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Study · In vitro (cells) · 2012

3 results

Growth hormone receptor blockade inhibits growth hormone-induced chemoresistance by restoring cytotoxic-induced apoptosis in breast cancer cells independently of estrogen receptor expression.

Minoia M, Gentilin E, Molè D, Rossi M, Filieri C, Tagliati F, Baroni A, Ambrosio MR, degli Uberti E, Zatelli MC

The Journal of clinical endocrinology and metabolism22 Mar 2012Cited by 36 (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: Publisher copyright. Results still quote short attributed sentences.

Results from this study3

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

  1. 01LabIn vitro (cells)Mechanism

    In MDA-MB-231 breast cancer cells, pegvisomant reduced GH-induced DNA synthesis compared with GH without pegvisomant.

    In plain wordsIn cells, pegvisomant reduced GH-induced DNA synthesis compared with GH without pegvisomant.

    Outcome
    DecreaseGH-induced DNA synthesis
    Study

    humann: not reported in source

    ER-negative MDA-MB-231 breast cancer cells
    Comparator
    GH without pegvisomant
    Outcome group
    Tumor growth · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    GH protects ER-negative MDA-MB-231 cells from the cytotoxic effects of D and GH receptor antagonist pegvisomant reduces GH-induced DNA synthesis also in these cells.
  2. 02LabIn vitro (cells)Mechanism

    In MDA-MB-231 and MCF7 breast cancer cells, pegvisomant blocked GH-mediated reduction of basal apoptosis.

    In plain wordsIn cells, pegvisomant blocked GH-mediated suppression of basal cell death compared with GH without pegvisomant.

    Outcome
    IncreaseBasal apoptosis
    Study

    humann: not reported in source

    MDA-MB-231 and MCF7 breast cancer cells
    Comparator
    GH without pegvisomant
    Outcome group
    Tumor growth · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In both MDA-MB-231 and MCF7 cells, GH does not revert D-induced G2/M accumulation but significantly reduces basal and D-induced apoptosis, an effect blocked by pegvisomant.
    1 context sentence
    Summary · context
    GH protects ER-negative MDA-MB-231 cells from the cytotoxic effects of D and GH receptor antagonist pegvisomant reduces GH-induced DNA synthesis also in these cells.
  3. 03LabIn vitro (cells)Mechanism

    In MDA-MB-231 and MCF7 breast cancer cells, pegvisomant blocked GH-mediated reduction of doxorubicin-induced apoptosis.

    In plain wordsIn cells, adding pegvisomant blocked GH-mediated suppression of doxorubicin-induced cell death compared with GH and doxorubicin alone.

    Outcome
    IncreaseDoxorubicin-induced apoptosis
    Study

    humann: not reported in source

    MDA-MB-231 and MCF7 breast cancer cells
    Comparator
    GH and doxorubicin without pegvisomant
    Outcome group
    Tumor growth · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In both MDA-MB-231 and MCF7 cells, GH does not revert D-induced G2/M accumulation but significantly reduces basal and D-induced apoptosis, an effect blocked by pegvisomant.
    2 context sentences
    Summary · context
    We previously demonstrated that GH protects the estrogen receptor (ER) positive BC-derived MCF7 cell line toward the cytotoxic effects of doxorubicin (D), independently of IGF-I.
    Summary · context
    GH protects ER-negative MDA-MB-231 cells from the cytotoxic effects of D and GH receptor antagonist pegvisomant reduces GH-induced DNA synthesis also in these 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

    28 Oct 2026, 02:03 UTC

    Study results updated

  2. Version 1

    27 Oct 2026, 16:34 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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