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ASCT2/SLC1A5 controls glutamine uptake and tumour growth in triple-negative basal-like breast cancer

PaperCitations, authors & open-access status

ASCT2/SLC1A5 controls glutamine uptake and tumour growth in triple-negative basal-like breast cancer is a paper indexed in PICO Portal from OpenAlex.

How many citations does ASCT2/SLC1A5 controls glutamine uptake and tumour growth in triple-negative basal-like breast cancer have?

PICO Portalcitation count

ASCT2/SLC1A5 controls glutamine uptake and tumour growth in triple-negative basal-like breast cancer has 590 citations in the OpenAlex counts PICO Portal stores.

When was ASCT2/SLC1A5 controls glutamine uptake and tumour growth in triple-negative basal-like breast cancer published?

PICO Portalyear

ASCT2/SLC1A5 controls glutamine uptake and tumour growth in triple-negative basal-like breast cancer has 2015 year in the PICO Portal index.

What is the open-access status of ASCT2/SLC1A5 controls glutamine uptake and tumour growth in triple-negative basal-like breast cancer?

PICO Portaloa status

ASCT2/SLC1A5 controls glutamine uptake and tumour growth in triple-negative basal-like breast cancer has hybrid oa status in the PICO Portal index.

What is the DOI of ASCT2/SLC1A5 controls glutamine uptake and tumour growth in triple-negative basal-like breast cancer?

PICO Portaldoi

The DOI for ASCT2/SLC1A5 controls glutamine uptake and tumour growth in triple-negative basal-like breast cancer is on the source record.

What is the PMID of ASCT2/SLC1A5 controls glutamine uptake and tumour growth in triple-negative basal-like breast cancer?

PICO Portalpmid

The PMID for ASCT2/SLC1A5 controls glutamine uptake and tumour growth in triple-negative basal-like breast cancer is on the source record.

What is the OpenAlex record for ASCT2/SLC1A5 controls glutamine uptake and tumour growth in triple-negative basal-like breast cancer?

PICO Portalopenalex

The OpenAlex for ASCT2/SLC1A5 controls glutamine uptake and tumour growth in triple-negative basal-like breast cancer is on the source record.

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