Results 61 to 70 of about 302,059 (295)

Meta‐analysis of the association between sodium‐glucose co‐transporter‐2 inhibitors and risk of skin cancer among patients with type 2 diabetes [PDF]

open access: yes, 2018
A slight increase in melanoma risk was observed among sodium‐glucose co‐transporter‐2 (SGLT‐2) inhibitor users in the regular reports. However, the association remains uncertain.
Bailey   +30 more
core   +1 more source

Inhibition of CDK9 enhances AML cell death induced by combined venetoclax and azacitidine

open access: yesMolecular Oncology, EarlyView.
The CDK9 inhibitor AZD4573 downregulates c‐MYC and MCL‐1 to induce death of cytarabine (AraC)‐resistant AML cells. This enhances VEN + AZA‐induced cell death significantly more than any combination of two of the three drugs in AraC‐resistant AML cells.
Shuangshuang Wu   +18 more
wiley   +1 more source

SGLT2 Inhibitors as Potential Anticancer Agents

open access: yesBiomedicines, 2023
Sodium-glucose cotransporter 2 (SGLT2) serves as a critical glucose transporter that has been reported to be overexpressed in cancer models, followed by increased glucose uptake in both mice and humans.
Debasish Basak, David Gamez, Subrata Deb
doaj   +1 more source

Decitabine impact on the endocytosis regulator RhoA, the folate carriers RFC1 and FOLR1, and the glucose transporter GLUT4 in human tumors. [PDF]

open access: yes, 2014
BackgroundIn 31 solid tumor patients treated with the demethylating agent decitabine, we performed tumor biopsies before and after the first cycle of decitabine and used immunohistochemistry (IHC) to assess whether decitabine increased expression of ...
A Kumari   +55 more
core   +2 more sources

Adaptaquin is selectively toxic to glioma stem cells through disruption of iron and cholesterol metabolism

open access: yesMolecular Oncology, EarlyView.
Adaptaquin selectively kills glioma stem cells while sparing differentiated brain cells. Transcriptomic and proteomic analyses show Adaptaquin disrupts iron and cholesterol homeostasis, with iron chelation amplifying cytotoxicity via cholesterol depletion, mitochondrial dysfunction, and elevated reactive oxygen species.
Adrien M. Vaquié   +16 more
wiley   +1 more source

Cyclic AMP pathway activation and extracellular zinc induce rapid intracellular zinc mobilization in Candida albicans [PDF]

open access: yes, 2018
LK was supported by Innovation Fund Denmark, DK (4019-00019B). Pcovery ApS received funding from Wellcome Trust, Research Councils, UK (100480/Z/12), Novo Seeds, DK and Boehringer Ingelheim Venture Fund, D.
Anja T. Fuglsang   +4 more
core   +3 more sources

LINC01116, a hypoxia‐lncRNA marker of pathological lymphangiogenesis and poor prognosis in lung adenocarcinoma

open access: yesMolecular Oncology, EarlyView.
The LINC01116 long noncoding RNA is induced by hypoxia and associated with poor prognosis and high recurrence rates in two cohorts of lung adenocarcinoma patients. Here, we demonstrate that besides its expression in cancer cells, LINC01116 is markedly expressed in lymphatic endothelial cells of the tumor stroma in which it participates in hypoxia ...
Marine Gautier‐Isola   +12 more
wiley   +1 more source

The role of zinc in renal pathological changes in diabetic status [PDF]

open access: yes, 2015
Diabetes mellitus (DM) was the 8th leading cause of death in 2011, resulting in 1.4 million deaths worldwide. One of the complications of DM is chronic kidney disease, which accounts for nearly 44% of all new cases of kidney failure in the US in 2011 ...
Fernando, Julie, Zhou, Shaobo
core   +1 more source

Therapeutic strategies for MMAE‐resistant bladder cancer through DPP4 inhibition

open access: yesMolecular Oncology, EarlyView.
We established monomethyl auristatin E (MMAE)‐resistant bladder cancer (BC) cell lines by exposure to progressively increasing concentrations of MMAE in vitro. RNA sequencing showed DPP4 expression was increased in MMAE‐resistant BC cells. Both si‐DPP4 and the DPP4 inhibitor sitagliptin suppressed the viability of MMAE‐resistant BC cells.
Gang Li   +10 more
wiley   +1 more source

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