ArticleOncogene2010
The BH3-only protein Bad confers breast cancer taxane sensitivity through a nonapoptotic mechanism.
Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 36 citations in OpenAlex.
- Article
- Brusatol Inhibits Esophageal Squamous Cell Carcinoma Tumorigenesis Through Bad-Mediated Mitochondrial Apoptosis Induction and Anti-Metastasis by Targeting Akt1.Biomolecules · 2025Article
- The non-cytotoxic small molecule NPB does not inhibit BAD phosphorylation and forms colloidal aggregates.Communications medicine · 2025Article
- Comparing the BAD Protein Interactomes in 2D and 3D Cell Culture Using Proximity Labeling.Journal of proteome research · 2024Article
- Androgens Modulate Bcl-2 Agonist of Cell Death (BAD) Expression and Function in Breast Cancer Cells.International journal of molecular sciences · 2023Article
- BAD regulates mammary gland morphogenesis by 4E-BP1-mediated control of localized translation in mouse and human models.Nature communications · 2021Article
- The Role of Necroptosis in ROS-Mediated Cancer Therapies and Its Promising Applications.Cancers · 2020Review
- BAD sensitizes breast cancer cells to docetaxel with increased mitotic arrest and necroptosis.Scientific reports · 2020Article
- Non-canonical BAD activity regulates breast cancer cell and tumor growth via 14-3-3 binding and mitochondrial metabolism.Oncogene · 2019Article
- Expression and Functional Analysis of the BCL2-Associated Agonist of Cell Death (Frontiers in endocrinology · 2018Article
- Prolonged mitotic arrest induced by Wee1 inhibition sensitizes breast cancer cells to paclitaxel.Oncotarget · 2017Article
- The pro-apoptotic paradox: the BH3-only protein Bcl-2 interacting killer (Bik) is prognostic for unfavorable outcomes in breast cancer.Oncotarget · 2016Article
- BCL-2 family protein, BAD is down-regulated in breast cancer and inhibits cell invasion.Experimental cell research · 2015Article
- Article
- Targeting proapoptotic protein BAD inhibits survival and self-renewal of cancer stem cells.Cell death and differentiation · 2014Article
- The chemotherapeutic agent paclitaxel inhibits autophagy through two distinct mechanisms that regulate apoptosis.Oncogene · 2013Article
- The BCL2 antagonist of cell death pathway influences endometrial cancer cell sensitivity to cisplatin.Gynecologic oncology · 2012Article
- Ceramide transfer protein and cancer.Anti-cancer agents in medicinal chemistry · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Antimitotic agents such as taxanes (paclitaxel and docetaxel) have greatly advanced the treatment of breast cancer, although variable patient response and drug toxicity are major limitations. Lack of validated predictive markers for taxane responsiveness precludes a priori identification of patients who are most likely to respond to treatment; thus, a subset of patients endure toxic side effects with marginal benefit. Mechanistic insights into taxane therapeutic activity may lead to rational therapeutic improvements. In this paper we report that the proapoptotic BH3-only protein Bad has a major role in taxane-induced cell death in vitro, and clinically is a prognostic indicator for overall survival of breast cancer patients after adjuvant taxane chemotherapy. Unexpectedly, Bad did not induce the mitochondrial apoptotic machinery in response to taxane treatment. Instead, Bad indirectly facilitated cell death by stimulating cellular proliferation. As dividing cells are the targets of taxane therapy, Bad-stimulated proliferation may be a marker of taxane sensitivity. Our studies indicate that quantification of Bad protein levels may have value as a diagnostic tool. They also suggest that cells expressing Bad are more sensitive to taxanes because of their altered cell cycle dynamics and reveal a clinically relevant proliferative role of Bad in breast cancer.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.