Anti-tumour activity of phosphoinositide-3-kinase antagonist AEZS 126 in models of triple-negative breast cancer

Hahne, Jens C.; Schmidt, Hermann; Meyer, Susanne; Engel, Jörg B.; Dietl, Johannes; Hönig, Arnd

doi:10.1007/s00432-013-1399-z

Cited by 3 publications

(5 citation statements)

References 44 publications

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“…In the present study we found that AEZS-126 executes its cytotoxicity in A2780 and Acis2780 cells only through necroptosis, a form of programmed cell death with features of necrosis. This observation is in good agreement with results from former studies where it was shown that AEZS-126 induced necroptosis in a broad panel of human breast cancer cell lines [28]. Nevertheless in the same study was demonstrated that the main mechanism of AEZS-126 mediated cytotoxicity must not always be based on necroptosis.…”

Section: Discussionsupporting

confidence: 91%

“…Previously we have reported that AEZS-126 showed also good anti-tumour activity in in vitro models of triple-negative breast cancer as well as in MCF-7 cells [28]. In the present study we found that AEZS-126 executes its cytotoxicity in A2780 and Acis2780 cells only through necroptosis, a form of programmed cell death with features of necrosis.…”

Section: Discussionmentioning

confidence: 55%

“…Nevertheless in the same study was demonstrated that the main mechanism of AEZS-126 mediated cytotoxicity must not always be based on necroptosis. In some breast cancer cell lines AEZS-126 induced caspase independent apoptosis beside necroptosis [28]. However, the mode of cell death seems to be a rather characteristic trait of treated cell line and not of the compound.…”

Section: Discussionmentioning

confidence: 99%

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Anti-tumour activity of phosphoinositide-3-kinase antagonist AEZS-126 in models of ovarian cancer

Hahne

Kurz

Meyer

et al. 2014

Arch Gynecol Obstet

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 55%

Section: Discussionmentioning

confidence: 99%

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Anti-tumour activity of phosphoinositide-3-kinase antagonist AEZS-126 in models of ovarian cancer

Hahne

Kurz

Meyer

et al. 2014

Arch Gynecol Obstet

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“…Clinical studies showed that the poor prognosis of TNBC was related to the activation of PI3K/AKT pathway [ 316 , 317 ]. A recent study exhibited that PI3K/AKT inhibitor AEZS 126 caused cell death by inducing apoptosis and necroptosis in TNBC cells [ 318 ]. Among the basal-like subtypes of TNBC, chemotherapy combined AEZS 126 with good toxicity characteristics and antitumor activity might be a potential strategy for TNBC clinical trials.…”

Section: Combination Therapies Of Rcd Subroutines With Small-molecule...mentioning

confidence: 99%

Targeting regulated cell death (RCD) with small-molecule compounds in triple-negative breast cancer: a revisited perspective from molecular mechanisms to targeted therapies

et al. 2022

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Triple-negative breast cancer (TNBC) is a subtype of human breast cancer with one of the worst prognoses, with no targeted therapeutic strategies currently available. Regulated cell death (RCD), also known as programmed cell death (PCD), has been widely reported to have numerous links to the progression and therapy of many types of human cancer. Of note, RCD can be divided into numerous different subroutines, including autophagy-dependent cell death, apoptosis, mitotic catastrophe, necroptosis, ferroptosis, pyroptosis and anoikis. More recently, targeting the subroutines of RCD with small-molecule compounds has been emerging as a promising therapeutic strategy, which has rapidly progressed in the treatment of TNBC. Therefore, in this review, we focus on summarizing the molecular mechanisms of the above-mentioned seven major RCD subroutines related to TNBC and the latest progress of small-molecule compounds targeting different RCD subroutines. Moreover, we further discuss the combined strategies of one drug (e.g., narciclasine) or more drugs (e.g., torin-1 combined with chloroquine) to achieve the therapeutic potential on TNBC by regulating RCD subroutines. More importantly, we demonstrate several small-molecule compounds (e.g., ONC201 and NCT03733119) by targeting the subroutines of RCD in TNBC clinical trials. Taken together, these findings will provide a clue on illuminating more actionable low-hanging-fruit druggable targets and candidate small-molecule drugs for potential RCD-related TNBC therapies. Graphical abstract

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“…3). 72,80–97 One of these targets is the androgen receptor, for which there have been some data on its ability to predict chemotherapy sensitivity and prognosticate patient outcomes. 98–100 Although there have only been preclinical and early phase studies looking at androgen receptor blockers as a targeted agent in mTNBC, larger clinical trials are currently ongoing.…”

Section: Future Directionsmentioning

confidence: 99%

A Review of Systemic Treatment in Metastatic Triple-Negative Breast Cancer

Zeichner

Terawaki²,

Gogineni³

2016

Breast Cancer�(Auckl)

152

153

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Patients with breast cancer along with metastatic estrogen and progesterone receptor (ER/PR)- and human epidermal growth factor receptor 2 (HER2)-negative tumors are referred to as having metastatic triple-negative breast cancer (mTNBC) disease. Although there have been many new treatment options approved by the Food and Drug Administration for ER/PR-positive and Her2/neu-amplified metastatic breast cancer, relatively few new agents have been approved for patients with mTNBC. There have been several head-to-head chemotherapy trials performed within the metastatic setting, and much of what is applied in clinical practice is extrapolated from chemotherapy trials in the adjuvant setting, with taxanes and anthracyclines incorporated early on in the patient’s treatment course. Select synergistic combinations can produce faster and more significant response rates compared with monotherapy and are typically used in the setting of visceral threat or symptomatic disease. Preclinical studies have implicated other possible targets and mechanisms in mTNBC. Ongoing clinical trials are underway assessing new chemotherapeutic strategies and agents, including targeted therapy and immunotherapy. In this review, we evaluate the standard systemic and future treatment options in mTNBC.

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Anti-tumour activity of phosphoinositide-3-kinase antagonist AEZS 126 in models of triple-negative breast cancer

Cited by 3 publications

References 44 publications

Anti-tumour activity of phosphoinositide-3-kinase antagonist AEZS-126 in models of ovarian cancer

Anti-tumour activity of phosphoinositide-3-kinase antagonist AEZS-126 in models of ovarian cancer

Targeting regulated cell death (RCD) with small-molecule compounds in triple-negative breast cancer: a revisited perspective from molecular mechanisms to targeted therapies

A Review of Systemic Treatment in Metastatic Triple-Negative Breast Cancer

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