Ectopic expression of either HMGA1 or HMGA2 also increased DNA compaction

Breast cancer stem cells are defined as a subpopu lation of breast cancer Gemcitabine Gemzar cells that will self renew and differentiate into other types of cancer cells. These cells are rare in cancers but 100-fold more tumori genic than cells of other phenotypes. Cancer stem cells are closely associated with tumor initiation, progression, metastasis and even drug-resistance. It is currently universally accepted that general chemo therapy is not successful in eradicating cancer stem,cells, particularly when the tumor becomes resistant. We hypothesized that cancer stem cells might confer growth resistance to endocrine therapeutic medicines. In 2003, Michael Clarkes team initially identified a CD44, CD24lo, ESA and lineage subpopulation of human breast cancer cells, which may start tumors in immune deficient NODSCID rodents. This subpopu lation could possibly be understood to be cancer stem cells according to the following features. Ability for self restore survival from anoikis, al, high tumorigenic potential and ability to efflux toxins Eumycetoma efficiently. Fillmore et al. Confirmed that breast cancer cell lines also have a stem like subpopulation depending on tumori genicity in vivo. Medical research using neoadjuvant treatment also suggested that these breast cancer stem cells could be selected by chemotherapy in place of by lapatinib. Therefore, drug-resistance to chemothera py is generally accepted as an intrinsic characteristic of breast cancer stem cells. Although some controversies remain, many re hunters believe that cancer stem cells are responsi ble for resistance to hormonal therapy. The response to endocrine treatment depends on the expression of oestrogen receptor, Lindeman and his col leagues reported that normal murine mammary stem cells are negative for ER, progesterone receptor and erbB2 during breast development. Smalley et al. Likewise confirmed by gene profiling and in vivo functional studies of Im Z-VAD-FMK expressing mouse mammary cells that ER-POSITIVE cells are not stem cells. In several in vitro tamoxifen resistance models, ER was down regulated as resistance created, that could be solved by inhibiting the epidermal growth factor receptorerbB2 signaling path while erbB2 was up-regulated. It had been also established that en hanced EGFRerbB2 signaling in tamoxifen resistant breast cancer cells probably benefits from selection for a more stem like phenotype. Utilizing a three di base cells. Breast cancer stem cells might be resistant to tamoxifen and survive, because tamoxifen only suppresses the growth of estrogen-related breast cancer cells after treatment.