martes, 8 de octubre de 2019

Breast Cancer Treatment (Adult) (PDQ®) 1/4 –Health Professional Version - National Cancer Institute

Breast Cancer Treatment (Adult) (PDQ®)–Health Professional Version - National Cancer Institute



National Cancer Institute

Breast Cancer Treatment (Adult) (PDQ®)–Health Professional Version

General Information About Breast Cancer

This summary discusses primary epithelial breast cancers in women. The breast is rarely affected by other tumors such as lymphomas, sarcomas, or melanomas. Refer to the following PDQ summaries for more information on these cancer types:
Breast cancer also affects men and children and may occur during pregnancy, although it is rare in these populations. Refer to the following PDQ summaries for more information:

Incidence and Mortality

Estimated new cases and deaths from breast cancer (women only) in the United States in 2019:[1]
  • New cases: 268,600.
  • Deaths: 41,760.
Breast cancer is the most common noncutaneous cancer in U.S. women, with an estimated 62,930 cases of in situ disease and 268,600 cases of invasive disease in 2019.[1] Thus, fewer than one of six women diagnosed with breast cancer die of the disease. By comparison, it is estimated that about 66,020 American women will die of lung cancer in 2019.[1] Men account for 1% of breast cancer cases and breast cancer deaths (refer to the Special Populations section in the PDQ summary on Breast Cancer Screening for more information).
Widespread adoption of screening increases breast cancer incidence in a given population and changes the characteristics of cancers detected, with increased incidence of lower-risk cancers, premalignant lesions, and ductal carcinoma in situ (DCIS). (Refer to the Ductal carcinoma in situ (DCIS) section in the Pathologic Evaluation of Breast Tissue section in the PDQ summary on Breast Cancer Screening for more information.) Population studies from the United States [2] and the United Kingdom [3] demonstrate an increase in DCIS and invasive breast cancer incidence since the 1970s, attributable to the widespread adoption of both postmenopausal hormone therapy and screening mammography. In the last decade, women have refrained from using postmenopausal hormones, and breast cancer incidence has declined, but not to the levels seen before the widespread use of screening mammography.[4]

Anatomy

ENLARGEDrawing of female breast anatomy showing  the lymph nodes, nipple, areola, chest wall, ribs, muscle, fatty tissue, lobe, ducts, and lobules.
Anatomy of the female breast. The nipple and areola are shown on the outside of the breast. The lymph nodes, lobes, lobules, ducts, and other parts of the inside of the breast are also shown.

Risk Factors

Increasing age is the most important risk factor for most cancers. Other risk factors for breast cancer include the following:
  • Family health history.[5]
  • Major inheritance susceptibility.[6,7]
    • Germline mutation of the BRCA1 and BRCA2 genes and other breast cancer susceptibility genes.[8,9]
  • Alcohol intake.
  • Breast tissue density (mammographic).[10]
  • Estrogen (endogenous).[11-13]
    • Menstrual history (early menarche/late menopause).[14,15]
    • Nulliparity.
    • Older age at first birth.
  • Hormone therapy history.
    • Combination estrogen plus progestin hormone replacement therapy.
  • Obesity (postmenopausal).[16]
  • Personal history of breast cancer.[17]
  • Personal history of benign breast disease (BBD) (proliferative forms of BBD).[18-20]
  • Radiation exposure to breast/chest.[21]
Age-specific risk estimates are available to help counsel and design screening strategies for women with a family history of breast cancer.[22,23]
Of all women with breast cancer, 5% to 10% may have a germline mutation of the genes BRCA1 and BRCA2.[24] Specific mutations of BRCA1 and BRCA2 are more common in women of Jewish ancestry.[25] The estimated lifetime risk of developing breast cancer for women with BRCA1 and BRCA2 mutations is 40% to 85%. Carriers with a history of breast cancer have an increased risk of contralateral disease that may be as high as 5% per year.[26] Male BRCA2 mutation carriers also have an increased risk of breast cancer.[27]
Mutations in either the BRCA1 or the BRCA2 gene also confer an increased risk of ovarian cancer [27,28] or other primary cancers.[27,28] Once a BRCA1 or BRCA2 mutation has been identified, other family members can be referred for genetic counseling and testing.[29-32] (Refer to the PDQ summaries on Genetics of Breast and Gynecologic CancersBreast Cancer Prevention; and Breast Cancer Screening for more information.)
(Refer to the PDQ summary on Breast Cancer Prevention for more information about factors that increase the risk of breast cancer.)

Protective Factors

Protective factors and interventions to reduce the risk of female breast cancer include the following:
  • Estrogen use (after hysterectomy).[33-35]
  • Exercise.[36-38]
  • Early pregnancy.[39-41]
  • Breast feeding.[42]
  • Selective estrogen receptor modulators (SERMs).[43]
  • Aromatase inhibitors or inactivators.[44,45]
  • Risk-reducing mastectomy.[46]
  • Risk-reducing oophorectomy or ovarian ablation.[47-50]
(Refer to the PDQ summary on Breast Cancer Prevention for more information about factors that decrease the risk of breast cancer.)

Screening

Clinical trials have established that screening asymptomatic women using mammography, with or without clinical breast examination, decreases breast cancer mortality. (Refer to the PDQ summary on Breast Cancer Screening for more information.)

Diagnosis

Patient evaluation

When breast cancer is suspected, patient management generally includes the following:
  • Confirmation of the diagnosis.
  • Evaluation of the stage of disease.
  • Selection of therapy.
The following tests and procedures are used to diagnose breast cancer:
  • Mammography.
  • Ultrasound.
  • Breast magnetic resonance imaging (MRI), if clinically indicated.
  • Biopsy.

Contralateral disease

Pathologically, breast cancer can be a multicentric and bilateral disease. Bilateral disease is somewhat more common in patients with infiltrating lobular carcinoma. At 10 years after diagnosis, the risk of a primary breast cancer in the contralateral breast ranges from 3% to 10%, although endocrine therapy decreases that risk.[51-53] The development of a contralateral breast cancer is associated with an increased risk of distant recurrence.[54] When BRCA1/BRCA2 mutation carriers were diagnosed before age 40 years, the risk of a contralateral breast cancer reached nearly 50% in the ensuing 25 years.[55,56]
Patients who have breast cancer will undergo bilateral mammography at the time of diagnosis to rule out synchronous disease. To detect either recurrence in the ipsilateral breast in patients treated with breast-conserving surgery or a second primary cancer in the contralateral breast, patients will continue to have regular breast physical examinations and mammograms.
The role of MRI in screening the contralateral breast and monitoring women treated with breast-conserving therapy continues to evolve. Because an increased detection rate of mammographically occult disease has been demonstrated, the selective use of MRI for additional screening is occurring more frequently despite the absence of randomized, controlled data. Because only 25% of MRI-positive findings represent malignancy, pathologic confirmation before treatment is recommended. Whether this increased detection rate will translate into improved treatment outcome is unknown.[57-59]

Prognostic and Predictive Factors

Breast cancer is commonly treated by various combinations of surgery, radiation therapy, chemotherapy, and hormone therapy. Prognosis and selection of therapy may be influenced by the following clinical and pathology features (based on conventional histology and immunohistochemistry):[60]
  • Menopausal status of the patient.
  • Stage of the disease.
  • Grade of the primary tumor.
  • Estrogen receptor (ER) and progesterone receptor (PR) status of the tumor.
  • Human epidermal growth factor type 2 receptor (HER2/neu) overexpression and/or amplification.
  • Histologic type. Breast cancer is classified into a variety of histologic types, some of which have prognostic importance. Favorable histologic types include mucinous, medullary, and tubular carcinomas.[61-63]
The use of molecular profiling in breast cancer includes the following:[64]
  • ER and PR status testing.
  • HER2/neu receptor status testing.
  • Gene profile testing by microarray assay or reverse transcription-polymerase chain reaction (e.g., MammaPrint, Oncotype DX).
On the basis of ER, PR, and HER2/neu results, breast cancer is classified as one of the following types:
  • Hormone receptor positive.
  • HER2/neu positive.
  • Triple negative (ER, PR, and HER2/neu negative).
ER, PR, and HER2 status are important in determining prognosis and in predicting response to endocrine and HER2-directed therapy. The American Society of Clinical Oncology/College of American Pathologists consensus panel has published guidelines to help standardize the performance, interpretation, and reporting of assays used to assess the ER-PR status by immunohistochemistry and HER2 status by immunohistochemistry and in situ hybridization.[65,66]
Gene profile tests include the following:
  • MammaPrint: The first gene profile test to be approved by the U.S. Food and Drug Administration was the MammaPrint gene signature. The 70-gene signature classifies tumors into high- and low-risk prognostic categories. [67-71] The aim of the MINDACT (NCT00433589) trial (see below) is to determine the clinical usefulness and patient benefit of adjuvant chemotherapy .
  • Oncotype DX: The Oncotype DX 21 gene assay is the gene profile test with the most extensive clinical validation thus far and applies to hormone receptor–positive breast cancer. A 21-gene recurrence score is generated based on the level of expression of each of the 21 genes:
    • Recurrence score <18: low risk.
    • Recurrence score ≥18 and <31: intermediate-risk.
    • Recurrence score ≥31: high risk.
The following trials describe the prognostic and predictive value of multigene assays in early breast cancer:
  1. The prognostic ability of the Oncotype DX 21-gene assay was assessed in two randomized trials.
    • The National Surgical Adjuvant Breast and Bowel Project (NSABP B-14Exit Disclaimer) trial randomly assigned patients to receive tamoxifen or placebo; the results favoring tamoxifen changed clinical practice in the late 1980s.[72] Formalin-fixed, paraffin-embedded tissue was available for 668 patients. The 10-year distant recurrence risk for patients treated with tamoxifen was 7% for those with a low recurrence score, 14% for those with an intermediate recurrence score, and 31% for those with high recurrence score (P < .001).[73]
    • A community-based, case-control study examined the prognostic ability of the recurrence score to predict breast cancer deaths after 10 years in a group of tamoxifen-treated patients and observed a similar prognostic pattern to that seen in patients from NSABP B-14.[74]
  2. The use of Oncotype Dx to predict benefit from chemotherapy in patients with node-negative, ER-positive breast cancer was initially assessed in a prospective-retrospective way using the tamoxifen alone (n = 227) and the combination arms (n = 424) of the NSABP B-20Exit Disclaimer trial.[72] Patients in the NSABP B-20 trial were randomly assigned to receive tamoxifen alone or tamoxifen concurrently with methotrexate and 5-fluorouracil (MF) or cyclophosphamide with MF (CMF).[75]
    • The 10-year distant disease-free survival (DFS) improved from 60% to 88% by adding chemotherapy to tamoxifen in the high-risk group, while no benefit was observed in the low recurrence score group.[76]
  3. Similar findings were reported in the prospective-retrospective evaluation of the Southwestern Oncology Group (SWOG-8814 [NCT00929591]) trial in hormone receptor–positive lymph node-positive postmenopausal patients treated with tamoxifen with or without cyclophosphamide, doxorubicin, and fluorouracil.[77] However, the sample size in this analysis was small, follow-up was only 5 years, and the prognostic impact of having positive nodes needs to be taken into consideration.
    • Of note, both analyses (NSABP B-20 and S8814) were underpowered for any conclusive predictive analysis among patients identified as having an intermediate recurrence score.
  4. Results from the prospective, randomized TAILORx (NCT00310180) trial indicate that chemotherapy is unlikely to provide substantial benefit to patients older than 50 years with ER-PR–positive and node-negative disease and a recurrence score of 11 to 25.[78] In this study, a low-risk score was defined as less than 11, an intermediate score was 11 to 25, and a high-risk score was greater than 25. These cut points differ from those described above.
    Patients in this study with a low-risk score were found to have very low rates of recurrence at 5 years with endocrine therapy.[79]
    • Rate of invasive DFS was 93.8% at 5 years and 84.0% at 9 years.
    • Rate of freedom from recurrence of breast cancer at a distant site was 99.3% at 5 years and 96.8% at 9 years.
    • Rate of freedom from recurrence of breast cancer at a distant or local-regional site was 98.7% at 5 years and 95.0% at 9 years.
    • Rate of overall survival (OS) was 98.0% at 5 years and 93.7% at 9 years.
    In the middle-risk group in the TAILORx study (recurrence score, 11–25), 6,907 women were randomly assigned to endocrine therapy alone or endocrine therapy plus chemotherapy.[78] Of these, 3,399 women on the endocrine therapy-alone arm and 3,312 women on the endocrine therapy-plus-chemotherapy arm were available for an analysis according to the randomized treatment assignments. After a median follow-up of 90 months, the difference in invasive DFS, the main study endpoint, met the prespecified noninferiority criterion (P > .10 for a test of no difference after 835 events had occurred) suggesting the noninferiority of endocrine therapy compared with endocrine therapy plus chemotherapy.
    • In this population, the 9-year invasive DFS was 83.3% for endocrine therapy alone and 84.3% for endocrine therapy plus chemotherapy (hazard ratio [HR], 1.08; 95% confidence interval [CI], 0.94–1.24; P = .26).[78][Level of evidence: 1iiD]
    • One hundred eighty-five patients in the endocrine-only arm received chemotherapy, and 608 patients in the endocrine therapy-plus-chemotherapy arm did not receive their assigned chemotherapy. In an analysis based on the actual treatment received, the HR for invasive DFS was 1.14 (95% CI, 0.99–1.31; P =.06).
    • Outcomes for the other endpoints examined (freedom of distant breast cancer recurrence, freedom from local and distant recurrence, and OS) were similar between the two treatment arms and none were significant at P < 0.10.
    • There was a significant interaction between treatment assignment and age (P = .03) with respect to invasive DFS, suggesting that chemotherapy might be beneficial in women younger than 50 years with recurrence scores ranging from 11 to 25.
    • A secondary analysis of TAILORx demonstrated that integration of clinical risk (assessed by tumor size and grade) adds prognostic information to the recurrence score in women with a recurrence score of at least 11; however, clinical risk was not predictive of a chemotherapy benefit.[80] The interaction between age and chemotherapy benefit was further explored in this secondary analysis. Among women aged 50 years or younger, rates of distant recurrence were lower with chemotherapy in the setting of recurrence scores of 16 to 20 and high clinical risk; and in the setting of recurrence scores of 21 to 25, regardless of clinical risk.
    • The majority of women received tamoxifen as their endocrine therapy. It is not certain if any of the observed benefits of chemotherapy are attributable to ovarian function suppression and if they could be achieved through endocrine therapy.
  5. The MINDACT (NCT00433589) trial tested whether adding MammaPrint genomic risk to a clinical-risk classification (modified from Adjuvant! Online) might guide more appropriate choices of chemotherapy in women with node negative- or 1-to-3 node-positive disease.[81][Level of evidence: 3iiiDii] Unlike the TAILORx study, which only had hormone receptor–positive patients, this trial included hormone receptor–negative patients. In this prospective study, women with both genomic and clinical high-risk classification received chemotherapy, while those with both genomic and clinical low-risk classification did not receive chemotherapy. Participants with discordant results (clinical high-risk- with genomic low-risk classification, or clinical low-risk- with genomic high-risk classification) were randomly assigned to receive or not receive chemotherapy. A total of 1,550 women with high clinical risk and low genomic risk, and 592 women with low clinical risk and high genomic risk, were randomly assigned to receive or not receive chemotherapy. The primary goal of the study was to determine whether patients with high clinical risk, but low genomic risk, who did not receive chemotherapy had a 5-year survival rate without distant metastases (primary study endpoint) of 92% or lower (a noninferiority design).
    • This endpoint was met because the observed rate in the group was 94.7% (95% CI, 92.5%–96.2%). However, among patients with high clinical risk but low genomic risk, the rate of 5-year survival without distant metastases was 1.5% higher in the arm that did receive chemotherapy than in the arm that did not receive chemotherapy, although the study was not powered to detect a difference between these arms (HR chemotherapy vs. no chemotherapy, 0.78; 95% CI, 0.50–1.21; P = .27)
    • Patients in the low clinical risk group with high genomic risk did well, and there was little evidence of benefit from chemotherapy in this group (5-year survival without distant metastases, 95.8% with chemotherapy vs. 95.0% without; HR, 1.17; 95% CI, 0.59–2.28; P = .66).
Results from the prospective, randomized RxPONDER (NCT01272037) trial will help to determine if there is a benefit from adjuvant chemotherapy in patients with ER-positive-, node-positive early breast cancer treated with endocrine therapy, and a recurrence score below 25.
Many other gene-based assays may guide treatment decisions in patients with early breast cancer (e.g., Predictor Analysis of Microarray 50 [PAM50] Risk of Recurrence [ROR] score, EndoPredict, Breast Cancer Index).
Although certain rare inherited mutations, such as those of BRCA1 and BRCA2, predispose women to develop breast cancer, prognostic data on BRCA1/BRCA2 mutation carriers who have developed breast cancer are conflicting. These women are at greater risk of developing contralateral breast cancer. (Refer to the Prognosis of BRCA1- and BRCA2-related breast cancer section of the PDQ Genetics of Breast and Gynecologic Cancers summary for more information.)

Posttherapy Considerations

Hormone replacement therapy

After careful consideration, patients with severe symptoms may be treated with hormone replacement therapy. For more information, refer to the following PDQ summaries:

Related Summaries

Other PDQ summaries containing information related to breast cancer include the following:
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