Results 51 to 60 of about 2,343,487 (194)

PKM2–c-Myc–Survivin Cascade Regulates the Cell Proliferation, Migration, and Tamoxifen Resistance in Breast Cancer

open access: yesFrontiers in Pharmacology, 2020
The M2 isoform of pyruvate kinase (PKM2), as a key glycolytic enzyme, plays important roles in tumorigenesis and chemotherapeutic drug resistance. However, the intricate mechanism of PKM2 as a protein kinase regulating breast cancer progression and ...
Pian Yu   +13 more
doaj   +1 more source

Tripartite motif-containing 3 (TRIM3) enhances ER signaling and confers tamoxifen resistance in breast cancer

open access: yesOncogenesis, 2021
Tamoxifen resistance remains a clinical problem in estrogen receptor (ER)-positive breast cancer. SUMOylation of ERα enhances ERα-induced transcription activity.
Runyi Ye   +7 more
doaj   +1 more source

A potential role for naringenin in reversing tamoxifen resistance in MCF-7 breast cancer cells [PDF]

open access: yes, 2012
Tamoxifen has been used as an effective treatment against breast cancer for over 30 years. However, tamoxifen resistance has become a major hurdle to effective treatment.
Ramos, Joseph   +1 more
core  

Oxidative stress mediates estrogen receptor independent killing and contributes to tamoxifen resistance

open access: yes, 2016
Tamoxifen is the accepted therapy for patients with estrogen receptor-α (ERα)-positive breast cancer. However, clinical resistance to tamoxifen, as demonstrated by recurrence or progression on therapy, is frequent and precedes death from metastases.
Brindley, David N.   +10 more
core   +1 more source

Understanding Tamoxifen Resistance in Breast cancer [PDF]

open access: yes, 2016
Tamoxifen is the accepted therapy for patients with estrogen receptor α (ERα)−positive breast cancer. However, clinical resistance to tamoxifen, as demonstrated by recurrence or progression on therapy, is frequent and precedes death from metastases.
Bekele, Raie Taye
core   +1 more source

Mutant KRAS‐m6A Epitranscriptome Axis Promotes Colorectal Cancer and is a Therapeutic Target

open access: yesAdvanced Science, EarlyView.
Mutant KRAS‐m6A axis promotes colorectal cancer (CRC) progression. Mutant KRAS stabilizes METTL3, leading to increased m6A‐modified BCL9L mRNA and translation of BCL9L protein. BCL9L in turn mediates TGF‐β secretion to induce differentiation of Treg and an immunosuppressive microenvironment.
Danyu Chen   +12 more
wiley   +1 more source

Lnc-DC promotes estrogen independent growth and tamoxifen resistance in breast cancer

open access: yesCell Death and Disease, 2021
Selective estrogen receptor modulators (SERMs) such as tamoxifen have proven to be effective in the treatment of estrogen receptor (ER) positive breast cancer.
Wan-Xin Peng   +6 more
doaj   +1 more source

Targeting the YAP‐BST2 Axis Overcomes Intrinsic Anti‐PD‐1 Resistance in Metastatic Gastric Cancer

open access: yesAdvanced Science, EarlyView.
Concurrent YAP hyperactivation and Tp53 loss in Atp4b‐expressed parietal cell lineage drives gastric cancer initiation, multi‐organ metastasis, and intrinsic resistance to anti‐PD‐1 therapy. BST2 emerges as a direct YAP‐TEAD transcriptional target that engages PIRA2 on myeloid cells to establish an immunosuppressive microenvironment.
Weihong Zhang   +17 more
wiley   +1 more source

The role of CtIP (RBBP8) in tamoxifen resistance and human breast cancer [PDF]

open access: yes, 2007
textAcquired resistance to the antiestrogen tamoxifen constitutes a major clinical challenge in breast cancer therapy. However, the mechanisms involved are still poorly understood.
Wu, Minhao, 1976-
core  

A Gut‐Brain Axis Underlying Succinate‐Associated Compulsive‐Like Behavior

open access: yesAdvanced Science, EarlyView.
Gut‐derived succinate is associated with an excitatory‐inhibitory imbalance in dmPFC glutamatergic neurons, involving microglial SUCNR1 activation and vagal afferent signaling via upregulated gut 5‐HT4 receptors along the DVC‐CeA‐dmPFC circuit, changes that are linked to excessive compulsive‐like behavior.
Yi Li   +12 more
wiley   +1 more source

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