Results 121 to 130 of about 9,917,709 (290)

What are multiple primary malignancies? [PDF]

open access: yes, 2017
Over the past 30 years, the incidence of cancer in Poland has more than doubled. Advances in technology, early diagnosis and improved treatment make more and more malignancies curable. An increase in the survival of cancer patients has also been observed.
Anna Doboszyńska   +3 more
core   +2 more sources

Case series of multiple primary cancers in single individuals: diagnostic and therapeutic dilemmas

open access: yesJournal of Community Hospital Internal Medicine Perspectives, 2017
Background and Objectives: Cancer recurrence represents treatment failure; the development of new primary tumors is suggestive of persistent exposure to etiological risk factors or genetic predisposition due to mutations in multiple cell lines.
Faizan Malik   +4 more
doaj   +1 more source

Castration‐resistant prostate cancer cells are addicted to the high activity of cyclin‐dependent kinase 2

open access: yesMolecular Oncology, EarlyView.
We show that emergence of castration‐resistant prostate (CRPC) is associated with significant upregulation of cyclins that positively regulate cyclin‐dependent kinase 2 (CDK2) and concomitant downregulation of CDK4 cyclins. This renders CRPC cells dependent on the high activity of CDK2, and CDK2 inhibitors synergistically sensitize CRPC cells to both ...
Joyeeta Chatterjee   +3 more
wiley   +1 more source

Synchronous multiple primary colorectal cancer in patients with extraintestinal malignancies

open access: yesСибирский онкологический журнал
Introduction. The incidence of colorectal cancer (CRC) is steadily increasing in Russia. Patients with cancers of extra-intestinal malignancies are at increased risk of developing CRC.
V. V. Podolskiy, E. A. Podolskaya
doaj   +1 more source

Mechanisms and therapeutic opportunities of the ribotoxic stress response in cancer

open access: yesMolecular Oncology, EarlyView.
Cancer cells' high translational demand creates opportunities to therapeutically target ribosome function. Ribosome stalling and collisions activate ZAKα and the ribotoxic stress response (RSR), which can trigger rapid, p53‐independent apoptosis in cancer.
Anastassiya Kim   +7 more
wiley   +1 more source

Gut microbiota alterations in patients with non‐small‐cell lung cancer undergoing chemoradiotherapy

open access: yesMolecular Oncology, EarlyView.
We investigated the impact of concurrent chemoradiotherapy (CRT) on the gut microbiota in patients with locally advanced non‐small‐cell lung cancer. Overall gut microbiota composition remained largely stable throughout CRT while antibiotic exposure may influence microbial diversity.
Hanne Marte Nymoen   +19 more
wiley   +1 more source

Clinical and molecular analysis of synchronous double lung cancers [PDF]

open access: yes, 2012
Background: Since multiple lung cancer treatment strategies differ, it is essential for clinicians to be able to distinguish between separate primary lesions and metastasis. In the present study, we used array comparative genomic hybridization (aCGH) and
Oikawa, Masahiro   +10 more
core   +1 more source

DEVELOPMENT OF MULTIPLE PRIMARY CANCERS IN LUNG CANCER PATIENTS: APPALACHIAN VS. NON-APPALACHIAN POPULATIONS OF KENTUCKY [PDF]

open access: yes, 2016
OBJECTIVE: This study examined whether there were differences in the development of multiple primary cancers in lung cancer patients residing in the Appalachian versus Non-Appalachian regions of Kentucky.
Pravosud, Vira
core   +1 more source

NAPRT loss promotes lung tumor initiation and growth through AKT signaling independently of NAD+ biosynthesis

open access: yesMolecular Oncology, EarlyView.
Loss of NAPRT promotes lung tumor initiation and growth through a noncanonical mechanism, independent of its role in NAD+ biosynthesis. Mechanistically, NAPRT depletion activates the mTORC2‐driven AKT/β‐catenin signaling axis to enhance clonogenic and invasive phenotypes. Furthermore, lung‐specific Naprt deletion significantly increases tumor burden in
Myung Joon Oh   +11 more
wiley   +1 more source

Regulation of the lncRNA NEAT1 by p53‐ΔNp63 crosstalk modulates the DNA damage response and therapeutic efficacy in HNSCC

open access: yesMolecular Oncology, EarlyView.
In head and neck squamous cell carcinoma (HNSCC) p53 and p63 exert opposite roles on the transcription regulation of the lncRNA NEAT1. Under basal conditions, p53 levels are low and p63 represses NEAT1 expression. Upon genotoxic stress, p53 is rapidly induced, displacing p63 from the NEAT1 promoter leading to NEAT1 transcriptional activation and ...
Sara De Domenico   +5 more
wiley   +1 more source

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