Introduction “when the purple color is on the skin over the tumur accompanied by shooting pains it is a very unpropitious beginning” Charles Bell 1814. Lee and Tannenbaum in 1924- Inflammatory Breast Cancer (IBC)
An aggressive subset of breast cancer diagnosed clinically(no current molecular definition) 2-5% of breast cancer incidence with mortality of 10% Women diagnosed with IBC have a poorer diagnosis “No Lump Still Cancer”
Risk factors Major : Age, sex, genetic, previous breast ca Intermediate : Hormonal, irradiation, benign dx with atypia, diet, alcohol Minor: obesity, benign dx with mild atypia
Types 2 types of IBC -PRIMARY-in previously normal breast - SECONDARY- features of IBC on chest wall post mastectomy for non-IBC or recurrence with inflammatory features in a breast that already had cancer Palpable lump is present only in a 3 rd of IBC patient at diagnosis
Pathology Growth pattern is characterized by minimal insitu component or lack of insitu component Has extensive component of intraparenchymal lymphovascular tumour emboli Its less compact than non- ibc , leaving more available space for migration of cncers
Skin changes are due to dermal lymphatic invasions, a state where dermal dermal lymphovascular spaces are filled with tumor emboli that retracted away from the surrounding endothelia lining Considered as hallmark of ibc as it leads to lymphatics obstruction and high metastatic potential of ibc
Clinical presentation Rapid onset of; Redness(erythema) >1/3 breast Edema(Orange peel appearance) Often Warm, pain Enlarged without a mass
Enlarged axillary nodes Nipple changes Highly metastatic 35% at presentation
Diagnosis Made from minimum criteria in clinical definition with confirmed breast cancer; rapid onset 3-6months Imaging helps in management
IBC STAGING Per AJCC Guidelines- TMN T-always T4D regardless of size of redness N-N1-N3depending on the number and location of clinically positive nodes M-Distant metastasis Clinical stage iii-iv
IBC imaging No lump in 2/3, most common findings is skin thickening Mammogram often miss >50% of IBC Uss of breast and nodes MRI Metastatic workup-PET/CT if not possible the CT chest, abdomen and pelvis Bone scan
Difference from LABC Rapidly changing appearance More difficult to detect by routine imaging Often in young women before age of screening Worse prognosis(often TNBC, higher frequency of HER2 amplification and elevated Ki67)
Differential diagnosis Mastitis or cellulitis post radiation Radiation dermatitis Duct ectasia Breast abscess
Histological concept Confirmed by core biopsy for biomarker analysis(ER,PR,HER2) 2punch biopsy to determine presence of lymphovascular emboli Targeted genes VEGF genes Its not an histological subtype of BC
Molecular subtypes Similar to BC as a whole , IBC can be ER,PR and or HER2 + difference in proportion IBC non IBC ER/PR+ 50% 60-70% HER2+ 40% 15-20% TNBC 30% 15-20%
Metastasis High recurrence 50-60% by 5yrs Early spread via lymphatics and blood Recurrence-2types, local including skin and distant bone,lungs , brain
Management Multidisciplinary approach Management protocol from IBC consensus treatment strategy Involving systemic therapy and locoregional therapy
SYSTEMIC THERAPY Its essentially a systemic disease at diagnosis Options include -chemotherapy anthracycline+taxane -Herceptin based regimen if indicated -Lapatinib based if indicated -Hormonal based if indicated - sutent ?
Neoadjuvant chemotherapy is starting point( anthracycline+taxanes ) if chemoresistant then a non-cross resistant drugs recommended(personalized management) HER2 targeted therapy - transtuzumab+pertuzumab TCH-P-effective anthracycline free options
Conclusions IBC has unique tumur biology from non-IBC, consensus exist on minimal diagnostic criteria and given to its aggressive biology, patient will benefit from aggressive treatment and more clinical trial participation is needed for a better treatment outcomes