Hyperbaric oxygen: Does it promote growth or recurrence of malignancy?

J. Feldmeier, U. Carl, K. Hartmann, P. Sminia

Research output: Contribution to journalReview articleAcademicpeer-review

Abstract

It has been a concern that a therapeutic modality recommended as an adjunct to healing and administered to promote proliferation of fibroblasts, epithelial cells and blood vessels in a wound could also lead to proliferation of malignant cells and angiogenesis in a malignant tumor. The first reported concern that hyperbaric oxygen (HBO2) might have cancer growth enhancing effects appeared in a paper by Johnson and Lauchlan in 1966. In a series of patients treated with HBO2 radiosensitization, they reported a more frequent than expected incidence of metastases and an unusual pattern of metastases. The published literature from clinical reports, animal studies and cell culture studies are reviewed. Putative mechanisms whereby HBO2 could have carcinogenic effects are discussed. The processes of angiogenesis in wound healing and in cancer growth are compared and contrasted. In vitro, in vivo and clinical studies strongly suggest no more than a neutral effect of HBO2 on tumor growth. In fact some studies suggest a negative impact of HBO2 on malignant progression or formation. For angiogenesis, similarities in wound healing and cancer are striking but significant differences are found including the relative importance of angiogenic factors and the process of cessation of angiogenesis. Tumors that grow in hypoxic environments are more prone to metastases and more lethal to the patient. They are also more likely to mutate toward resistant genotypes. Discussion of postulated mechanisms of carcinogenesis including free radical and immunosuppressive effects points out why they are not likely to enhance or cause cancer growth or initiation. In conclusion, the published literature on tumor angiogenesis mechanisms and other possible mechanisms of cancer causation or accelerated growth provides little basis for HBO2 to enhance malignant growth or metastases. A history of malignancy should not be considered a contraindication for HBO2 therapy.

Original languageEnglish
Pages (from-to)1-18
Number of pages18
JournalUndersea Hyperb Med
Volume30
Issue number1
Publication statusPublished - 1 Mar 2003

Cite this

Feldmeier, J. ; Carl, U. ; Hartmann, K. ; Sminia, P. / Hyperbaric oxygen : Does it promote growth or recurrence of malignancy?. In: Undersea Hyperb Med. 2003 ; Vol. 30, No. 1. pp. 1-18.
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abstract = "It has been a concern that a therapeutic modality recommended as an adjunct to healing and administered to promote proliferation of fibroblasts, epithelial cells and blood vessels in a wound could also lead to proliferation of malignant cells and angiogenesis in a malignant tumor. The first reported concern that hyperbaric oxygen (HBO2) might have cancer growth enhancing effects appeared in a paper by Johnson and Lauchlan in 1966. In a series of patients treated with HBO2 radiosensitization, they reported a more frequent than expected incidence of metastases and an unusual pattern of metastases. The published literature from clinical reports, animal studies and cell culture studies are reviewed. Putative mechanisms whereby HBO2 could have carcinogenic effects are discussed. The processes of angiogenesis in wound healing and in cancer growth are compared and contrasted. In vitro, in vivo and clinical studies strongly suggest no more than a neutral effect of HBO2 on tumor growth. In fact some studies suggest a negative impact of HBO2 on malignant progression or formation. For angiogenesis, similarities in wound healing and cancer are striking but significant differences are found including the relative importance of angiogenic factors and the process of cessation of angiogenesis. Tumors that grow in hypoxic environments are more prone to metastases and more lethal to the patient. They are also more likely to mutate toward resistant genotypes. Discussion of postulated mechanisms of carcinogenesis including free radical and immunosuppressive effects points out why they are not likely to enhance or cause cancer growth or initiation. In conclusion, the published literature on tumor angiogenesis mechanisms and other possible mechanisms of cancer causation or accelerated growth provides little basis for HBO2 to enhance malignant growth or metastases. A history of malignancy should not be considered a contraindication for HBO2 therapy.",
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Feldmeier, J, Carl, U, Hartmann, K & Sminia, P 2003, 'Hyperbaric oxygen: Does it promote growth or recurrence of malignancy?' Undersea Hyperb Med, vol. 30, no. 1, pp. 1-18.

Hyperbaric oxygen : Does it promote growth or recurrence of malignancy? / Feldmeier, J.; Carl, U.; Hartmann, K.; Sminia, P.

In: Undersea Hyperb Med, Vol. 30, No. 1, 01.03.2003, p. 1-18.

Research output: Contribution to journalReview articleAcademicpeer-review

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T1 - Hyperbaric oxygen

T2 - Does it promote growth or recurrence of malignancy?

AU - Feldmeier, J.

AU - Carl, U.

AU - Hartmann, K.

AU - Sminia, P.

PY - 2003/3/1

Y1 - 2003/3/1

N2 - It has been a concern that a therapeutic modality recommended as an adjunct to healing and administered to promote proliferation of fibroblasts, epithelial cells and blood vessels in a wound could also lead to proliferation of malignant cells and angiogenesis in a malignant tumor. The first reported concern that hyperbaric oxygen (HBO2) might have cancer growth enhancing effects appeared in a paper by Johnson and Lauchlan in 1966. In a series of patients treated with HBO2 radiosensitization, they reported a more frequent than expected incidence of metastases and an unusual pattern of metastases. The published literature from clinical reports, animal studies and cell culture studies are reviewed. Putative mechanisms whereby HBO2 could have carcinogenic effects are discussed. The processes of angiogenesis in wound healing and in cancer growth are compared and contrasted. In vitro, in vivo and clinical studies strongly suggest no more than a neutral effect of HBO2 on tumor growth. In fact some studies suggest a negative impact of HBO2 on malignant progression or formation. For angiogenesis, similarities in wound healing and cancer are striking but significant differences are found including the relative importance of angiogenic factors and the process of cessation of angiogenesis. Tumors that grow in hypoxic environments are more prone to metastases and more lethal to the patient. They are also more likely to mutate toward resistant genotypes. Discussion of postulated mechanisms of carcinogenesis including free radical and immunosuppressive effects points out why they are not likely to enhance or cause cancer growth or initiation. In conclusion, the published literature on tumor angiogenesis mechanisms and other possible mechanisms of cancer causation or accelerated growth provides little basis for HBO2 to enhance malignant growth or metastases. A history of malignancy should not be considered a contraindication for HBO2 therapy.

AB - It has been a concern that a therapeutic modality recommended as an adjunct to healing and administered to promote proliferation of fibroblasts, epithelial cells and blood vessels in a wound could also lead to proliferation of malignant cells and angiogenesis in a malignant tumor. The first reported concern that hyperbaric oxygen (HBO2) might have cancer growth enhancing effects appeared in a paper by Johnson and Lauchlan in 1966. In a series of patients treated with HBO2 radiosensitization, they reported a more frequent than expected incidence of metastases and an unusual pattern of metastases. The published literature from clinical reports, animal studies and cell culture studies are reviewed. Putative mechanisms whereby HBO2 could have carcinogenic effects are discussed. The processes of angiogenesis in wound healing and in cancer growth are compared and contrasted. In vitro, in vivo and clinical studies strongly suggest no more than a neutral effect of HBO2 on tumor growth. In fact some studies suggest a negative impact of HBO2 on malignant progression or formation. For angiogenesis, similarities in wound healing and cancer are striking but significant differences are found including the relative importance of angiogenic factors and the process of cessation of angiogenesis. Tumors that grow in hypoxic environments are more prone to metastases and more lethal to the patient. They are also more likely to mutate toward resistant genotypes. Discussion of postulated mechanisms of carcinogenesis including free radical and immunosuppressive effects points out why they are not likely to enhance or cause cancer growth or initiation. In conclusion, the published literature on tumor angiogenesis mechanisms and other possible mechanisms of cancer causation or accelerated growth provides little basis for HBO2 to enhance malignant growth or metastases. A history of malignancy should not be considered a contraindication for HBO2 therapy.

KW - Animals

KW - Free Radicals/adverse effects

KW - Growth Substances/metabolism

KW - Humans

KW - Hyperbaric Oxygenation/adverse effects

KW - Immune Tolerance

KW - Immunity, Cellular

KW - Mice

KW - Neoplasm Recurrence, Local/etiology

KW - Neovascularization, Pathologic/etiology

KW - Rats

KW - Tumor Cells, Cultured

KW - Wound Healing/physiology

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M3 - Review article

VL - 30

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JO - Undersea Hyperb Med

JF - Undersea Hyperb Med

SN - 1066-2936

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