Ten-year outcome after combined modality therapy for inflammatory breast cancer

Harris, Eleanor; Schultz, Delray; Bertsch, Helaine; Fox, Kevin R.; Glick, John H.; Solin, Lawrence J.

doi:10.1016/s0360-3016(02)04201-3

Cited by 110 publications

(65 citation statements)

References 29 publications

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“…Despite significant improvements in the disease-free survival rates of non-IBC (nIBC) patients, IBC patient survival rates remain low, with a 5-year disease-free survival rate of less than 40%, in comparison to the $90% of nIBC (4,(7)(8)(9). The poor prognosis is due to infiltration of tumor emboli that metastasize within the dermal lymphatic vessels of the skin overlying the breast (3,4).…”

Section: Introductionmentioning

confidence: 99%

Regulation of Inflammatory Breast Cancer Cell Invasion through Akt1/PKBα Phosphorylation of RhoC GTPase

Lehman

Laere

Golen

et al. 2012

Molecular Cancer Research

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With a 42% and 18% 5-and 10-year respective disease-free survival rate, inflammatory breast cancer (IBC) is arguably the deadliest form of breast cancer. IBC invades the dermal lymphatic vessels of the skin overlying the breast and as a consequence nearly all women have lymph node involvement and $1/3 have gross distant metastases at the time of diagnosis. One year after diagnosis $90% of patients have detectable metastases, making IBC a paradigm for lymphovascular invasion. Understanding the underlying mechanisms of the IBC metastatic phenotype is essential for new therapies. Work from our laboratory and others show distinct molecular differences between IBC and non-IBCs (nIBCs). Previously we showed that RhoC GTPase is a metastatic switch responsible for the invasive phenotype of IBC. In this study we integrate observations made in IBC patients with in vitro analysis. We show that the PI3K/Akt signaling pathway is crucial in IBC invasion. Key molecules involved in cytoskeletal control and cell motility are specifically upregulated in IBC patients compared with stage and cell-typeof-origin matched nIBCs patients. Distinctively, RhoC GTPase is a substrate for Akt1 and its phosphorylation is absolutely essential for IBC cell invasion. Further our data show that Akt3, not Akt1 has a role in IBC cell survival. Together our data show a unique and targetable pathway for IBC invasion and survival.

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Section: Introductionmentioning

confidence: 99%

Regulation of Inflammatory Breast Cancer Cell Invasion through Akt1/PKBα Phosphorylation of RhoC GTPase

Lehman

Laere

Golen

et al. 2012

Molecular Cancer Research

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“…The 5-year survival rate for patients with IBC is o40%, while the 5-year survival rate of all other breast cancers combined is approximately 90%. [1][2][3][4] This poor prognosis can be attributed to a number of factors, including the propensity for misdiagnosis of the disease due to its unique clinical presentation. [5][6][7] In contrast to most breast cancers, IBC is characterized by the lack of discernible primary tumor formation and the accumulation of cancerous epithelial cells in the dermal lymphatic vessels.…”

mentioning

confidence: 99%

Anoikis evasion in inflammatory breast cancer cells is mediated by Bim-EL sequestration

et al. 2014

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Inflammatory breast cancer (IBC) is a rare and highly invasive type of breast cancer, and patients diagnosed with IBC often face a very poor prognosis. IBC is characterized by the lack of primary tumor formation and the rapid accumulation of cancerous epithelial cells in the dermal lymphatic vessels. Given that normal epithelial cells require attachment to the extracellular matrix (ECM) for survival, a comprehensive examination of the molecular mechanisms underlying IBC cell survival in the lymphatic vessels is of paramount importance to our understanding of IBC pathogenesis. Here we demonstrate that, in contrast to normal mammary epithelial cells, IBC cells evade ECM-detachment-induced apoptosis (anoikis). ErbB2 and EGFR knockdown in KPL-4 and SUM149 cells, respectively, causes decreased colony growth in soft agar and increased caspase activation following ECM detachment. ERK/MAPK signaling was found to operate downstream of ErbB2 and EGFR to protect cells from anoikis by facilitating the formation of a protein complex containing Bim-EL, LC8, and Beclin-1. This complex forms as a result of Bim-EL phosphorylation on serine 59, and thus Bim-EL cannot localize to the mitochondria and cause anoikis. These results reveal a novel mechanism that could be targeted with innovative therapeutics to induce anoikis in IBC cells.

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“…As sometimes happens, patients elect to go with different means of treatment and not the mastectomy with lymph node dissection, radiation, and chemotherapy that is the standard of care. 3,4,8,9,10,11,12,13 Even though the patient elected not to attempt the full surgery, there are still surgical options that could have helped her quality of life and are important to consider. Wound care can be curative for many different wounds but can also greatly improve the quality of life that is present.…”

Section: Introductionmentioning

confidence: 99%

Fungating Metastatic Breast Cancer, a Challenging Case Report of Bleeding Control and Palliative Wound Care

Addison¹

2014

EJPM

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This case will discuss the palliative care in an advanced metastatic and fungating breast cancer. As sometimes happens, patients elect to go with different means of treatment and not the mastectomy with lymph node dissection, radiation, and chemotherapy that is the standard of care. Even though the patient elected not to attempt the full surgery, there are still surgical options that could have helped her quality of life and are important to consider. Wound care can be curative for many different wounds but can also greatly improve the quality of life that is present. Wounds leave the body exposed to secondary infections and can produce foul odor which is not conducive to patient or family comfort and happiness. It can be used in conjunction with many different treatments and should not be forgotten in the treatment of all patients. In this case we also discussed a variety of methods for bleeding control of this cancerous mass.

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Ten-year outcome after combined modality therapy for inflammatory breast cancer

Cited by 110 publications

References 29 publications

Regulation of Inflammatory Breast Cancer Cell Invasion through Akt1/PKBα Phosphorylation of RhoC GTPase

Regulation of Inflammatory Breast Cancer Cell Invasion through Akt1/PKBα Phosphorylation of RhoC GTPase

Anoikis evasion in inflammatory breast cancer cells is mediated by Bim-EL sequestration

Fungating Metastatic Breast Cancer, a Challenging Case Report of Bleeding Control and Palliative Wound Care

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