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What is Estrogen Receptor Positive Breast Cancer?


Breast cancer is the most common female cancer in the US.

Important risk factors for breast cancer are age, gender, reproductive history, hormonal factors, and family history. Although a family history of breast and/or ovarian cancer is common in patients diagnosed with breast cancer, less than ten percent of all breast cancers are associated with genetic mutations.

Assay of hormone receptors (estrogen [ER] and progesterone [PR] receptors) is an important component of the pathologic evaluation of breast cancer, for both prognostic and predictive purposes, as patients with hormone receptor-positive tumors benefit from the addition of endocrine treatments.

 

 What are the Molecular SubTypes of Breast Cancer:

 Molecular profiling, based upon variations in gene expression, has identified several distinct breast cancer subtypes, named the breast cancer intrinsic subtypes.

Luminal A and B are the most common subtypes and make up the majority of estrogen receptor (ER)-positive breast cancers. Luminal A tumors carry the best prognosis of all of the subtypes. Luminal B tumors have a lower expression of ER-related genes, variable expression of the human epidermal growth factor receptor-2 (HER2) cluster, and higher expression of the proliferation cluster. Consequently, luminal B tumors have a poorer prognosis.

HER2-enriched (HER2+/ER-) subtype cancers are typically negative for ER and progesterone receptor (PR), and positive for HER2. The poor prognosis associated with these tumors has been undoubtedly altered by HER2-directed therapies

Basal-like tumors are typically ER-negative, PR-negative, and HER2-negative on clinical assays, which has prompted the nickname "triple-negative" to describe them. They have a strong association with cancers arising in breast cancer gene 1, early onset (BRCA1) mutation carriers and are overrepresented in breast cancer developing during the premenopausal years and in African-American women. They have the worst prognosis of the subtypes

Staging of Breast Cancer:

Tumor node metastases (TNM) staging system for carcinoma of the breast

Primary tumor (T)

TX

Primary tumor cannot be assessed

T0

No evidence of primary tumor

Tis

Carcinoma in situ

Tis (DCIS)

Ductal carcinoma in situ

Tis (LCIS)

Lobular carcinoma in situ

Tis (Paget's)

Paget's disease (Paget disease) of the nipple NOT associated with invasive carcinoma and/or carcinoma in situ (DCIS and/or LCIS) in the underlying breast parenchyma. Carcinomas in the breast parenchyma associated with Paget's disease are categorized based on the size and characteristics of the parenchymal disease, although the presence of Paget's disease should still be noted.

T1

Tumor ≤20 mm in greatest dimension

T1mi

Tumor ≤1 mm in greatest dimension

T1a

Tumor >1 mm but ≤5 mm in greatest dimension

T1b

Tumor >5 mm but ≤10 mm in greatest dimension

T1c

Tumor >10 mm but ≤20 mm in greatest dimension

T2

Tumor >20 mm but ≤50 mm in greatest dimension

T3

Tumor >50 mm in greatest dimension

T4◊

Tumor of any size with direct extension to the chest wall and/or to the skin (ulceration or skin nodules)

T4a

Extension to the chest wall, not including only pectoralis muscle adherence/invasion

T4b

Ulceration and/or ipsilateral satellite nodules and/or edema (including peau d'orange) of the skin, which do not meet the criteria for inflammatory carcinoma

T4c

Both T4a and T4b

T4d

Inflammatory carcinoma§

The use of neoadjuvant therapy does not change the clinical (pretreatment) stage. Clinical (pretreatment) T will be defined by clinical and radiographic findings, while y pathologic (posttreatment) T will be determined by pathologic size and extension. The ypT will be measured as the largest single focus of invasive tumor, with the modifier "m" indicating multiple foci. The measurement of the largest tumor focus should not include areas of fibrosis within the tumor bed.

Regional lymph nodes (N)

Clinical

NX

Regional lymph nodes cannot be assessed (eg, previously removed)

N0

No regional lymph node metastases

N1

Metastases to movable ipsilateral level I, II axillary lymph node(s)

N2

Metastases in ipsilateral level I, II axillary lymph nodes that are clinically fixed or matted; or in clinically detected‡ ipsilateral internal mammary nodes in the absence of clinically evident axillary lymph node metastases

N2a

Metastases in ipsilateral level I, II axillary lymph nodes fixed to one another (matted) or to other structures

N2b

Metastases only in clinically detected‡ ipsilateral internal mammary nodes and in the absence of clinically evident level I, II axillary lymph node metastases

N3

Metastases in ipsilateral infraclavicular (level III axillary) lymph node(s) with or without level I, II axillary lymph node involvement; or in clinically detected‡ ipsilateral internal mammary lymph node(s) with clinically evident level I, II axillary lymph node metastases; or metastases in ipsilateral supraclavicular lymph node(s) with or without axillary or internal mammary lymph node involvement

N3a

Metastases in ipsilateral infraclavicular lymph node(s)

N3b

Metastases in ipsilateral internal mammary lymph node(s) and axillary lymph node(s)

N3c

Metastases in ipsilateral supraclavicular lymph node(s)

Pathologic (pN)†**

pNX

Regional lymph nodes cannot be assessed (eg, previously removed, or not removed for pathologic study)

pN0

No regional lymph node metastasis identified histologically

pN0(i-)

No regional lymph node metastases histologically, negative immunohistochemistry (IHC)

pN0(i+)

Malignant cells in regional lymph node(s) no greater than 0.2 mm (detected by H&E or IHC including isolated tumor cell clusters (ITC))

pN0(mol-)

No regional lymph node metastases histologically, negative molecular findings (RT-PCR)••

pN0(mol+)

Positive molecular findings (RT-PCR)••, but no regional lymph node metastases detected by histology or IHC

pN1

Micrometastases; or metastases in 1-3 axillary lymph nodes; and/or in internal mammary nodes with metastases detected by sentinel lymph node biopsy but not clinically detected ΔΔ

pN1mi

Micrometastases (greater than 0.2 mm and/or more than 200 cells, but none greater than 2.0 mm)

pN1a

Metastases in 1-3 axillary lymph nodes, at least one metastasis greater than 2.0 mm

pN1b

Metastases in internal mammary nodes with micrometastases or macrometastases detected by sentinel lymph node biopsy but not clinically detected ΔΔ

pN1c

Metastases in 1-3 axillary lymph nodes and in internal mammary lymph nodes with micrometastases or macrometastases detected by sentinel lymph node biopsy but not clinically detected

pN2

Metastases in 4-9 axillary lymph nodes; or in clinically detected◊◊ internal mammary lymph nodes in theabsence of axillary lymph node metastases

pN2a

Metastases in 4-9 axillary lymph nodes (at least one tumor deposit greater than 2.0 mm)

pN2b

Metastases in clinically detected◊◊ internal mammary lymph nodes in the absence of axillary lymph node metastases

pN3

Metastases in ten or more axillary lymph nodes; or in infraclavicular (level III axillary) lymph nodes; or in clinically detected◊◊ ipsilateral internal mammary lymph nodes in the presence of one or more positive level I, II axillary lymph nodes; or in more than three axillary lymph nodes and in internal mammary lymph nodes with micrometastases or macrometastases detected by sentinel lymph node biopsy but not clinically detected ΔΔ; or in ipsilateral supraclavicular lymph nodes

pN3a

Metastases in ten or more axillary lymph nodes (at least one tumor deposit greater than 2.0 mm); or metastases to the infraclavicular (level III axillary lymph) nodes

pN3b

Metastases in clinically detected◊◊ ipsilateral internal mammary lymph nodes in the presence of one or more positive axillary lymph nodes; or in more than three axillary lymph nodes and in internal mammary lymph nodes with micrometastases or macrometastases detected by sentinel lymph node biopsy but not clinically detected ΔΔ

pN3c

Metastases in ipsilateral supraclavicular lymph nodes

Posttreatment ypN

- Post-treatment yp "N" should be evaluated as for clinical (pretreatment) "N" methods above. The modifier "sn" is used only if a sentinel node evaluation was performed after treatment. If no subscript is attached, it is assumed that the axillary nodal evaluation was by axillary node dissection (AND).

- The X classification will be used (ypNX) if no yp posttreatment SN or AND was performed

- N categories are the same as those for pN

Distant metastasis (M)

M0

No clinical or radiographic evidence of distant metastases

cM0(i+)

No clinical or radiographic evidence of distant metastases, but deposits of molecularly or microscopically detected tumor cells in circulating blood, bone marrow, or other nonregional nodal tissue that are no larger than 0.2 mm in a patient without symptoms or signs of metastases

M1

Distant detectable metastases as determined by classic clinical and radiographic means and/or histologically proven larger than 0.2 mm

Posttreatment yp M classification. The M category for patients treated with neoadjuvant therapy is the category assigned in the clinical stage, prior to initiation of neoadjuvant therapy. Identification of distant metastases after the start of therapy in cases where pretherapy evaluation showed no metastases is considered progression of disease. If a patient was designated to have detectable distant metastases (M1) before chemotherapy, the patient will be designated as M1 throughout.

Anatomic stage/prognostic groups§§

0

Tis

N0

M0

IA

T1 ¥¥

N0

M0

IB

T0

N1mi

M0

T1 ¥¥

N1mi

M0

IIA

T0

N1 ‡‡

M0

T1 ¥¥

N1 ‡‡

M0

T2

N0

M0

IIB

T2

N1

M0

T3

N0

M0

IIIA

T0

N2

M0

T1 ¥¥

N2

M0

T2

N2

M0

T3

N1

M0

T3

N2

M0

IIIB

T4

N0

M0

T4

N1

M0

T4

N2

M0

IIIC

Any T

N3

M0

IV

Any T

Any N

M1

.

 

 Treatment of hormone receptor positive breast cancer:

 The treatment of early stage breast cancer includes the treatment of locoregional disease with surgery, radiation therapy, or both, and the treatment of systemic disease with one or a combination of chemotherapy, endocrine therapy, or biologic therapy. 

 Neoadjuvant (before Surgery) systemic therapy has become a frequently used option in the treatment of breast cancer.

For patients with locally advanced, inoperable breast cancer and inflammatory breast cancer, neoadjuvant systemic therapy is standard treatment. The goal of neoadjuvant systemic therapy is to induce tumor response, to facilitate local control through surgical resection and radiation therapy, and to improve disease-free and overall survival.

For patients with early stage, operable breast cancer, neoadjuvant systemic therapy may be used rather than primary surgery in order to increase the chance of successful breast conserving surgery. For these patients, neoadjuvant systemic therapy results in long-term distant disease-free survival and overall survival comparable to that achieved with adjuvant systemic therapy.

 

Here, Dr. Tony Talebi discusses the general concepts of estrogen receptor positive breast cancer with world renowned breast cancer expert Dr. Marc Lippman, professor and chairman of the department of medicine at the University of Miami. Dr. Marc Lippman pioneered the use of tamoxifen in estrogen receptor positive breast cancer with his early research while at the National Cancer Institute which revolutionized the treatment of breast cancer.   The discussion includes breast cancer stage treatment, advanced breast cancer treatment, symptom of breast cancer, new treatments for breast cancer, stage 1 breast cancer treatment, stage 4 cancer treatment, early symptoms of breast cancer, early symptoms of breast cancer, staging of breast cancer, symptoms for breast cancer, stage iv breast cancer treatment, breast cancer cells, men breast cancer, breast cancer in women, risk factors of breast cancer, radiation for breast cancer, chemotherapy for breast cancer, breast cancer radiation, advanced cancer treatment, what causes breast cancer, articles on breast cancer, facts on breast cancer, stage 3 breast cancer, risk factors for breast cancer, symptoms of cancer, breast cancer survival rates, what cause breast cancer, breast cancer risk factors, stage 3 breast cancer prognosis, survival rate for breast cancer, early stage breast cancer, images of breast cancer, inflammatory breast cancer symptoms, how is breast cancer diagnosed, breast cancer holistic treatment, triple negative breast cancer prognosis, triple negative breast cancer survival, effects of breast cancer, holistic cancer treatment, different types of breast cancer, first signs of breast cancer, stage 4 breast cancer prognosis, definition of breast cancer, statistics of breast cancer.

 





Dr. Marc Lippman credentials:

Certifications
                                           American Board of Internal Med-Medical Oncology

American Board of Internal Medicine

American Bd of Int Med-Endocrinology Diabetes & Metabolism

Specialties

  • Hematology/Oncology - Internal Medicine
  • Internal Medicine

Roles

  • Interim Deputy Director, Sylvester Comprehensive Cancer Center
  • Professor and Chairman

Biography

Marc E. Lippman, M.D. was named the Kathleen and Stanley Glaser Professor of Medicine at the University of Miami Leonard M. Miller School of Medicine, and was named Chairman of the Department of Medicine in May 2007. Previously Dr. Lippman was the John G. Searle Professor and Chair of Internal Medicine at the University of Michigan, Ann Arbor, Michigan. From 1988 through 1999 Dr. Lippman was Professor of Medicine and Pharmacology, and Chair, Department of Oncology at Georgetown University in Washington, D.C., and served as Director of the Lombardi Cancer Center at Georgetown University Medical Center. From 1978 through 1990 he was Clinical Professor of Medicine and Pharmacology, Uniformed Services, University of the Health Sciences. Dr. Lippman served as Head of the Medical Breast Cancer Section, Medicine Branch, at the National Institute of Health. He was a Senior Investigator at the National Cancer Institute of the National Institute of Health. Dr. Lippman completed a Fellowship in Endocrinology at Yale Medical School in New Haven, CT from 1973-1974. In addition, he was Clinical Associate at the National Cancer Institute from 1970-1971 and Clinical Associate at the Laboratory of Biochemistry of the National Cancer Institute of the National Institute of Health. From 1970 to 1988 he served as an Officer and Medical Director of the United States Public Health Service. Dr. Lippman completed his residency on the Osler Medical Service, John Hopkins Hospital, in Baltimore, Maryland from 1968-1970.

A native of New York, Dr. Lippman received his Bachelor's Degree from Cornell University, Magna Cum Laude, and medical school degree at Yale Medical School in New Haven, CT where he was elected to AOA.

Dr. Lippman is widely known for his research in breast cancer. Throughout his illustrious career he has received numerous awards including Mallinckrodt Award of the Clinical Radioassay Society in 1978; the Commendation Medal USPHS in 1982; Meritorius Service Medal, USPHS in 1987; Clinical Investigator Award, American Federation for Clinical Research in 1985; D.R. Edwards Lecture and Medal, Tenovus Institute, Wales 1985; Plenary Lecturer, British Association of Cancer Research in 1987; Gosse Lecture, Dalhuosie University, Halifax Nova Scotia in 1987; the American Cancer Society.