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Group 2 (luminal B). This type includes tumors that are ER positive, PR negative and HER2 positive.

Luminal B breast cancers are likely to benefit from chemotherapy and may benefit from hormone therapy and treatment targeted to HER2.

In fact, recent clinical trial data indicate that patients with hormone receptor-negative tumors (basal-like or HER2-positive) show better responses to adjuvant and neoadjuvant chemotherapy regimens than patients with luminal A and B tumors.

Patients who achieved a pCR had good prognosis regardless of tumor subtype; however, patients with basal-like or HER2-positive tumors who did not achieve pCR had a higher risk of relapse and poorer prognosis than other subgroups.

Molecular Subtypes of Breast Cancer:

Group 3 (HER2 positive). This type includes tumors that are ER negative and PR negative, but HER2 positive.

HER2 breast cancers are likely to benefit from chemotherapy and treatment targeted to HER2.

Group 4 (basal-like). This type, which is also called triple-negative breast cancer, includes tumors that are ER negative, PR negative and HER2 negative.

Basal-like breast cancers are likely to benefit from chemotherapy

  • Group 1 (luminal A). This group includes tumors that are ER positive and PR positive, but negative for HER2.

  • Luminal A breast cancers are likely to benefit from hormone therapy and may also benefit from chemotherapy.

Microtubule Stabilization

Ixabepilone:

a member of the epothilone class of macrolide antibiotics, possesses high microtubule stabilizing activity and low susceptibility to drug resistance mechanisms, including multidrug-resistant protein and P-glycoprotein .

In the US, ixabepilone is approved for use in combination with capecitabine for the treatment of metastatic or locally advanced breast cancer after failure of an anthracycline and a taxane.

What's TNBC?

Angiogenesis Inhibition:

Risk factor of TNBC:

Sunitinib :

a dual inhibitor of the receptors for platelet-derived growth factor and vascular endothelial growth factor, has been investigated in a preliminary phase II trial in TNBC patients with metastatic disease who had received prior anthracycline and taxane therapy.

- Breast cancer that lacks expression of estrogen receptor/progesterone receptor, and overexpression of the human epidermal growth factor receptor 2 (HER2), or triple-negative breast cancer (TNBC), accounts for around 15–20% of breast cancers in the US.

- It typically carries a poorer prognosis than other breast cancer subgroups, with shorter periods of disease-free and overall survival. TNBC also has a propensity for visceral or central nervous system metastases

The Paradox of Triple Negative Breast Cancer

  • Premenopausal status
  • African descent
  • Younger age at menarche
  • Higher parity
  • Younger age at first term birth
  • Choosing not to breastfeed
  • Pharmacological lactation suppression
  • Elevated waist-to-hip ratio.
  • Recent evidence suggests that metabolic syndrome may also increase the risk of TNBC

Neoadjuvant/Adjuvant Setting

  • Triple-negative breast cancer is sensitive to chemotherapy, and patients who achieve a pathological complete response (pCR) with neoadjuvant treatment have good OS.

What's the TNBC Paradox?

Epidermal Growth Factor Receptor Inhibition

- A retrospective analysis of 1601 breast cancer patients showed that compared with other breast cancer subgroups, those with TNBC have a significantly higher risk of distant recurrence and death within 5 years of diagnosis.

- TNBC tend to have a better response to neoadjuvant chemotherapy than other subtypes.

SRC Kinase Inhibition:

In vitro studies have indicated that TNBC cell lines display greater sensitivity to growth inhibition by the multitarget kinase inhibitor, dasatinib, than luminal or HER2-overexpressed breast cancer cell lines.

Aberrant Deoxyribonucleic Acid Repair

Platinum Agents:

Triple-negative breast cancer cells exhibit an abundance of DNA aberrations, suggesting that their DNA repair mechanisms are defective. Consequently, these tumors may have an increased sensitivity to agents that cause inter-strand DNA breaks (e.g., platinum agents)

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