Target intelligence / Profile preview

Breast cancer survival pathways

Molecular classification
Signaling pathway, Intracellular signaling cascade
01

Overview

Breast cancer survival pathways represent a diverse set of interconnected signaling networks that enable malignant cells to evade apoptosis and maintain proliferative capacity. Primary among these are the PI3K/Akt/mTOR and MAPK/ERK pathways, which integrate extracellular signals from growth factor receptors like HER2 and hormone receptors like the Estrogen Receptor (Source: PubMed, PMID: 30545854). Dysregulation of these pathways, often through genetic mutations such as PIK3CA or loss of the PTEN tumor suppressor, is a hallmark of breast cancer progression and therapeutic resistance (Source: NIH/NCI). Pharmacological targeting of these pathways involves the use of kinase inhibitors and monoclonal antibodies designed to block specific signaling nodes, thereby restoring the cell's natural apoptotic mechanisms (Source: Journal of Clinical Oncology). However, the complexity and redundancy of these networks often lead to the activation of compensatory pathways, presenting a significant challenge for long-term treatment efficacy (Source: StatPearls).

Other names
Pro-survival signaling in breast cancerOncogenic survival networksBreast cancer cell survival signaling
02

Mechanism of action

Inhibition of specific enzymatic or receptor nodes within intracellular cascades to disrupt pro-survival signaling and promote programmed cell death (Source: Nature Reviews Cancer).

03

Biological functions

Cell survivalApoptosis inhibitionCell proliferationSignal transductionMetabolic regulation
04

Disease associations

Breast cancerMalignant neoplasm of breast
05

Safety considerations

HyperglycemiaGastrointestinal toxicity (diarrhea, nausea)StomatitisPneumonitisAcquired drug resistance via bypass signalingCardiotoxicity (associated with HER2 inhibition)
06

Interacting drugs

Alpelisib

7 more in the full profile.

07

Biomarkers

PIK3CA mutationPTEN lossHER2/neu (ERBB2) amplificationEstrogen receptor (ER) expressionProgesterone receptor (PR) expressionAKT1 mutation

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