Modulating the Epigenetic Machinery for Increased SSTR2 Expression in Small-Cell Lung Cancer Cells

M. J. Klomp; L. J. Hofland; L. van den Brink; P. M. van Koetsveld; M. de Jong; S. U. Dalm

doi:10.1007/s00259-022-05924-4

Modulating the Epigenetic Machinery for Increased SSTR2 Expression in Small-Cell Lung Cancer Cells

M. J. Klomp, L. J. Hofland, L. van den Brink, P. M. van Koetsveld, M. de Jong, S. U. Dalm

Research output: Contribution to journal › Meeting Abstract › Academic › peer-review

Abstract

Aim/Introduction: Peptide receptor radionuclide therapy for neuroendocrine tumor (NET) patients is effective, however, complete responses are rare. To improve treatment outcome, we aim to enhance somatostatin type-2 receptor (SSTR2) expression using histone deacetylase inhibitors (HDACis). Our previous studies using the HDACi valproic acid showed promising results in vitro, however, in vivo studies did not demonstrate increased SSTR2-mediated [¹⁷⁷Lu]Lu-DOTATATE uptake. Therefore we investigated the potential of other HDACis, targeting different HDAC enzyme classes and/or having longer half-lives in vivo, in high SSTR2-expressing small-cell lung cancer (SCLC) cells. In addition, we compared the results to that obtained in low SSTR2-expressing NET cells.

Original language	English
Article number	OP-166
Pages (from-to)	S57-S57
Number of pages	1
Journal	European Journal of Nuclear Medicine and Molecular Imaging
Volume	49
Issue number	Suppl 1
DOIs	https://doi.org/10.1007/s00259-022-05924-4
Publication status	Published - Sept 2022

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title = "Modulating the Epigenetic Machinery for Increased SSTR2 Expression in Small-Cell Lung Cancer Cells",

abstract = "Aim/Introduction: Peptide receptor radionuclide therapy for neuroendocrine tumor (NET) patients is effective, however, complete responses are rare. To improve treatment outcome, we aim to enhance somatostatin type-2 receptor (SSTR2) expression using histone deacetylase inhibitors (HDACis). Our previous studies using the HDACi valproic acid showed promising results in vitro, however, in vivo studies did not demonstrate increased SSTR2-mediated [177Lu]Lu-DOTATATE uptake. Therefore we investigated the potential of other HDACis, targeting different HDAC enzyme classes and/or having longer half-lives in vivo, in high SSTR2-expressing small-cell lung cancer (SCLC) cells. In addition, we compared the results to that obtained in low SSTR2-expressing NET cells.",

author = "Klomp, {M. J.} and Hofland, {L. J.} and {van den Brink}, L. and {van Koetsveld}, {P. M.} and {de Jong}, M. and Dalm, {S. U.}",

year = "2022",

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language = "English",

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T1 - Modulating the Epigenetic Machinery for Increased SSTR2 Expression in Small-Cell Lung Cancer Cells

AU - Klomp, M. J.

AU - Hofland, L. J.

AU - van den Brink, L.

AU - van Koetsveld, P. M.

AU - de Jong, M.

AU - Dalm, S. U.

PY - 2022/9

Y1 - 2022/9

N2 - Aim/Introduction: Peptide receptor radionuclide therapy for neuroendocrine tumor (NET) patients is effective, however, complete responses are rare. To improve treatment outcome, we aim to enhance somatostatin type-2 receptor (SSTR2) expression using histone deacetylase inhibitors (HDACis). Our previous studies using the HDACi valproic acid showed promising results in vitro, however, in vivo studies did not demonstrate increased SSTR2-mediated [177Lu]Lu-DOTATATE uptake. Therefore we investigated the potential of other HDACis, targeting different HDAC enzyme classes and/or having longer half-lives in vivo, in high SSTR2-expressing small-cell lung cancer (SCLC) cells. In addition, we compared the results to that obtained in low SSTR2-expressing NET cells.

AB - Aim/Introduction: Peptide receptor radionuclide therapy for neuroendocrine tumor (NET) patients is effective, however, complete responses are rare. To improve treatment outcome, we aim to enhance somatostatin type-2 receptor (SSTR2) expression using histone deacetylase inhibitors (HDACis). Our previous studies using the HDACi valproic acid showed promising results in vitro, however, in vivo studies did not demonstrate increased SSTR2-mediated [177Lu]Lu-DOTATATE uptake. Therefore we investigated the potential of other HDACis, targeting different HDAC enzyme classes and/or having longer half-lives in vivo, in high SSTR2-expressing small-cell lung cancer (SCLC) cells. In addition, we compared the results to that obtained in low SSTR2-expressing NET cells.

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JO - European Journal of Nuclear Medicine and Molecular Imaging

JF - European Journal of Nuclear Medicine and Molecular Imaging

IS - Suppl 1

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ER -

Modulating the Epigenetic Machinery for Increased SSTR2 Expression in Small-Cell Lung Cancer Cells

Abstract

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