Figures & data
Figure 1 Image depicting the development of therapeutic regimens against breast cancer.
![Figure 1 Image depicting the development of therapeutic regimens against breast cancer.](/cms/asset/3a50c5ab-23ba-49c5-8b3d-84458a2e9be2/dbct_a_30881110_f0001_c.jpg)
Figure 2 Snapshot of various chemotherapeutic modalities that are being prescribed in clinics and the novel therapeutic drugs that are being developed.
![Figure 2 Snapshot of various chemotherapeutic modalities that are being prescribed in clinics and the novel therapeutic drugs that are being developed.](/cms/asset/3fde896f-c921-43d3-89da-f583dc211d5c/dbct_a_30881110_f0002_c.jpg)
Figure 3 Schematic diagram showing intrinsic and extrinsic factors that aid the breast cancer stem cells to evade and survive against therapeutic insults.
Notes: Two widely accepted theories regarding the origins of CSCs are highlighted. According to “Cancer stem cell theory,” an inherent subpopulation of dormant cancer cells that are pluripotent in nature with the ability to repopulate the depleted pool of cancer cells following therapy. The “cancer stem cell plasticity theory” describes that therapeutic insults and EMT triggers a few breast cancer cells to undergo a switch, converting epithelial cells to pluripotent CSCs. The interplay of microenvironment and intrinsic cascades of CSCs aids them to elude the conventional therapy. Intrinsic factors depict microRNAs, drug transporters, ALDH, and altered cellular metabolism as pivotal processes that can be targeted. Further, extrinsic factors include a plethora of various components from the tumor microenvironment. Some of the important players being hypoxia, angiogenesis, EMT, immune cells, and stromal cells promoting proliferative signaling like cytokines, TGF-β, and self-renewal signals like Wnt/Notch/Hedgehog. Some of the inhibitors/mAbs against these resistance promoting factors have also been depicted.
![Figure 3 Schematic diagram showing intrinsic and extrinsic factors that aid the breast cancer stem cells to evade and survive against therapeutic insults.Notes: Two widely accepted theories regarding the origins of CSCs are highlighted. According to “Cancer stem cell theory,” an inherent subpopulation of dormant cancer cells that are pluripotent in nature with the ability to repopulate the depleted pool of cancer cells following therapy. The “cancer stem cell plasticity theory” describes that therapeutic insults and EMT triggers a few breast cancer cells to undergo a switch, converting epithelial cells to pluripotent CSCs. The interplay of microenvironment and intrinsic cascades of CSCs aids them to elude the conventional therapy. Intrinsic factors depict microRNAs, drug transporters, ALDH, and altered cellular metabolism as pivotal processes that can be targeted. Further, extrinsic factors include a plethora of various components from the tumor microenvironment. Some of the important players being hypoxia, angiogenesis, EMT, immune cells, and stromal cells promoting proliferative signaling like cytokines, TGF-β, and self-renewal signals like Wnt/Notch/Hedgehog. Some of the inhibitors/mAbs against these resistance promoting factors have also been depicted.](/cms/asset/e57fb721-81a4-4450-8fe9-c6f2b6d5b02a/dbct_a_30881110_f0003_c.jpg)
Table 1 Upcoming therapeutic modalities against breast cancer stem cells
Figure 4 Schematic showing TRAIL therapy against CSC and TAM.
Abbreviations: BCSC, breast cancer stem cell; CSC, cancer stem cell; FAS, Fas cell surface death receptor; TAM, tumor-associated macrophage; TRAIL, tumor necrosis factor-related apoptosis inducing ligand.
![Figure 4 Schematic showing TRAIL therapy against CSC and TAM.](/cms/asset/1f40afd0-c53e-4e5f-acb5-ee82c07f7c04/dbct_a_30881110_f0004_c.jpg)