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 Inflammatory Breast Cancer

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Inflammatory Breast Cancer

Abstract
                       
                       Inflammatory breast cancer (IBC) represents
the most virulent form of breast cancer, characterized by involvement of
the skin and rapid progression of the disease. Management involves
careful coordination of multidisciplinary modalities, including imaging,
systemic chemotherapy, surgery, and radiation therapy. The use of
neoadjuvant chemotherapy has contributed significantly to improvement in
overall survival since the first descriptions of this entity, and has
made the role of locoregional therapy, including surgery and radiation,
critical to continued improvements in this disease. This article
examines the unique epidemiology and pathology of IBC, and reviews the
various treatment modalities, noting the significance of a multimodality
approach and delineating each of the specific components. Moreover, the
current research in IBC is briefly described, which experts hope will
further improve systemic therapies. (JNCCN 2011;9:233–241)



Overview/Epidemiology

                       Inflammatory breast cancer (IBC) is an
aggressive form of disease accounting for 1% to 5% of all breast cancers
diagnosed in the United States.[1] Lee and Tannenbaum[2] first used the term inflammatory breast cancer in 1924 to describe this clinical presentation. Subsequently, Haagensen[3]
described diagnostic criteria for IBC, including a rapidly enlarging
breast, erythema involving at least one third of the breast, generalized
induration, and biopsy-proven carcinoma.
                       IBC is a clinicopathologic entity
characterized by distinct skin changes, including diffuse erythema and
edema (peau d’orange), often without a clinically evident underlying
mass.[4]
It is associated with abrupt onset and rapid progression, with a high
risk of axillary lymph node involvement, and distant metastases at
initial diagnosis.[5]
Despite multimodality therapy, survival rates are lower than those for
other breast cancers. Its aggressive course, together with accumulating
molecular and epidemiologic data, also supports the concept that IBC may
be a distinct biologic entity rather than a subtype on the spectrum of
locally advanced breast cancer. In fact, several important epidemiologic
aspects of IBC are known and support this notion, such as the higher
incidence in African-Americans, the younger age at onset, the
association with high body mass index, and the relatively poor prognosis
compared with breast cancer overall.[6]
                       
                       Other aspects, such as the incidence of
disease, the identification of risk factors, the consistency of
biomarker assays, and even the effectiveness of different therapeutic
modalities, are difficult to interpret largely because of the
differences in the definition of this entity. Currently, the most widely
referenced case definition is that of the American Joint Committee on
Cancer (AJCC),[7] which states in part that
                       <blockquote>“inflammatory carcinoma is a
clinicopathologic entity characterized by diffuse erythema and edema
(peau d’orange) of the breast, often without an underlying mass. These
clinical findings should involve the majority of the breast…It is
important to remember that inflammatory carcinoma is primarily a
clinical diagnosis. Involvement of the dermal lymphatics alone does not
indicate inflammatory carcinoma in the absence of clinical findings.”
Clinical and Biologic Characteristics

                       IBC is primarily a clinical diagnosis. One of
the commonly described changes associated with IBC is erythema, with
the skin overlying the breast showing a pink or mottled pink hue (Figure
1A). The erythema may be associated with a sensation of heat in the
affected breast. Concurrently or soon after, the breast begins to
enlarge rapidly, sometimes increasing in size 2- to 3-fold within a few
weeks (Figure 1B). This rapid rate of progress, along with diffuse
erythema of more than one third of the skin overlying the breast,
distinguishes IBC from neglected locally advanced breast cancer with
skin involvement. In more advanced and aggressive cases, the area can
change color dramatically within a few days, turning from pinkish to
dark red or purple, spreading diffusely over the entire breast. The
increased size of the breast is the result of edema caused by tumor
blockage of the lymphatic channels. Although nipple involvement is not a
principal feature of IBC, flattening, retraction, crusting, or
blistering may be apparent on examination. These nonspecific
characteristics can ultimately result in delayed diagnosis, and other
disease states can be confused with IBC. Infectious mastitis and abscess
typically occur only in lactating women. The inflammation associated
with ductal ectasia is more localized and responds quickly to supportive
measures. Sarcomatous, lymphomatous, or leukemic involvement of the
breast requires histologic examination for accurate diagnosis.[8]
                   

  
                                                   

(Enlarge Image)



                                   Figure 1.
                               

Clinical Signs of Inflammatory Breast Cancer.  A) Patient presenting
with erythema and increased breast size. B) Detailed view of involved
breast.
[ CLOSE WINDOW ]

<blockquote>
</blockquote>

                                   Figure 1.
                               


Clinical Signs of Inflammatory Breast Cancer.  A)
Patient presenting with erythema and increased breast size. B) Detailed
view of involved breast.

                       It is important to distinguish 2 distinct
clinical varieties of IBC that are commonly cited in the literature.
Primary IBC is used to describe the de novo development of IBC in a
previously normal breast. Unlike primary IBC, secondary IBC describes
the development of inflammatory skin changes that mimic IBC in either a
breast that already has cancer or on the chest wall after a mastectomy
for a noninflammatory breast cancer. (Figure 2). The breasts are usually
photographed during the examination, because response to treatment can
be monitored by reduction of the erythema and edema.

                                                   

(Enlarge Image)



                                   Figure 2.
                               

Clinical Presentation of Diffuse Recurrent Inflammatory Breast Cancer. The patient presented with skin rash and skin nodules.
<blockquote></blockquote>

                                   Figure 2.

                               

Clinical Presentation of Diffuse Recurrent Inflammatory Breast Cancer. The patient presented with skin rash and skin nodules.

                       IBC is not a specific histologic subtype and
can occur with invasive ductal and lobular, small cell, medullary, and
large cell carcinomas. Although skin changes in IBC resemble an acute
inflammatory process, these changes in fact result from dermal lymphatic
invasion by tumor emboli, leading to obstruction of lymphatic drainage.[9]
Although dermal lymphatic invasion is not a prerequisite for diagnosis,
because it can also be found in locally advanced or neglected breast
cancers, the presence of tumor emboli is a more distinct pathologic
feature of IBC. Therefore, in addition to diagnostic core biopsy, a
full-thickness skin biopsy is often obtained if IBC is suspected.
                       Distinct biologic characteristics typical of
IBC are associated with poor outcome, including high S-phase fraction,
high grade, aneuploidy, lack of estrogen and progesterone receptor
expression, and overexpression of human epidermal growth factor receptor
2 (HER2).[10–12] Inflammatory breast tumors are more likely to have mutations in p53, associated with decreased response to chemotherapy and decreased survival outcomes.[13]
Several genes have been identified that are believed to contribute to
the aggressive nature of IBC. Expression of nuclear factor kappa
β–related genes, which mediate cell migration, invasion, and metastasis,
was reported to be higher in IBC.[14]
Overexpression of RhoC GTPase, a member of the Ras family of
guanosine-5'-triphosphate (GTP)–binding proteins, upregulate angiogenic
factors (e.g., vascular endothelial growth factor [VEGF], basic
fibroblast growth factor), promoting cell motility and invasion.[15] IBC is associated with loss of expression of Wisp-3,
a tumor suppressor gene coding for insulin-like growth factor binding
protein–related protein (IGFBP-rP9) regulates tumor cell growth and
invasion.[16] Currently, except for HER2 status, these features are rarely used for treatment decisions in IBC.
Diagnostic Modalities

                       In most cases of IBC no discrete mass is
palpable on clinical examination, but imaging studies may show an
underlying mass and characteristic thickening of the skin (Figure 3).[17]
Although IBC is a clinicopathologic entity, the key role of imaging
studies is to identify a primary breast tumor, facilitate biopsy for
evaluation of biomarkers, stage locoregional and metastatic disease, and
evaluate tumor response to neoadjuvant therapy.
                                                   

(Enlarge Image)



                                   Figure 3.
                               

A 33-year-old Woman with Right Inflammatory Breast Cancer. An exial
postcontrast T1-weighted VIBRANT MR image shows diffuse skin thickening
in the right breast, with large multifocal disease mostly localized in
the right lower quadrant.
[ CLOSE WINDOW ]

<blockquote></blockquote>

                                   Figure 3.
                               

A 33-year-old Woman with Right Inflammatory
Breast Cancer. An exial postcontrast T1-weighted VIBRANT MR image shows
diffuse skin thickening in the right breast, with large multifocal
disease mostly localized in the right lower quadrant.

                       Although mammography is believed to be the
gold standard in breast imaging, findings in IBC are less sensitive,
detecting only 43% of primary lesions.[18]
The most common mammographic finding is skin thickening, and this may
be missed without clinical correlation. The advent of digital
mammography with improved contrast resolution, however, has increased
detection of skin thickening and diffuse increased breast density often
associated with IBC. Ultrasonography can identify an area of
heterogeneous infiltration and may be used in conjunction with
mammography. The greatest benefit of ultrasound, however, may be
detection of nodal involvement, both for locoregional therapeutic
planning and for evaluating response to induction therapy.
Ultrasonography has been reported to detect up to 93% of ipsilateral
axillary nodal involvement and up to 50% of infraclavicular, internal
mammary, or supraclavicular nodal involvement.[19]
                       
                       The use of MRI has been found to be the most accurate test for detecting a primary breast lesion in IBC.[20]
MRI findings frequently observed in IBC include diffuse skin
thickening, breast enlargement, edema, and a mass or parenchymal
enhancement. Other findings can include dilated lymphatic ducts or chest
wall edema. MRI has also been used to monitor response to chemotherapy,
correlating better with actual residual disease than measurements
determined through clinical examination, mammography, or
ultrasonography.[21]
                       
                       FDG-PET/CT is an emerging imaging method that
is widely gaining clinical acceptance because of its ability to
co-register both anatomic and functional information on one image.
Although prospective studies on the current use of FDG-PET/CT in primary
breast cancer have suggested limited value in evaluating local lymph
nodal disease,[22]
they have focused primarily on patients with early or small volume
disease who have a low probability of lymph node involvement. These
findings do not necessarily apply to patients with IBC who frequently
have extensive locoregional disease and in whom appropriate delineation
of disease extent is helpful for planning treatment, including
radiotherapy and chemotherapy (Figure 4). A single study of 7 patients
described increased uptake in enlarged breasts, with associated
prominent skin uptake, and intense scattered foci.[23]
Associated ipsilateral axillary adenopathy was seen in 86% of patients,
infraclavicular and supraclavicular adenopathy in 1 patient, and bone
metastases in another.
                                                   

(Enlarge Image)



                                   Figure 4.
                               

Three-dimensional (Coronal, Sagittal, and Transaxial) Display of the
PET/CT Images for a 47-year-old White Female with Nnewly Diagnosed
Inflammatory Breast Cancer. Extensive active lesions are shown for this
patient: 1) primary lesions of inflammatory breast cancer in the left
breast (white arrow), 2) extensive left axillary lymph node involvement
(blue arrow), and 3) an additional lesion in the left internal mammary
node (green arrow); this lesion will likely change the radiation field.
[ CLOSE WINDOW ]

<blockquote>
</blockquote>
                                   Figure 4.
                               

Three-dimensional (Coronal, Sagittal, and
Transaxial) Display of the PET/CT Images for a 47-year-old White Female
with Nnewly Diagnosed Inflammatory Breast Cancer. Extensive active
lesions are shown for this patient: 1) primary lesions of inflammatory
breast cancer in the left breast (white arrow), 2) extensive left
axillary lymph node involvement (blue arrow), and 3) an additional
lesion in the left internal mammary node (green arrow); this lesion will
likely change the radiation field.
                       
                       A preliminary study on the role of PET/CT in
24 patients with IBC showed that PET/CT is accurate at demonstrating
locoregional disease and distant metastases. Multicentric disease was
documented in 63% of patients, regional nodal disease in 88%, and
distant metastases in 38% of patients and primarily involved the liver,
skeleton, and contralateral supraclavicular node in this study.[19]
Furthermore, the test was useful in detecting internal mammary lymph
node involvement, predictive of recurrence risk and distant disease.[24]
                       
Multimodality Approach to Treatment
                       
                       Although IBC was once considered a uniformly
fatal disease with fewer than 5% of patients alive at 5 years,
management has evolved significantly over the past 40 years. A
multimodality approach, including primary systemic chemotherapy followed
by mastectomy and radiation therapy, has led to improved survival
outcomes.[25]
The NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines) for
Breast Cancer (in this issue; to view the most recent version of these
guidelines, visit the NCCN Web site at www.NCCN.org) list the standard
approach to treating IBC as neoadjuvant chemotherapy with an
anthracycline-based regimen and a taxane. If HER2 is overexpressed,
trastuzumab for a total of 1 year is indicated as part of the systemic
chemotherapy regimen. Mastectomy with axillary lymph node dissection is
standard in patients with IBC who respond to preoperative chemotherapy.
After surgery, postmastectomy radiation is recommended with adjuvant
endocrine therapy if indicated. A retrospective analysis of 179 patients
with IBC by Perez et al.[26]
showed an improvement in 5- and 10-year disease-free survival in those
who underwent multimodality therapy, including chemotherapy, surgery,
and radiation (40% and 35%), compared with those who underwent radiation
and surgery (24% and 24%) or radiation alone or with chemotherapy but
without surgery (6% and 0%).
Neoadjuvant Chemotherapy


                       Because of its relative rarity and poor
prognosis, most clinical trials of neoadjuvant chemotherapy have
excluded IBC, and therefore most studies reported are based on small
numbers of patients. The response to neoadjuvant chemotherapy has been
found to be the most important prognostic factor in patients, including
those with IBC (
Table 1
).[27] These results extended the prognostic significance of response to treatment in patients with IBC. In 1997, Ueno et al.[28]
updated the 20-year experience of 178 patients with IBC treated in 4
prospective trials at MD Anderson Cancer Center. All patients underwent
doxorubicin-based primary systemic chemotherapy, radiation therapy with
or without mastectomy, followed by adjuvant chemotherapy. The overall
response rate was 71%, with 5- and 10-year overall survival rates of 40%
and 33%, respectively. An estimated 28% of patients were reported alive
and without disease at 15 years.[28]
Other studies have also reported similar survival advantages for the
addition of preoperative anthracycline-based chemotherapy to
locoregional therapy, with higher disease-free and overall survival
rates in those experiencing a pathologic complete response.[29–32]
                       
                       The addition of taxanes to systemic
chemotherapy in IBC has also been investigated. A retrospective analysis
by Cristofanilli et al.[33]
reviewed 240 patients treated in 6 trials from 1973 to 2000. A total of
178 patients with IBC were treated with FAC alone (fluorouracil,
doxorubicin, and cyclophosphamide) and 62 with FAC followed by
paclitaxel. The pathologic complete response rate was significantly
higher in those treated with FAC and paclitaxel (25% vs. 10%). The
addition of paclitaxel led to improvement in progression-free (27 vs. 18
months) and median overall survival (54 vs. 32 months). In summary, the
incorporation of primary systemic therapy into the combined modality
approach has improved outcomes in the treatment of IBC; however, the
outcome remains poor, and additional therapeutic interventions should
consider the peculiar phenotype of the disease.
                       Several studies have documented increased frequency of HER2 overexpression in IBC.[34–39]
Trastuzumab has been studied in combination with chemotherapy in IBC
patients with pathologic complete response rates ranging from 17% to
40%.[40–42] Gianni et al.[43]
reported on a phase III prospective randomized trial evaluating the
addition of trastuzumab to anthracycline- and taxane-based induction
chemotherapy. Of 327 patients with locally advanced HER2-positive
disease, 27% had IBC. The addition of trastuzumab to neoadjuvant
chemotherapy led to a significantly increased 3-year event-free survival
(70% vs. 53%). Lapatinib, a reversible inhibitor of the HER1 (ErbB1)
and HER2 (ErbB2) tyrosine kinases, is also under evaluation in patients
with IBC. In a phase II study of 21 patients with HER2-positive IBC who
received induction lapatinib and paclitaxel, Boussen et al.[44] reported that the combination was associated with a clinical response rate of 80%.
                       Several other novel agents are currently
being studied for the treatment of IBC. IBC tumors are highly vascular
tumors that express angiogenic factors such as VEGF.[45] Gene expression patterns of human IBC xenografts have identified several angiogenesis-mediated genes, including VEGF, interleukin-8, bFGF, angiopoietin-13, Flt-1, Tie-2, and CD31.[46]
Based on studies indicating the importance of angiogenesis in IBC and
the results observed with the use of antiangiogenic agents in other
types of breast cancer, several studies evaluated the role of anti-VEGF
agents (bevacizumab) and SU5416 in combination with chemotherapy in the
treatment of IBC, but achieved no promising results.[47,48]
Multitargeted tyrosine kinases inhibitors directed at inhibition of the
various members of the family of VEGF receptors may represent more
active agents for the management of IBC and are currently being tested.[49]
                       
                       Several members of the Ras pathway have also
been proposed as potential molecular targets for treatment of IBC.
Farnesyl transferase inhibitors, known to block the farnesylation of
prenylated proteins (including the Rho subfamily of GTPases that is
highly expressed in IBC) are currently also being studied in combination
with chemotherapy in patients with breast cancer, including IBC.[50]
Locoregional Treatment

                       After neoadjuvant chemotherapy, standard
locoregional treatment includes mastectomy with axillary lymph node
dissection and radiation therapy. Patients who experience a pathologic
complete remission after neoadjuvant chemotherapy have a significantly
higher disease-free and overall survival compared with those who have
extensive residual disease. Patients whose disease does not respond to
induction chemotherapy may be considered for radiation therapy and then
reevaluated.
                       Mastectomy with axillary lymph node
dissection is the optimal surgical procedure for IBC. Axillary lymph
node involvement at presentation is noted in 55% to 85% of patients with
IBC and this remains an important prognostic factor. Case series have
shown that mastectomy improves local control, disease-free survival, and
cancer-specific survival.[50]
Removal of all gross disease is important, as skin lymphatic
involvement may extend beyond the area of visible skin change. Clinical
response by physical examination or imaging studies may underestimate
the extent of residual disease.[51] In a review of outcome data for patients with IBC after surgery, Curcio et al.[52]
found that negative margin status was associated with improved 3-year
local control, disease-free survival, and overall survival (60% vs. 31%,
37% vs. 17%, and 47% vs. 0%, respectively). In a series of 192 patients
with IBC treated at MD Anderson Cancer Center, the 5-year local control
rate was 91% for patients with negative margins and 68% for those with
positive margins.[29]
                       
                       Postmastectomy chest wall radiation therapy
is standard for patients with IBC after neoadjuvant chemotherapy
followed by mastectomy. The chest wall and lymph nodes within the
axillary, infraclavicular, supraclavicular, and internal mammary regions
are targeted with standard fractionation to 50 Gy to locoregional sites
followed by a 10-Gy boost to the scar. Given poor locoregional control
rates for IBC, an interest has been shown in dose escalation with
hyperfractionation. Liao et al.[53]
reported on 115 patients with IBC and found that escalating the dose
from 60 to 66 Gy delivered with twice-daily fractionation significantly
improved 5-year locoregional control rates (84% vs. 58%). Experience at
MD Anderson has shown that treatment to a chest wall with a cumulative
dose of 66 Gy was of clinical value for patients with a poor response to
induction chemotherapy, positive surgical margins, and 4 or more
positive lymph nodes after induction chemotherapy.[54]
Conclusions
                       
                       IBC is an aggressive and often lethal form of
breast cancer that can be misdiagnosed and therefore requires clinical
suspicion and appropriate workup. Early and accurate diagnosis is
essential. Diagnostic biopsies are extremely important; skin biopsy may
provide information regarding dermal lymphatic involvement and is
recommended. Although IBC is a clinicopathologic entity, imaging
modalities such as mammography, ultrasound, MRI, CT, and PET/CT have
been useful in diagnosing and staging this disease. Mammography
typically shows nonspecific findings, and therefore MRI is also
recommended. Such an aggressive disease with high incidence of
metastasis at presentation suggests the indication for PET/CT in staging
evaluation.
                       Although primary systemic chemotherapy with
anthracycline- and taxane-based regimens are the mainstay of therapy, a
multidisciplinary approach using adjuvant chemotherapy, radiation,
and/or surgery is utmost importance. The use of this multidisciplinary
approach in the treatment of IBC has resulted in significant increases
in survival over the past 4 decades, from less than 5% to 44% at 15
years in patients who experience a pathologic complete response. The use
of HER2 targeted therapy in the appropriate setting has improved
pathologic complete response and outcomes and is considered standard of
care. As knowledge of the biologic basis of IBC continues to expand,
further improvement in survival can be expected as targeted therapies
are added to these regimens.

References

  1. Hance KW, Anderson WF, Devesa SS, et al. Trends in
    inflammatory breast carcinoma incidence and survival: the Surveillance,
    Epidemiology, and End Results program at the National Cancer Institute. J
    Natl Cancer Inst 2005;97:966–975.
  2. Lee B, Tannenbaum N. Inflammatory carcinoma of the
    breast: a report of twenty-eight cases from the breast clinic of
    memorial hospital. Surg Gynecol Obstet 1924;38:580.
  3. Haagensen CD. Diseases of the female breast. Trans N Engl Obstet Gynecol Soc 1956;10:141–156.
  4. Walshe JM, Swain SM. Clinical aspects of inflammatory breast cancer. Breast Dis 2005;22:35–44.
  5. Jaiyesimi IA, Buzdar AU, Hortobagyi G. Inflammatory breast cancer: a review. J Clin Oncol 1992;10:1014–1024.
  6. Chang S, Parker SL, Pham T, et al. Inflammatory
    breast carcinoma incidence and survival: the Surveillance, Epidemiology,
    and End Results program of the National Cancer Institute, 1975–1992.
    Cancer 1998;82:2366–2372.
  7. Greene FL, Page DL, Fleming ID, et al. Breast. In:
    Greene FL, Page DL, Fleming ID, et al., eds. AJCC Cancer Staging Manual,
    6th ed. New York, NY: Springer-Verlag; 2002:255–281.
  8. Krishnan C, Moline S, Anders K, Warnke RA.
    Intravascular ALK-positive anaplastic large cell lymphoma mimicking
    inflammatory breast cancer. J Clin Oncol 2009;27:2563–2565.
  9. Gruber G, Ciriolo M, Altermatt HJ, et al. Prognosis
    of dermal lymphatic invasion with or without clinical signs of
    inflammatory breast cancer. Int J Cancer 2004;109:144–148.
  10. Paradiso A, Tommasi S, Brandi M, et al. Cell
    kinetics and hormonal receptor status in inflammatory breast carcinoma.
    Comparison with locally advanced disease. Cancer 1989;64:1922–1927.
  11. Kleer CG, van Golen KL, Merajver SD. Molecular
    biology of breast cancer metastasis. Inflammatory breast cancer:
    clinical syndrome and molecular determinants. Breast Cancer Res
    2000;2:423–429.
  12. Turpin E, Bieche I, Bertheau P, et al. Increased
    incidence of ERBB2 overexpression and TP53 mutation in inflammatory
    breast cancer. Oncogene 2002;21:7593–7597.
  13. Gonzalez-Angulo AM, Sneige N, Buzdar AU, et al. p53
    expression as a prognostic marker in inflammatory breast cancer. Clin
    Cancer Res 2004;10(18 Pt 1):6215–6221.
  14. Van Laere SJ, Van den Eynden GG, Van der Auwera, et
    al. Identification of cell-of-origin breast tumor subtypes in
    inflammatory breast cancer by gene expression profiling. Breast Cancer
    Res Treat 2006;95:243–255.
  15. van Golen KL, Wu ZF, Qiao XT, et al. RhoC GTPase
    overexpression modulates induction of angiogenic factors in breast
    cells. Neoplasia 2000;2:418–425.
  16. Kleer CG, Zhang Y, Pan Q, et al. WISP3 is a novel
    tumor suppressor gene of inflammatory breast cancer. Oncogene
    2002;21:3172–3180.
  17. Singletary SE, Cristofanilli M. Defining the clinical diagnosis of inflammatory breast cancer. Semin Oncol 2008;35:7–10.
  18. Chow CK. Imaging in inflammatory breast carcinoma. Breast Dis 2005;22:45–54.
  19. Yang WT, Le-Petross HT, Macapinlac H, et al.
    Inflammatory breast cancer: PET/CT, MRI, mammography, and sonography
    findings. Breast Cancer Res Treat 2008;109:417–426.
  20. Renz DM, Baltzer PA, Bottcher J, et al. Inflammatory
    breast carcinoma in magnetic resonance imaging: a comparison with
    locally advanced breast cancer. Acad Radiol 2008;15:209–221.
  21. Hamstra DA, Rehemtulla A, Ross BD. Diffusion
    magnetic resonance imaging: a biomarker for treatment response in
    oncology. J Clin Oncol 2007;25:4104–4109.
  22. Wahl RL, Siegel BA, Coleman RE, et al. Prospective
    multicenter study of axillary nodal staging by positron emission
    tomography in breast cancer: a report of the staging breast cancer with
    PET study group. J Clin Oncol 2004;22:277–285.
  23. Baslaim MM, Bakheet SM, Bakheet R, et al.
    18-Fluorodeoxyglucose-positron emission tomography in inflammatory
    breast cancer. World J Surg 2003;27:1099–1104.
  24. Carkaci S, Macapinlac HA, Cristofanilli M, et al.
    Retrospective study of 18F-FDG PET/CT in the diagnosis of inflammatory
    breast cancer: preliminary data. J Nucl Med 2009;50:231–238.
  25. Panades M, Olivotto IA, Speers CH, et al. Evolving
    strategies for inflammatory breast cancer: a population-based survival
    analysis. Clin Oncol 2005;23:1941–1950.
  26. Perez CA, Graham ML, Taylor ME, et al. Management of
    locally advanced carcinoma of the breast. I. Noninflammatory. Cancer
    1994;74(1 Suppl):453–465.
  27. Kuerer HM, Newman LA, Smith TL, et al. Clinical
    course of breast cancer patients with complete pathologic primary tumor
    and axillary lymph node response to doxorubicin-based neoadjuvant
    chemotherapy. J Clin Oncol 1999;17:460–469.
  28. Ueno NT, Buzdar AU, Singletary SE, et al.
    Combined-modality treatment of inflammatory breast carcinoma: twenty
    years of experience at M. D. Anderson Cancer Center. Cancer Chemother
    Pharmacol 1997;40:321–329.
  29. Harris EE, Schultz D, Bertsch H, et al. Ten-year
    outcome after combined modality therapy for inflammatory breast cancer.
    Int J Radiat Oncol Biol Phys 2003;55:1200–1208.
  30. Baldini E, Gardin G, Evangelista G, et al. Long-term
    results of combined-modality therapy for inflammatory breast carcinoma.
    Clin Breast Cancer 2004;5:358–363.
  31. Low JA, Berman AW, Steinberg SM, et al. Long-term
    follow-up for locally advanced and inflammatory breast cancer patients
    treated with multimodality therapy. J Clin Oncol 2004;22:4067–4074.
  32. Veyret C, Levy C, Chollet P, et al. Inflammatory
    breast cancer outcome with epirubicin-based induction and maintenance
    chemotherapy: ten-year results from the French Adjuvant Study Group
    GETIS 02 Trial. Cancer 2006;107:2535–2544.
  33. Cristofanilli M, Buzdar AU, Sneige N, et al.
    Paclitaxel in the multimodality treatment for inflammatory breast
    carcinoma. Cancer 2001;92:1775–1782.
  34. Guerin M, Gabillot M, Mathieu MC, et al. Structure
    and expression of c-erbB-2 and EGF receptor genes in inflammatory and
    non-inflammatory breast cancer: prognostic significance. Int J Cancer
    1989;43:201–208.
  35. Lerebours F, Bertheau P, Bieche I, et al. Evidence
    of chromosome regions and gene involvement in inflammatory breast
    cancer. Int J Cancer 2002;102:618–622.
  36. Charpin C, Bonnier P, Khouzami A, et al.
    Inflammatory breast carcinoma: an immunohistochemical study using
    monoclonal anti-pHER-2/neu, pS2, cathepsin, ER and PR. Anticancer Res
    1992;12:591–597.
  37. Sawaki M, Ito Y, Akiyama F, et al. High prevalence
    of HER-2/neu and p53 overexpression in inflammatory breast cancer.
    Breast Cancer 2006;13:172–178.
  38. Parton M, Dowsett M, Ashley S, et al. High incidence of HER-2 positivity in inflammatory breast cancer. Breast 2004;13:97–103.
  39. Prost S, Le MG, Douc-Rasy S, et al. Association of
    c-erbB2-gene amplification with poor prognosis in non-inflammatory
    breast carcinomas but not in carcinomas of the inflammatory type. Int J
    Cancer 1994;58:763–768.
  40. Limentani SA, Brufsky AM, Erban JK, et al. Phase II
    study of neoadjuvant docetaxel, vinorelbine, and trastuzumab followed by
    surgery and adjuvant doxorubicin plus cyclophosphamide in women with
    human epidermal growth factor receptor 2-overexpressing locally advanced
    breast cancer. J Clin Oncol 2007;25:1232–1238.
  41. Burstein HJ, Harris LN, Gelman R, et al.
    Preoperative therapy with trastuzumab and paclitaxel followed by
    sequential adjuvant doxorubicin/cyclophosphamide for HER2 overexpressing
    stage II or III breast cancer: a pilot study. J Clin Oncol
    2003;21:46–53.
  42. Hurley J, Doliny P, Reis I, et al. Docetaxel,
    cisplatin, and trastuzumab as primary systemic therapy for human
    epidermal growth factor receptor 2-positive locally advanced breast
    cancer. J Clin Oncol 2006;24:1831–1838.
  43. Gianni L, Eiermann W, Semiglazov V, et al.
    Neoadjuvant chemotherapy with trastuzumab followed by adjuvant
    trastuzumab versus neoadjuvant chemotherapy alone, in patients with
    HER2-positive locally advanced breast cancer (the NOAH trial): a
    randomised controlled superiority trial with a parallel HER2-negative
    cohort. Lancet 2010;375:377–384.
  44. Boussen H, Cristofanilli M, Zaks T, et al. Phase II
    study to evaluate the efficacy and safety of neoadjuvant lapatinib plus
    paclitaxel in patients with inflammatory breast cancer. J Clin Oncol
    2010;28:3248–3255.
  45. Van der Auwera I, Van den Eynden GG, Colpaert CG, et
    al. Tumor lymphangiogenesis in inflammatory breast carcinoma: a
    histomorphometric study. Clin Cancer Res 2005;11:7637–7642.
  46. Shirakawa K, Tsuda H, Heike Y, et al. Absence of
    endothelial cell, central necrosis, and fibrosis are associated with
    aggressive inflammatory breast cancer. Cancer Res 2001;61:445–451.
  47. Overmoyer B, Robertson K, Persons M, et al. A phase I
    pharmokinetic and pharmacodynamic study of SU5416 and doxorubicin (ADR)
    in inflammatory breast cancer (IBC) [abstract]. J Clin Oncol
    2001;20(Suppl 1):Abstract 391.
  48. Wedam S, Low J, Yang X, et al. A pilot study to
    evaluate response and angiogenesis after treatment with bevacizumab in
    patients with inflammatory breast cancer [abstract]. J Clin Oncol
    2004;21(Suppl 1):Abstract 578.
  49. Sonpavde G, Hutson TE. Pazopanib: a novel multitargeted tyrosine kinase inhibitor. Curr Oncol Rep 2007;9:115–119.
  50. Johnston SR, Hickish T, Ellis P, et al. Phase II
    study of the efficacy and tolerability of two dosing regimens of the
    farnesyl transferase inhibitor, R115777, in advanced breast cancer. J
    Clin Oncol 2003;21:2492–2499.
  51. Vlastos G, Fornage BD, Mirza NQ, et al. The
    correlation of axillary ultrasonography with histologic breast cancer
    downstaging after induction chemotherapy. Am J Surg 2000;179:446–452.
  52. Curcio LD, Rupp E, Williams WL, et al. Beyond
    palliative mastectomy in inflammatory breast cancer—a reassessment of
    margin status. Ann Surg Oncol 1999;6:249–254.
  53. Liao Z, Strom EA, Buzdar AU, et al. Locoregional
    irradiation for inflammatory breast cancer: effectiveness of dose
    escalation in decreasing recurrence. Int J Radiat Oncol Biol Phys
    2000;47:1191–1200.
  54. Woodward WA, Buchholz TA. The role of locoregional therapy in inflammatory breast cancer. Semin Oncol 2008;35:78–86.

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