Thalidomide

Franks, Michael; MacPherson, Gordon; Figg, William D.

doi:10.1016/s0140-6736(04)16308-3

Cited by 579 publications

(536 citation statements)

References 144 publications

(158 reference statements)

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“…During these years, in which thalidomide became the most popular sedative in Germany, about 10 000 children with phocomelia and other malformations were born [29] . It was only in 1994 that thalidomide was found to inhibit VEGF-and basic fibroblast growth factor-mediated angiogenesis; a detection that resulted from a side-effect-based literature screening in search of drugs with antiangiogenic activity that D'Amato and Folkman presumed should cause both amenorrhea and fetal malformations [30] .…”

Section: Thalidomide-the First Antiangiogenic Drugmentioning

confidence: 99%

“…In experimental models, the antiangiogenic activity of various thalidomide metabolites correlates with teratogenicity [30][31][32] , indicating that antiangiogenic effects are also mainly responsible for thalidomide-related birth defects in humans. The antiangiogenic potential of thalidomide is currently being evaluated for treatment of several malignant diseases [29] . Due to promising results in patients with therapyrefractory multiple myeloma, thalidomide is now evaluated as both first-line myeloma therapy and in combination with hematopoietic-cell transplantation [33,34] .…”

Section: Thalidomide-the First Antiangiogenic Drugmentioning

confidence: 99%

“…Thalidomide is a potent sedative, causes severe birth defects and can also induce sensible peripheral neuropathy, especially at higher cumulative doses [39] , therefore, it may not turn out to be the drug for treatment of vascular malformations hoped for by clinicians. Furthermore, in addition to its antiangiogenic activity, thalidomide exerts immunomodulating effects [29] . It is possible that other newly developed antiangiogenics will show more specific inhibition of VEGF or other steps within the angiogenic cascade, with possibly fewer side effects.…”

Section: Thalidomide-the First Antiangiogenic Drugmentioning

confidence: 99%

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Angiogenesis and vascular malformations: Antiangiogenic drugs for treatment of gastrointestinal bleeding

Juergen¹,

Bauditz²,

Herbert³

et al. 2007

WJG

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Treatment of gastrointestinal bleeding in patients with angiodysplasias and Osler's disease (hereditary hemorrhagic telangiectasia) is clinically challenging. Frequently, vascular malformations occur as multiple disseminated lesions, making local treatment an unfavorable choice or impossible. After local therapy, lesions often recur at other sites of the intestine. However, as there are few therapeutic alternatives, repeated endoscopic coagulations or surgical resections are still performed to prevent recurrent bleeding. Hormonal therapy has been employed for more than 50 years but has recently been shown to be ineffective. Therefore, new therapeutic strategies are required. Understanding of the pathophysiology of angiogenesis and vascular malformations has recently substantially increased. Currently, multiple inhibitors of angiogenesis are under development for treatment of malignant diseases. Experimental and clinical data suggest that antiangiogenic substances, which were originally developed for treatment of malignant diseases, may also represent long-awaited specific drugs for the treatment of vascular malformations. However, antiangiogenics display significantly different actions and side-effects. Although antiangiogenics like thalidomide seem to inhibit gastrointestinal bleeding, other substances like bevacizumab can cause mucosal bleeding. Therefore differential and cautious evaluation of this therapeutic strategy is necessary.

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Section: Thalidomide-the First Antiangiogenic Drugmentioning

confidence: 99%

Section: Thalidomide-the First Antiangiogenic Drugmentioning

confidence: 99%

Section: Thalidomide-the First Antiangiogenic Drugmentioning

confidence: 99%

See 1 more Smart Citation

Angiogenesis and vascular malformations: Antiangiogenic drugs for treatment of gastrointestinal bleeding

Juergen¹,

Bauditz²,

Herbert³

et al. 2007

WJG

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“…10 Approximately 40% patients with relapsed myeloma show a response, 11 and the drug is being investigated in other malignancies such as lung, renal, colon and breast cancer. Recently, Strupp et al 8 reported two patients with advanced, heavily treated AITL who had short-term good responses to thalidomide in combination with dexamethasone.…”

Section: Pathological Featuresmentioning

confidence: 99%

Pathology and clinical features of angioimmunoblastic T-cell lymphoma after successful treatment with thalidomide

Doğan

Ngu

et al. 2005

Leukemia

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“…Despite the very high risk of teratogenicity, thalidomide is emerging as a treatment for cancer and inflammatory diseases (1). Thalidomide is considered to be an effective drug for treating refractory multiple myeloma due to its antiangiogenic and immunomodulatory activities (2).…”

Section: Introductionmentioning

confidence: 99%

The G-rich promoter and G-rich coding sequence of basic fibroblast growth factor are the targets of thalidomide in glioma

Mei¹,

Wu²

2008

Molecular Cancer Therapeutics

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Thalidomide is considered to be a potent antiangiogenic and immunomodulatory drug for cancer therapy. Earlier clinical studies have found that patients responding to this drug often had high plasma levels of basic fibroblast growth factor (bFGF). This cytokine is a proangiogenic factor overexpressed in many tumors and is also a regulator of limb development; hence, it might be a target of thalidomide. Using U-87 MG cell lines, we found that thalidomide, especially when encapsulated in a liposome, down-regulated the transcription and translation of the FGF-2 gene by interacting with G-rich regions present in the promoter and the internal ribosome entry site of its transcript at concentrations much lower than therapeutic serum concentrations. Thalidomide treatment also dramatically suppressed the anchorage-independent growth of U-87 MG and other glioma cells by over a thousand fold without affecting its anchorage-dependent growth, which may be accomplished by knocking down endogenous bFGF expression in these cells. Accordingly, the addition of recombinant bFGF partially restored the anchorageindependent growth of these cells. Our data suggest that by targeting the G-rich regions of bFGF, thalidomide (at 0.1 Mg/mL) can reduce cellular bFGF levels and affect tumor anchorage-independent growth, the hallmark of tumorigenicity. Our results are promising for future clinical investigations using low doses of thalidomide.

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Thalidomide

Cited by 579 publications

References 144 publications

Angiogenesis and vascular malformations: Antiangiogenic drugs for treatment of gastrointestinal bleeding

Angiogenesis and vascular malformations: Antiangiogenic drugs for treatment of gastrointestinal bleeding

Pathology and clinical features of angioimmunoblastic T-cell lymphoma after successful treatment with thalidomide

The G-rich promoter and G-rich coding sequence of basic fibroblast growth factor are the targets of thalidomide in glioma

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