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Study · In vitro (cells) · 2022

4 results

Regulation of Chemosensitivity in Human Medulloblastoma Cells by p53 and the PI3 Kinase Signaling Pathway.

Naeem A, Harish V, Coste S, Parasido EM, Choudhry MU, Kromer LF, Ihemelandu C, Petricoin EF, Pierobon M, Noon MS, Yenugonda VM, Avantaggiati M and 4 more

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Kupfer GM, Fricke S, Rodriguez O, Albanese C

Molecular cancer research : MCR11 Oct 2021Cited by 16 (Europe PMC)

Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: CC BY-NC-ND. Results still quote short attributed sentences.

Results from this study4

4 results from studies that gave the peptide. No result from this study comes from people.

  1. 01LabIn vitro (cells)Mechanism

    In human medulloblastoma cells, co-treatment with Tβ4 induced p-AKT S473 in both p53-high and p53-low cells.

    In plain wordsIn cancer cells, Tβ4 raised the p-AKT signal in cells with high and low p53.

    Outcome
    Increasep-AKT S473 induction
    Study

    humann: not reported in source

    medulloblastoma cells, p53-high and p53-low
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Co-treatment with G-actin-sequestering peptide, thymosin β4 (Tβ4), induced p-AKTS473 in both p53-high and p53-low cells, enhancing chemosensitivity in D556 cells while enhancing chemoresistance in D283 and UW228 cells.
  2. 02LabIn vitro (cells)Efficacy outcome

    In D556 medulloblastoma cells, co-treatment with Tβ4 enhanced chemosensitivity.

    In plain wordsIn D556 cancer cells, Tβ4 made the cells respond better to chemotherapy.

    Outcome
    IncreaseChemosensitivity in D556 cells
    Study

    humann: not reported in source

    D556 medulloblastoma cells
    Outcome group
    Tumor growth · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Co-treatment with G-actin-sequestering peptide, thymosin β4 (Tβ4), induced p-AKTS473 in both p53-high and p53-low cells, enhancing chemosensitivity in D556 cells while enhancing chemoresistance in D283 and UW228 cells.
  3. 03LabIn vitro (cells)Efficacy outcome

    In D283 medulloblastoma cells, co-treatment with Tβ4 enhanced chemoresistance.

    In plain wordsIn D283 cancer cells, Tβ4 made the cells resist chemotherapy more.

    Outcome
    DecreaseChemosensitivity in D283 cells
    Study

    humann: not reported in source

    D283 medulloblastoma cells
    Outcome group
    Tumor growth · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Co-treatment with G-actin-sequestering peptide, thymosin β4 (Tβ4), induced p-AKTS473 in both p53-high and p53-low cells, enhancing chemosensitivity in D556 cells while enhancing chemoresistance in D283 and UW228 cells.
  4. 04LabIn vitro (cells)Efficacy outcome

    In UW228 medulloblastoma cells, co-treatment with Tβ4 enhanced chemoresistance.

    In plain wordsIn UW228 cancer cells, Tβ4 made the cells resist chemotherapy more.

    Outcome
    DecreaseChemosensitivity in UW228 cells
    Study

    humann: not reported in source

    UW228 medulloblastoma cells
    Outcome group
    Tumor growth · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Co-treatment with G-actin-sequestering peptide, thymosin β4 (Tβ4), induced p-AKTS473 in both p53-high and p53-low cells, enhancing chemosensitivity in D556 cells while enhancing chemoresistance in D283 and UW228 cells.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    13 Oct 2026, 01:52 UTC

    Study results updated

  2. Version 1

    12 Oct 2026, 18:17 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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