eMedicine Specialties > Oncology > Carcinoma of the Breast

Breast Cancer: Workup

Author: Rachel Swart, MD, PhD, Assistant Professor of Medicine, Department of Hematology and Oncology, Arizona Cancer Center, University of Arizona
Coauthor(s): Leona Downey, MD, Assistant Professor of Internal Medicine, Section of Oncology and Hematology, University of Arizona, Arizona Cancer Center; Julie Lang, MD, Assistant Professor of Surgery and the BIO5 Institute, Director of Breast Surgical Oncology, University of Arizona; Patricia A Thompson, PhD, Assistant Professor, Department of Pathology, University of Arizona, Tucson; Robert B Livingston, MD, Professor of Clinical Medicine and Director, Clinical Research Shared Services, Arizona Cancer Center; Alison T Stopeck, MD, Associate Professor of Medicine, Arizona Cancer Center, University of Arizona Health Sciences Center; Director of Clinical Breast Cancer Program, Arizona Cancer Center; Medical Director of Coagulation Laboratory, University Medical Center; Director of Arizona Hemophilia and Thrombosis Center
Contributor Information and Disclosures

Updated: Jan 15, 2010

Workup

Diagnostic Procedures

Percutaneous vacuum-assisted large gauge core biopsies with image guidance are the recommended diagnostic approach for newly diagnosed breast cancers. Image guided breast biopsy may be performed with ultrasound, stereotactic, or MRI guidance. Core biopsies spare the need for operative intervention (and subsequent scarring), often providing pathological results quicker than surgical excisions. Additionally, excisional biopsy, as the initial operative approach, has been shown to increase the rate of positive margins. Thus, core biopsies for diagnosing breast cancer can eliminate the need for additional surgeries for definitive margin control and assessment of nodal status.

In some cases, a breast mass may be palpable but not correlate with imaging by either ultrasound or mammogram. Under this circumstance, palpation directed core biopsy, fine needle aspiration, or open excisional biopsy may be required to diagnose a suspicious palpable breast mass. Typically, patients who undergo a core needle biopsy, whether directed by imaging studies or palpation, have a titanium marker clip placed at the biopsy site. These clips are particularly helpful when planning a lumpectomy for non-palpable breast lesions that require preoperative image-guided wire-localization or for patients who undergo neoadjuvant chemotherapy, resulting in a pathological complete response. Complications of a diagnostic core or excisional biopsy include hematoma, infection, scarring, re-operation, and sampling error resulting in inaccurate diagnosis.

Histologic Findings

In situ carcinoma

Ductal carcinoma in situ (DCIS)

Increased use of screening mammography has resulted in a dramatic increase in the detection of DCIS. Approximately 64,000 cases of DCIS are diagnosed annually in the United States. Today, 90% of DCIS cases are identified on mammography as suspicious calcifications, linear, clustered, segmental, focal, or mixed distribution. DCIS is divided into comedo (ie, cribriform, micropapillary, solid) and noncomedo subtypes, which provides additional prognostic information regarding likelihood of progression or local recurrence.

Table 3. Ductal Carcinoma in Situ Subtypes

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Table
DCIS CharacteristicComedoNoncomedo
Nuclear gradeHighLow
Estrogen receptorNegativePositive
HER2/neu overexpressionPresentAbsent
DistributionContinuousMultifocal
NecrosisPresentAbsent
Local recurrenceHighLow
PrognosisWorseBetter
DCIS CharacteristicComedoNoncomedo
Nuclear gradeHighLow
Estrogen receptorNegativePositive
HER2/neu overexpressionPresentAbsent
DistributionContinuousMultifocal
NecrosisPresentAbsent
Local recurrenceHighLow
PrognosisWorseBetter

However, mammography often underestimates the multifocality and extent of DCIS. This has led to the use of breast MRI for the detection and staging of DCIS. Several studies, however, have demonstrated high sensitivity and low specificity for MRI in the detection of DCIS leading to unnecessary biopsies and more aggressive surgeries. Currently, the standard treatment of DCIS is surgical resection with or without radiation. Adjuvant radiation and hormonal therapies are often reserved for younger women, patients undergoing lumpectomy, or comedo subtype.

Approximately 30% of women with DCIS in the United States are treated with mastectomy with or without reconstruction, 30% with conservative surgery alone, and 40% with conservative surgery followed by whole-breast radiation therapy. Axillary or sentinel lymph node dissection is not routinely recommended for patients with DCIS. Current studies have identified metastatic disease to the axillary node in 10% of patients. In DCIS, whole-breast radiotherapy is delivered over 5-6 weeks after surgery, reducing the local recurrence rate by approximately 60%. Roughly 50% of local recurrences are invasive breast cancer. Meta-analyses of randomized controlled trials comparing radiation therapy versus observation after surgery for DCIS have demonstrated slightly higher rates of contralateral breast cancer after radiation therapy (3.85% vs 2.5%). Studies comparing accelerated partial breast radiation given over 5 days to standard whole breast radiotherapy are currently underway.

Tamoxifen is the only hormonal therapy currently approved for adjuvant therapy in patients treated with breast-conserving surgery and radiation for DCIS. Currently, a clinical trial evaluating the role of the aromatase inhibitor anastrozole as adjuvant therapy in DCIS has met its accrual and results are anticipated.

Lobular carcinoma in situ (LCIS)

LCIS arises from the terminal duct apparatus and shows a rather diffuse distribution throughout the breast, which explains its presentation as a non-palpable mass in most cases. Over the last 25 years, LCIS incidence has doubled and is now 2.8% per 100,000 women. The peak incidence is in women aged 40-50 years. Because LCIS is nonpalpable, it has no consistent features on breast imaging and is most often an incidental finding associated with a breast biopsy performed for an unrelated mammographic abnormality. Approximately, 10-20% of women with LCIS develop invasive breast cancer within 15 years from their LCIS diagnosis. Thus, LCIS is considered a biomarker of increased breast cancer risk. Treatment options for LCIS include chemoprevention with a SERM, bilateral mastectomy with or without reconstruction, and close observation.

Other invasive breast cancer histology
  • Medullary carcinoma: Medullary carcinoma is relatively uncommon (5%) and generally occurs in younger women. Most patients present with a bulky palpable mass with axillary lymphadenopathy. Diagnosis of this type of breast cancer depends on a histologic triad of (1) sheets of anaplastic tumor cells with scant stroma, (2) moderate or marked stromal lymphoid infiltrate, and (3) histologic circumscription or a pushing border. DCIS may be observed in the surrounding normal tissues. ER, PR, and HER2/neu are typically negative, and TP53 is commonly mutated. Roughly 30% of patients have lymph node metastasis. Typical or classic medullary carcinomas are often associated with a good prognosis despite the unfavorable prognostic features associated with this type of breast cancer. However, a recent analysis of 609 medullary breast cancer specimens from various stage I and II NSABP protocols indicate that overall survival and prognosis are not as good as previously reported.
  • Mucinous carcinoma: Mucinous carcinoma is another rare histologic type seen in fewer than 5% of invasive breast cancer cases. It usually presents during the seventh decade of life. It often presents as a palpable mass or mammographically as a poorly defined tumor with rare calcifications. Mucin production is the histologic hallmark with 2 main forms, type A and B, with AB lesions possessing features of both. Type A mucinous carcinoma represented the classic variety with larger quantities of extracellular mucin, whereas type B is a distinct variant with endocrine differentiation. DCIS is not a frequent occurrence, though it may be found. Most cases are ER and PR positive, but HER2/neu overexpression is rare. Additionally, these carcinomas predominantly express glycoproteins MUC2 and MUC6. Overall, patients with mucinous carcinoma have an excellent prognosis (>80% 10-year survival).
  • Tubular carcinoma: Tubular carcinoma of the breast is an uncommon histologic type involving 1-2% of all breast cancers. Characteristic features of this type include a single layer of epithelial cells with low-grade nuclei and apical cytoplasmic snoutings arranged in well-formed tubules and glands. Tubular components comprise more than 90% of pure tubular carcinomas and at least 75% of mixed tubular carcinomas. This type of breast cancer has a low incidence of lymph node involvement and a very high overall survival rate. Because of its favorable prognosis, patients are often treated with only breast-conserving surgery and local radiation therapy.
  • Papillary carcinoma
    • Papillary carcinoma of the breast encompasses a spectrum of histological subtypes. There are two common types: cystic (noninvasive form) and micropapillary ductal carcinoma (invasive form). This form of breast cancer is usually seen in women older than 60 years and accounts for approximately 1-2% of all breast cancers. Papillary carcinomas are centrally located in the breast and can present with bloody nipple discharge. They are strongly ER and PR positive.
    • Cystic papillary carcinoma has a low mitotic activity, which results in a more indolent course and good prognosis. However, invasive micropapillary ductal carcinoma has a more aggressive phenotype even though approximately 70% of cases are ER positive. A retrospective review of 1400 cases of invasive carcinoma identified 83 cases (6%) with at least one component of invasive micropapillary ductal carcinoma. Additionally, lymph node metastasis is frequently seen in this subtype (70-90% incidence), and the number of lymph nodes involved appears to correlate with survival.
  • Metaplastic breast cancer (MBC)
    • MBC accounts for less than 1% of breast cancer cases. It is characterized by a combination of adenocarcinoma plus mesenchymal and epithelial components. A wide variety of histological patterns include spindle-cell carcinoma, carcinosarcoma, squamous cell carcinoma of ductal origin, adenosquamous carcinoma, carcinoma with pseudosarcomatous metaplasia, and matrix-producing carcinoma. This diverse group of malignancies is identified as a single entity based on a similarity in clinical behavior. When compared with infiltrating ductal carcinoma, metaplastic breast cancer tumors are larger, more rapidly growing, commonly node negative, and typically ER, PR, and HER-2 negative. The disease tends to occur in older women with an average age of onset in the sixth decade and has a higher incidence in African Americans.
    • The majority of published case series have demonstrated a worse prognosis for metaplastic breast cancer as compared to infiltrating ductal carcinoma, even when adjusted for stage, with a 3-year overall survival rate of 48-71% and 3-year disease-free survival rate of 15-60%. In most case series, large tumor size and advanced stage have emerged as predictors of poor overall survival and prognosis. Nodal status does not appear to impact survival in metaplastic breast cancer.
    • Surgery is used to treat up to 95% of women with metaplastic breast cancer. Few data support the effectiveness of systemic chemotherapy in patients with metaplastic breast cancer and its use has been extrapolated from the treatment of more common types of breast cancer. A review of chemotherapy and response in a series of 27 patients with metaplastic breast cancer found only one partial response with a doxorubicin-containing regimen in the setting of metastatic disease. As in soft-tissue sarcomas, metaplastic breast cancer shows a tendency for local recurrence and for hematogenous spread to lung, liver, and bone.
  • Mammary Paget disease (MPD)
    • MPD is relatively rare, comprising 1-4% of all breast cancers. Peak incidence is seen in the sixth decade of life (mean age 57 y). This adenocarcinoma is localized within the epidermis of the nipple-areola complex and composed of the histologic hallmark, Paget cells, within the basement membrane. Paget cells are large, pale epithelial cells with hyperchromatic, atypical nucleus, dispersed between the keratinocytes as a single or cluster of cells. Lesions are predominantly unilateral developing insidiously as a scaly, fissured, oozing, or erythematous nipple-areola complex. Retraction or ulceration of the nipple is often noted, along with symptoms of itching, tingling, burning, or pain.
    • Mammary Paget disease is associated with an underlying breast cancer in 75% of cases. Standard treatment of mammary Paget disease is surgical excision (modified radical mastectomy with lymph node excision). Breast conserving surgery can achieve satisfactory results, but at the risk of local recurrence. Adjuvant chemotherapy with tamoxifen may increase survival in premenopausal patients with lymph node metastasis. Poor prognostic factors include a palpable breast tumor, lymph node involvement, histological type, and patient younger than 60 years. The overall 5-year and 10-year survival rates are 59% and 44%, respectively.

Prognostic and predictive factors

Numerous prognostic and predictive factors for breast cancer have been identified by the College of American Pathologists to guide the clinical management of women with breast cancer. Breast cancer prognostic factors include the following:

  • Axillary lymph node status
  • Tumor size
  • Lymphatic/vascular invasion
  • Patient age
  • Histologic grade
  • Histologic subtypes (eg, tubular, colloid [mucinous], papillary)
  • Response to neoadjuvant therapy
  • Estrogen receptor/progesterone receptor status
  • Her2/neu gene amplification and/or overexpression
  • Breast cancer predictive factors include the following:
  • Estrogen receptor/progesterone receptor status
  • Her2/neu gene amplification and/or overexpression
  • Lymph node status: Fluid from the breast tissue normally drains into the lymph nodes located in the axilla. Cancerous involvement of these nodes is an indication of the likelihood that the breast cancer has spread to other organs. Axillary nodal involvement and survival have been evaluated relative to the number and sites in breast cancer patients. For any given number of positive nodes, survival was independent of the level of involvement but directly related to the number of involved nodes. Patients with node-negative disease have an overall 10-year survival rate of 70% and 5-year recurrence rate of 19%. As the number of positive nodes increase, so does the probability of relapse. With 1-3 positive nodes, the recurrence rate at 5 years is 30-40%. Four to 9 positive nodes have a recurrence rate of 44-70%. Patients with more than 10 positive lymph nodes have a recurrence rate of 72-82%.
  • Hormone receptor status: Estrogen receptor (ER) and progesterone receptor (PR) assays are routinely performed by pathologists on tumor material. Immunohistochemistry (IHC) is a semiquantitative technique that is observer and antibody dependent. In general, hormone-positive tumors have a more indolent course and are responsive to hormonal therapy.
  • HER2
    • Eighteen to twenty percent of invasive breast cancers overexpress HER2, which has both prognostic and predictive implications. Prior to the routine use of adjuvant trastuzumab therapy, HER2 overexpression was associated with a more aggressive tumor phenotype and worse prognosis (higher rate of recurrence and mortality) especially in patients who do not receive adjuvant chemotherapy. Additionally, HER2 status has been shown to be predictive for response to certain chemotherapeutic agents (ie, doxorubicin, and HER2 targeted therapies, trastuzumab, a monoclonal antibody, and lapatinib, a small molecule oral tyrosine kinase inhibitor) directed specifically to the HER2 receptor. Retrospectively analyzed results from clinical trials have shown HER2-positive patients benefit from anthracycline-based regimens secondary to the co-amplification of topoisomerase II with HER2. Preliminary data also suggest that HER2 may predict response and benefit from paclitaxel in the adjuvant setting.
    • A recent phase III, double-blind, randomized study evaluated the efficacy of lapatinib in HER2-negative and HER2 uncharacterized metastatic breast cancer. The study concluded that while patients with HER2-negative or HER2-untested metastatic breast cancer did not experience benefit from the addition of lapatinib to paclitaxel, first-line therapy with paclitaxel-lapatinib significantly improved clinical outcomes in patients who were HER2-positive.8
    • Several methods for HER2 testing have been developed. Since approximately 20% of current HER2 testing may be inaccurate, the American Society of Clinical Oncology and the College of American Pathologists have recommended guidelines in HER2 testing to ensure accuracy. Breast cancer specimens should initially undergo HER2 testing by a validated immunohistochemistry assay (ie, DAKO Hercep Test [DAKO Cytomation]) for HER2 protein expression.9 The scoring method for HER2 expression is based on the cell membrane staining pattern and is listed below.
      • 3+: Positive HER2 expression - Uniform intense membrane staining of more than 30% of invasive tumor cells
      • 2+: Equivocal for HER2 protein expression – Complete membrane staining that is either nonuniform or weak in intensity but has circumferential distribution in at least 10% of cells
      • 0 or 1+: Negative for HER2 protein expression
    • Breast cancer specimens with equivocal immunohistochemistry should undergo validation using a HER2 gene amplification method (ie, fluorescence in situ hybridization [FISH]). More centers are relying on FISH alone for determining HER2 status. In general, FISH testing is thought to be more reliable, but it is more expensive than immunohistochemistry. Newer methodologies for establishing HER2 status including RT-PCR and CISH (chromogenic in situ hybridization) have not yet been validated. Equivocal immunohistochemistry results can be seen in 15% of invasive breast cancers. The interpretation for HER2 FISH testing (HER2/CEP17 ratio and gene copy number) is given below.
      • Positive HER2 amplification: FISH ratio greater than 2.2 or HER2 gene copy greater than 6.0
      • Equivocal HER2 amplification: FISH ratio 1.8-2.2 or HER2 gene copy 4.0-6.0
      • Negative HER2 amplification: FISH less than 1.8 or HER2 gene copy less than 4.0
    • Discordant results (IHC3+/FISH negative or IHC less than 3+/FISH positive) have been observed in approximately 4%. Equivocal HER2 FISH results are seen in less than 3% of invasive breast cancer specimens and had previously been considered HER2 positive. Currently, no data support excluding this group from treatment with trastuzumab.
  • Oncotype DX
    • The Oncotype Dx assay (Genomic Health, San Francisco, Calif) is a reverse transcriptase-polymerase chain reaction (RT-PCR)-based assay of 21 genes (16 cancer genes and 5 reference genes) performed on paraffin-embedded breast tumor tissue. Using a formula based on the expression of these genes, a recurrence score (RS) can be calculated that correlates with the likelihood of distant recurrence at 10 years. Breast tumors with a recurrence score of less than 18 are considered low risk, recurrence score of 18-30 intermediate-risk, and more than 30 are high risk. Currently, Oncotype Dx has been validated and FDA approved in women with early-stage, ER-positive, node-negative breast cancer treated with tamoxifen where the recurrence score correlated with both relapse-free interval and overall survival. Furthermore, the Oncotype Dx assay has been shown to predict benefit from chemotherapy and hormonal therapy in hormone-sensitive, node-negative tumors retrospectively in the NSABP B-14 and B-20 studies.
    • Women with low recurrence score showed a significantly higher improvement in disease-free survival (DFS) with the addition of tamoxifen versus chemotherapy. Whereas, women with a high recurrence score had a significant improvement in disease-free survival by adding chemotherapy. Among women with 1-3 node-positive, hormone receptor-positive disease, the Oncotype Dx recurrence score was a significant predictor of recurrence, with a 21% decrease in recurrence risk for each 10-point drop in recurrence score. In general, results from these studies would indicate a selective group of node-positive, hormone receptor-positive patients with a low recurrence score would not benefit from an anthracycline based regimen. The benefit of adding chemotherapy to hormonal therapy in tumors with an intermediate score is still controversial, and a large prospective, randomized phase III study (TAILORx Trial) is addressing this important question.

Staging

The American Joint Committee on Cancer staging system groups patients based on the tumor size (T), lymph node status (N), and distant metastasis (M) into 4 stages.

  • Primary tumor (T)
    • Tx: Primary tumor cannot be assessed
    • T0:  No evidence of primary tumor
    • Tis: (DCIS) Carcinoma in situ
    • Tis: (LCIS) Carcinoma in situ
    • Tis: Paget disease of the nipple with no tumor (Paget disease associated with a tumor is classified according to the size of the tumor.)
    • T1:  Tumor 2 cm or smaller in greatest diameter
      • T1mic: Microinvasion 0.1 cm or less in greatest dimension
      • T1a: Tumor >0.1 but not >0.5 cm in greatest diameter
      • T1b: Tumor >0.5 but not >1 cm in greatest diameter
      • T1c: Tumor >1 cm but not >2 cm in greatest diameter
    • T2:  Tumor >2 cm but not >5 cm in greatest diameter
    • T3: Tumor >5 cm in greatest diameter
    • T4:  Tumor of any size, with direct extension to (a) the chest wall or (b) skin only, as described below
      • T4a: Extension to the chest wall, not including the pectoralis muscle
      • T4b: Edema (including peau d’orange) or ulceration of the skin of the breast or satellite skin nodules confined to the same breast
      • T4c: Both T4a and T4b
      • T4d: Inflammatory disease
  • Regional lymph nodes (N)
    • Nx: Regional lymph nodes cannot be assessed (eg, previously removed)
    • N0: No regional lymph node metastasis
    • N1: Metastasis in movable ipsilateral axillary lymph node(s)
    • N2: Metastasis in ipsilateral axillary lymph node(s) fixed or matted, or in clinically apparent ipsilateral internal mammary nodes in the absence of clinically evident axillary lymph node metastasis
      • N2a: Metastasis in ipsilateral axillary lymph nodes fixed to one another or to other structures
      • N2b: Metastasis only in clinically apparent ipsilateral internal mammary nodes and in the absence of clinically evident axillary lymph nodes
    • N3: Metastasis in ipsilateral infraclavicular or supraclavicular lymph node(s) with or without axillary lymph node involvement, or clinically apparent ipsilateral internal mammary lymph node(s) and in the presence of axillary lymph node
      • N3a: Metastasis in ipsilateral infraclavicular lymph node(s)
      • N3b: Metastasis in ipsilateral internal mammary lymph node(s) and axillary lymph node(s)
      • N3c: Metastasis in ipsilateral supraclavicular lymph node(s)
  • Distant metastasis
    • Mx: Distant metastasis cannot be assessed
    • M0:  No distant metastasis
    • M1: Distant metastasis

Table 2. TNM Staging System for Breast Cancer


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Table
StageTumorNodeMetastases
Stage 0TisN0M0
Stage IT1N0M0
Stage IIAT0
T1
T2		N1
N1
N0		M0
M0
M0
Stage IIBT2
T3		N1
N0		M0
M0
Stage IIIAT0
T1
T2
T3		N2
N2
N2
N1-2		M0
M0
M0
M0
Stage IIIBT4
T4
T4		N0
N1
N2		M0
M0
M0
Stage IIICAny TN3M0
Stage IVAny TAny NM1
StageTumorNodeMetastases
Stage 0TisN0M0
Stage IT1N0M0
Stage IIAT0
T1
T2		N1
N1
N0		M0
M0
M0
Stage IIBT2
T3		N1
N0		M0
M0
Stage IIIAT0
T1
T2
T3		N2
N2
N2
N1-2		M0
M0
M0
M0
Stage IIIBT4
T4
T4		N0
N1
N2		M0
M0
M0
Stage IIICAny TN3M0
Stage IVAny TAny NM1


Five-year survival rates are highly correlated with tumor stage, 99-100% for stage 0, 95-100% for stage I, 86% for stage II, 57% for stage III, and 20% for stage IV. This prognostic information can guide physicians in making therapeutic decisions. Pathologic review of the tumor tissue for histological grade along with the determination of estrogen/progesterone receptor (ER/PR), HER2 status, and lymph node involvement as determined by sentinel lymph node biopsy or axillary lymph node dissection is necessary for determining prognosis.

See also the Best Evidence rated reference, Trends in survival over the past two decades among white and black patients with newly diagnosed stage IV breast cancer.10

The National Cancer Center Network (NCCN) guideline recommends a history and physical examination followed by laboratory studies (CBC with differential, liver and renal function tests, and calcium levels) for all asymptomatic women with early stage breast cancer (Stage I and II). Women with stage III (locally advanced or inflammatory breast cancer) or symptomatic disease should have a chest x-ray or CT scan of the chest, CT scan of the abdomen and pelvis, and bone scan for evaluation of distant metastasis. Tumor markers (CEA and CA15.3 or CA27.29) may also be obtained in these patients.11

Currently, the use of positron emission tomography (PET) or PET/CT is not indicated in the staging of clinical stage I, II, or operable stage III breast cancer; however, the use of PET/CT scans for staging locally advanced and inflammatory breast cancer to assist in identification of nonaxillary lymph node metastasis (ie, internal mammary or supraclavicular lymph nodes) prior to starting neoadjuvant therapy is appropriate.

More on Breast Cancer

Overview: Breast Cancer
Workup: Breast Cancer
Treatment: Breast Cancer
Follow-up: Breast Cancer
Multimedia: Breast Cancer
References
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Further Reading

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Keywords

breast cancer, breast carcinoma, breast cancer treatment, breast cancer diagnosis, breast cancer pictures, breast cancer prognosis, breast cancer etiology, breast cancer symptoms, breast cancer surgery, invasive breast cancer, in situ breast cancer, ductal carcinoma in situ, DCIS, lobular carcinoma in situ, LCIS, inflammatory breast cancer, breast cancer subtypes, luminal A breast cancer, luminal B breast cancer, basal breast cancer, ERBB2+ breast cancer, normal breast breast cancer, probability models, BRCAPRO, Myriad I, Myriad II, Manchester, Breast and Ovarian Analysis of Disease Incidence and Carrier Estimation Algorithm, BOADICEA, Ontario Family History Assessment Tool, FHAT, cancer in women, carcinoma of the breast, hormone replacement therapy, hrt, oral contraceptives, oral contraception, OCs, birth control pills, women’s health, female breast cancer, male breast cancer, breast cancer in men

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Contributor Information and Disclosures

Author

Rachel Swart, MD, PhD, Assistant Professor of Medicine, Department of Hematology and Oncology, Arizona Cancer Center, University of Arizona
Rachel Swart, MD, PhD is a member of the following medical societies: American Association for Cancer Research, American Society of Clinical Oncology, Arizona Medical Association, and Southwest Oncology Group
Disclosure: Nothing to disclose.

Coauthor(s)

Leona Downey, MD, Assistant Professor of Internal Medicine, Section of Oncology and Hematology, University of Arizona, Arizona Cancer Center
Leona Downey, MD is a member of the following medical societies: American Geriatrics Society, American Society of Clinical Oncology, and Southwest Oncology Group
Disclosure: Nothing to disclose.

Julie Lang, MD, Assistant Professor of Surgery and the BIO5 Institute, Director of Breast Surgical Oncology, University of Arizona
Julie Lang, MD is a member of the following medical societies: American College of Surgeons, American Society of Breast Surgeons, American Society of Clinical Oncology, Association for Academic Surgery, and Society of Surgical Oncology
Disclosure: Genomic Health Grant/research funds Speaking and teaching; Agendia Grant/research funds Speaking and teaching

Patricia A Thompson, PhD, Assistant Professor, Department of Pathology, University of Arizona, Tucson
Disclosure: Nothing to disclose.

Robert B Livingston, MD, Professor of Clinical Medicine and Director, Clinical Research Shared Services, Arizona Cancer Center
Robert B Livingston, MD is a member of the following medical societies: American Association for Cancer Research, American Federation for Clinical Research, and American Society of Clinical Oncology
Disclosure: Nothing to disclose.

Alison T Stopeck, MD, Associate Professor of Medicine, Arizona Cancer Center, University of Arizona Health Sciences Center; Director of Clinical Breast Cancer Program, Arizona Cancer Center; Medical Director of Coagulation Laboratory, University Medical Center; Director of Arizona Hemophilia and Thrombosis Center
Alison T Stopeck, MD is a member of the following medical societies: American Association for Cancer Research, American College of Physicians, American Society of Clinical Oncology, American Society of Hematology, Hemophilia and Thrombosis Research Society, and Southwest Oncology Group
Disclosure: Genentech Honoraria Speaking and teaching; AstraZeneca Honoraria Speaking and teaching; AstraZeneca Grant/research funds Other

Medical Editor

Robert C Shepard, MD, FACP, Associate Professor of Medicine in Hematology and Oncology at University of North Carolina at Chapel Hill; Vice President of Scientific Affairs, Therapeutic Expertise, Oncology, at PRA International
Robert C Shepard, MD, FACP is a member of the following medical societies: American Association for Cancer Research, American College of Physician Executives, American College of Physicians, American Federation for Clinical Research, American Federation for Medical Research, American Medical Association, American Medical Informatics Association, American Society of Hematology, Association of Clinical Research Professionals, Eastern Cooperative Oncology Group, European Society for Medical Oncology, Massachusetts Medical Society, and Society for Biological Therapy
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Chief Editor

Jules E Harris, MD, Clinical Professor of Medicine, Division of Hematology/Medical Oncology, Department of Internal Medicine, University of Arizona College of Medicine at Tucson; Consulting Staff, Arizona Cancer Center
Jules E Harris, MD is a member of the following medical societies: American Association for Cancer Research, American Association for the Advancement of Science, American Association of Immunologists, American Society of Hematology, and Central Society for Clinical Research
Disclosure: GlobeImmune Salary Consulting; Amplimed Consulting fee Consulting; FibroGen Consulting fee Consulting

 
 
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