3.7% with extended tamoxifen, whereas breast cancer mortality was reduced by 2.8% . In the Adjuvant Tamoxifen-To Offer More study, almost 7,000 patients were randomized to stop tamoxifen after 5 years, or to continue to year 10. Ten years of tamoxifen was associated with a 2.6% reduction in breast cancer recurrence, which was most notable beyond year 7, and a 1.4% reduction in breast cancer mortality .

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What Is A Hormone Receptor

In breast cancer, hormone receptors are the proteins located in and around breast cells. These receptors signal cells both healthy and cancerous to grow. In the case of breast cancer, the hormone receptors tell the cancer cells to grow uncontrollably, and a tumor results.

Hormone receptors can interact with estrogen or progesterone. Estrogen receptors are the most common. This is why ER-positive is the most common form of breast cancer.

Some people are diagnosed with progesterone receptor-positive breast cancer. The key difference is whether cancerous cells are getting growth signals from estrogen or progesterone.

Testing for hormone receptors is important in treating breast cancer. In some cases, there are no hormone receptors present, so hormone therapy isnt a good treatment option. This is called hormone receptor-negative breast cancer.

According to, about 2 out of 3 people with breast cancer have some form of hormone receptors present. This makes them candidates for hormone therapy.

What Is The Survival Rate For Hr Positive Breast Cancers

Hormone Receptor Positive Breast Cancer

The survival rate for breast cancers are excellent if the cancer is detected early, and in general HR positive cancers grow slower and have a better prognosis. Overall, breast cancers that are both HR positive and HER2 negative have the best outcomes.

According to recent National Cancer Institute data, the four-year survival rate for combined stages of cancer, based on HR and HER2 status are:

  • HR positive/HER2 negative: 92.5%

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Hormone Receptors & Receptor Tests

All breast cancers are examined under a microscope for biomarkers of estrogen and progesterone receptors. About 70% of breast cancers are hormone receptor-positive.

Your hormone receptor status should appear on your pathology report after biopsy or surgery. Receptors will be retested if you ever have a recurrence or metastases as well, as your status can change.

Hormones and receptors go together kind of like a lock and key. Receptors are proteins on the surface of breast cells, and when hormones bind to them, the receptors tell the cells to grow and divide. All breast cells have receptors, but they are found in much greater numbers on breast cancer cells that are considered positive.

A goal of treatment is to block the signal created when the hormones attach to receptors. Doing that requires one of two things:

  • Reducing the amount of the hormone in the body
  • Blocking the receptor so that hormone cant bind with it
  • Most of the time, breast cancers tend to be positive or negative for both estrogen and progesterone receptors. Now and then, one will be positive for estrogen but not progesterone. The treatment is the same either way.

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    Less Common Types Of Hormone Therapy

    Some other types of hormone therapy that were used more often in the past, but are rarely given now include:

    • Megestrol acetate , a progesterone-like drug
    • High doses of estrogen

    These might be options if other forms of hormone therapy are no longer working, but they can often cause side effects.

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    When Is Hormone Therapy Used For Breast Cancer

    Hormone therapy is often used after surgery to help reduce the risk of the cancer coming back. Sometimes it is started before surgery .

    It is usually taken for at least 5 years. Treatment longer than 5 years might be offered to women whose cancers have a higher chance of coming back. A test called the Breast Cancer Index might be used to help decide if a woman will benefit from more than 5 years of hormone therapy.

    Hormone therapy can also be used to treat cancer that has come back after treatment or that has spread to other parts of the body.

    A Hormone Receptor Status Is Either Hormone Receptor Positive Or Hormone Receptor Negative

    • Hormone receptor-positive breast cancer cells have either estrogen or progesterone receptors. These breast cancers can be treated with hormone therapy drugs that lower estrogen levels or block estrogen receptors. HR-positive cancers tend to grow more slowly than those that are HR-negative. HR-positive cancers are generally more common in women after menopause.
    • Hormone receptor-negative breast cancers do not have estrogen or progesterone receptors. These types of cancers will not benefit from hormone therapy drugs and typically grow faster than HR-positive cancers. HR-negative cancers are more common in women who have not yet gone through menopause.

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