melanoma/proline

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Cytotoxic T cell recognition of a human melanoma derived peptide with a carboxyl-terminal alanine-proline sequence.

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Recently, we defined the antigenic epitope recognized by the human monoclonal antibody L94 to be a protein with a C-terminal sequence of alanine-proline (AP). An antigenic peptide no. 707 (RVAALARDAP), which was identified by the use of cDNA libraries of an antigen positive melanoma cell line M14,

Proline substitution independently enhances H-2D(b) complex stabilization and TCR recognition of melanoma-associated peptides.

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The immunogenicity of H-2D(b) (D(b)) restricted epitopes can be significantly increased by substituting peptide position 3 to a proline (p3P). The p3P modification enhances MHC stability without altering the conformation of the modified epitope allowing for T-cell cross-reactivity with the native

Cell-mediated cytotoxicity for melanoma tumor cells: detection by a (3H) proline release assay.

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An in vitro lymphocyte-mediated cytotoxicity assay using [3H]proline-labeled target cells is described. The assay, modified from an original procedure of Bean et al., assesses the release of [3-H]proline by filtering the total culture fluid containing both trypsinized tumor cells and effector cells.

Proline prodrug of melphalan, prophalan-L, demonstrates high therapeutic index in a murine melanoma model.

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The therapeutic efficacy of prophalan-L, the L-proline prodrug of melphalan that demonstrated prolidase-dependent bioactivation to melphalan, was examined in vivo in a mouse melanoma model. Prophalan-L exhibited 2- to 2.5-fold higher hydrolytic and cytotoxic activity than prophalan-D, the D-analog,

Prolidase, a potential enzyme target for melanoma: design of proline-containing dipeptide-like prodrugs.

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Bioinformatics tools such as Perl, Visual Basic, Cluster, and TreeView were used to analyze public gene expression databases in order to identify potential enzyme targets for prodrug strategies. The analyses indicated that prolidase might be a desirable enzyme target based on its differential

In vivo and in vitro antitumor effect of ascorbic acid, lysine, proline and green tea extract on human melanoma cell line A2058.

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BACKGROUND Melanoma, a very serious form of skin cancer, causes the most skin cancer-related deaths, due to metastasis. Structural changes in the extracellular matrix (ECM) are necessary for cell migration during tissue remodeling. MMPs, VEGF, Ki-67 (proliferative protein) and constituents of ECM

Disruption of Proline Synthesis in Melanoma Inhibits Protein Production Mediated by the GCN2 Pathway.

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Many processes are deregulated in melanoma cells and one of those is protein production. Although much is known about protein synthesis in cancer cells, effective ways of therapeutically targeting this process remain an understudied area of research. A process that is upregulated in melanoma

Proline prodrug of melphalan targeted to prolidase, a prodrug activating enzyme overexpressed in melanoma.

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OBJECTIVE To determine the bioactivation and uptake of prolidase-targeted proline prodrugs of melphalan in six cancer cell lines with variable prolidase expression and to evaluate prolidase-dependence of prodrug cytotoxicity in the cell lines compared to that of the parent drug,

Functional specialization in proline biosynthesis of melanoma.

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Proline metabolism is linked to hyperprolinemia, schizophrenia, cutis laxa, and cancer. In the latter case, tumor cells tend to rely on proline biosynthesis rather than salvage. Proline is synthesized from either glutamate or ornithine; both are converted to pyrroline-5-carboxylate (P5C), and then

First detection of the melanoma-predisposing proline-48-threonine mutation of p16 in Hungarians: was there a common founder either in Italy or in Hungary?

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The P48T germ line mutation of p16 was detected in a Hungarian multiple primary melanoma patient (deceased at the age of 39) with no affected family members. Genetic analysis of the patient and his family revealed that the patient was homozygous for the mutation, whereas his parents (father

Inhibition of pulmonary metastasis of melanoma b16fo cells in C57BL/6 mice by a nutrient mixture consisting of ascorbic Acid, lysine, proline, arginine, and green tea extract.

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The authors investigated the effect of a nutrient mixture (NM) on lung metastasis by B16F0 melanoma cells in C57BL/6 female mice. Mice were divided into equal groups (1 to 6) and injected via tail vein with B16F0 cells (groups 1 to 4), B16FO cells pretreated with NM (group 5), or saline (group 6).

Splicing factor proline/glutamine-rich is a novel autoantigen of dermatomyositis and associated with anti-melanoma differentiation-associated gene 5 antibody.

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Anti-MDA5 antibody positive dermatomyositis (DM) and clinically amyopathic DM (CADM) often develop into rapidly progressive interstitial lung disease, but their pathogenesis remains unclear. We observed that sera from DM/CADM patients immunoprecipitated a common 110 kDa polypeptide. We investigated

Proline-rich Akt substrate of 40kDa (PRAS40): a novel downstream target of PI3k/Akt signaling pathway.

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Modifications in signaling of the proline-rich Akt substrate of 40-kDa (PRAS40) pathway is implicated in type 2 diabetes and melanoma. PRAS40 is known for its ability to regulate the mammalian target of rapamycin complex 1 (mTORC1) kinase activity, possessing a key regulatory role at the cross point

Selective degradation of basement membrane macromolecules by metastatic melanoma cells.

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The extracellular matrix deposited in culture by the mouse endodermal cell line (PF HR9) was used as an experimental model to study the interactions between basement membranes and several tumorigenic and nontumorigenic cell lines, including the metastatic B16 melanoma cell sublines. Analysis by

Salubrinal in Combination With 4E1RCat Synergistically Impairs Melanoma Development by Disrupting the Protein Synthetic Machinery

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Increased protein synthesis is a key process in melanoma, which is regulated by the ALDH18A1 gene encoding pyrroline-5-carboxylate synthase (P5CS). P5CS is involved in proline biosynthesis and targeting ALDH18A1 has previously been shown to inhibit melanoma development by decreasing intracellular

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