Dacarbazine, cisplatin and carmustine, with or without tamoxifen, for metastatic melanoma: 5-year follow-up

Lattanzi, S C; Tosteson, Tor D.; Chertoff, Jocelyn D.; Maurer, L. Herbert; O’Donnell, Jacqueline; LeMarbre, Paul J.; Mott, Leila A.; Delprete, Stefano; Forcier, R. Jackson; Ernstoff, Marc S.

doi:10.1097/00008390-199510000-00010

Cited by 58 publications

(35 citation statements)

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“…Metastatic melanomas are typically resistant to chemotherapy (1), with response rates of 15 -20% achieved with dacarbazine, the best single agent, and reported response rates ranging from 15 to 43% with combination dacarbazine, cisplatin, carmustine, and tamoxifen, but with no survival benefit (2)(3)(4). It has been suggested that the underlying resistance of metastatic melanomas to radiation and chemotherapy may be due at least in part to over-expression of apoptosis inhibitory proteins (1).…”

Section: Introductionmentioning

confidence: 99%

RelA, p50 and Inhibitor of kappa B alpha are Elevated in Human Metastatic Melanoma Cells and Respond Aberrantly to Ultraviolet Light B

McNulty

Tohidian

Meyskens

2001

Pigment Cell Research

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melanocytes. We also found that melanoma cells expressed Metastatic melanomas are typically resistant to radiation and chemotherapy. The underlying basis for this phenomenon may higher cytoplasmic levels of RelA, p105/p50 and the inhibitory protein, inhibitor of kappa B alpha (IkBa) than melanocytes. result in part from defects in apoptotic pathways. Nuclear factor kappa B (NFkB) has been shown to control apoptosis in To directly test whether RelA expression has an impact on melanoma cell survival, we used antisense RelA phosphorothmany cell types and normally functions as an immediate stress ioate oligonucleotides and found that melanoma cell viability response mechanism that is rigorously controlled by multiple inhibitory complexes. We have previously shown that NFkB was significantly decreased compared with untreated or conbinding is elevated in metastatic melanoma cells relative to trol cultures. The constitutive activation of NFkB in metastatic melanoma cell cultures may, therefore, support an normal melanocytes. In the current study, Western blot analysis showed that, compared with normal melanocytes, inappropriate cell survival pathway that can be therapeutically manipulated. melanoma cell lines have higher nuclear levels of the NFkB subunits p50 (7-fold) and RelA (5-10-fold). In response to Key words: Melanocyte, Melanoma, NFkB, Antisense, TNF, tumor necrosis factor-alpha (TNFa), both melanocytes and UVB melanoma cells showed increased nuclear p50 and RelA levels, but levels in melanoma cells remained higher than in Nuclear factor kappa B (NFkB) activation has been shown to have both pro-and anti-apoptotic functions in various cell types (5, 6). There are five mammalian NFkB/ Rel family members, p50, p52, RelA, RelB, and cRel, that share a highly conserved 300-amino acid Rel homology domain containing dimerization, nuclear localization, and DNA binding regions (5 -8). These proteins can form homoand heterodimers, which bind DNA at NFkB sequences found in the promoters of a variety of genes and specific dimer pairs elicit differential induction of these genes (5,8,9). Several studies have suggested that NFkB transcription

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Section: Introductionmentioning

confidence: 99%

RelA, p50 and Inhibitor of kappa B alpha are Elevated in Human Metastatic Melanoma Cells and Respond Aberrantly to Ultraviolet Light B

McNulty

Tohidian

Meyskens

2001

Pigment Cell Research

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“…17 Chemotherapeutic agents in various combination have been used in the treatment of stage IV patients. In phase II trials, 29,31 two of the most effective combinations (produced response rates ranging from 30 to 50%) were the three-drug combination of cisplatin/vinblastine/dacarbazine (CVD) and the four-drug combination(Dartmouth combination) of cisplatin/dacarbazine/carmustine and tamoxifen (CDBT). Although in randomized phase III trials showed no differences in either response duration or survival.…”

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confidence: 99%

Malignant mucosal melanoma of the head and neck — a review

Lengyel

Gilde

Remenár

et al. 2003

Pathol. Oncol. Res.

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“…The two most active combinations are the four-drug combination of cisplatin, DTIC, carmustine (BCNU), and tamoxifen (the Dartmouth regimen) and cisplatin, vinblastine, and DTIC (the CVD regimen). The Dartmouth regimen was initially evaluated in 42 patients and demonstrated a response rate of 54% and overall survival of 412 days (Lattanzi et al 1995). The Darthmouth regimen was then evaluated against DTIC in a large (n=240) phase III randomized trial (Chapman et al 1999).…”

Section: Single Agent Vs Combination Chemotherapymentioning

confidence: 99%