Arrest of Growth of Ovarian Tumor by Tranexamic Acid

Åstedt, Birger; Glifberg, Ingemar; Mattsson, W.; Tropé, Claes G.

doi:10.1001/jama.1977.03280020058026

Cited by 31 publications

(11 citation statements)

References 6 publications

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“…At the time this subject was originally reviewed [1], two studies reported patients with advanced malignancy who had been treated with anticoagulants plus the protease inhibitor, tranexamic acid [65,66]. These reports were reviewed from the perspective of the anticoagulant use.…”

Section: Summary Of Recent Clinical Trialsmentioning

confidence: 99%

“…The hypothesis that progression of such tumor types may be mediated, at least to some extent, by this pathway, is supported by studies of the role of urokinase in experimental models of malignancy [40]. Clues to the relevance of urokinase to progression of human malignancy are provided by the 427 studies reviewed previously [65,66] and the studies of Monden et al [24] cited above. In addition, Kikuchi and associates [67] described 11 patients with advanced ovarian carcinoma complicated by ascites who were treated with intraperitoneal injections of tranexamic acid.…”

Section: Summary Of Recent Clinical Trialsmentioning

confidence: 99%

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Clinical trials with anticoagulant and antiplatelet therapies

1992

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Clinical trials of drugs that influence coagulation and fibrinolysis pathways have been undertaken in patients with malignancy because these pathways are capable of influencing malignant progression. The validity of this concept was originally confirmed in experimental animal models of malignancy. Earlier pilot studies in human disease have been succeeded by definitive prospective randomized clinical trials that have revealed heterogeneity of responsiveness to anticoagulant and fibrinolytic agents that may be attributable to differences in mechanisms of interaction of the tumor cells of various types of malignancy with these pathways in vivo. In certain tumor types studied thus far, increased tumor response rates and prolongation of survival have been observed that suggest the possibility that substantial benefit may be realized from this treatment approach in patients with malignancy. In addition, the availability of newer and potentially more effective therapeutic agents holds promise for even greater gains in previously tested tumor types. The ability to design treatment regimens that correspond to defined mechanisms that pertain to specific tumor types should permit future studies to be designed rationally. Current data suggest that anticoagulant and fibrinolytic agents might reasonably be tested in tumor types characterized by the existence of a tumor cell-associated coagulation pathway with thrombin generation and conversion of fibrinogen to fibrin (such as small cell carcinoma of the lung). By contrast, protease inhibitors might reasonably be tested in tumor types characterized by expression of tumor cell plasminogen activators. Expansion of current views on the possible role of antithrombic drugs in cancer therapy is justified. For example, antithrombotic drugs classified as non-steroidal anti-inflammatory agents may inhibit carcinogenesis while polyanionic drugs with anticoagulant properties, such as suramin and heparin, may inhibit growth factor interactions with cells. Intriguing new opportunities clearly exist for interactions between clinical and basic investigators that may provide both novel biologic insights and improved patient care.

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Section: Summary Of Recent Clinical Trialsmentioning

confidence: 99%

Section: Summary Of Recent Clinical Trialsmentioning

confidence: 99%

Clinical trials with anticoagulant and antiplatelet therapies

1992

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“…This means that metastasis has almost certainly already occurred in humans so treated and clinical measures of outcome have correspondingly been improved survival and delayed time to tumor progression rather than inhibition of metastasis per se [17][18][19][20][21][22]. To complicate matters further, fibrinolytic therapy has been shown to be effective in certain clinical settings [20,21,24] while success has been claimed for antifibrinolytic therapy in others [25].…”

Section: Introductionmentioning

confidence: 99%

The role of fibrin in tumor metastasis

Costantini

Zacharski

1992

Cancer Metast Rev

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A volume of data that has accumulated for over a century has suggested that fibrin may facilitate the persistence and progression of malignancy. Techniques that have been developed recently have shown that fibrin is indeed a component of the connective tissue stroma in human malignancy but in only a few tumor types. However, therapeutic intervention studies with drugs that limit thrombin activity or enhance fibrinolysis have shown favorable clinical effects in at least one such tumor type. These favorable findings affirm the concept that cause-and-effect relationships do, in fact, exist between thrombin generation with fibrin formation and tumor progression, and suggest that a rational basis exists for the design of future drug intervention trials that target reactions relevant to specific tumor types. These findings also provide a basis for the design of experiments capable of defining further the role of fibrin in the integrity of these tumor types. Because fibrinogen is found much more commonly than fibrin in the connective tissue of a variety of human malignancies, attention might reassumably be directed to determining the possible contribution of this molecule as well as of fibrin to tumor progression.

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“…Several case reports have documented the successful use of heparin to treat cancer [25][26][27][28]. The last [28] documents a case of pancreatic cancer in which a partial response to cytotoxic chemotherapy was converted to complete tumour regression by adding heparin to the chemotherapeutic regimen.…”

Section: Investigations In Humansmentioning

confidence: 99%

The Use of Heparin for Treating Human Malignancies

Ornstein

Zacharski

1999

Pathophysiol Haemos Thromb

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There is a substantial amount of data implicating coagulation mechanisms in the pathogenesis of malignancy. Studies in some experimental animal models have shown that the anticoagulant heparin limits tumour growth and metastasis and prolongs survival. Experience with the effects of heparin on human malignancy is limited primarily to settings in which it was given either to prevent or to treat thrombosis in patients who also had cancer. However, these studies have shown noteworthy apparent improvement in cancer outcome with heparin, especially with low-molecular-weight heparin. There are several possible mechanisms by which heparin could potentially alter the natural history of cancer progression because of its ability to modify the cellular and molecular environment of tumour cells. This experience provides the rationale for definitive clinical trials of heparin in patients with cancer and also for further experimentation to define the mechanisms of antineoplastic activity by this familiar class of drugs.

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Arrest of Growth of Ovarian Tumor by Tranexamic Acid

Cited by 31 publications

References 6 publications

Clinical trials with anticoagulant and antiplatelet therapies

Clinical trials with anticoagulant and antiplatelet therapies

The role of fibrin in tumor metastasis

The Use of Heparin for Treating Human Malignancies

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