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1

Antitumor effect of RGD-4C-GG-D(KLAKLAK)2 peptide in mouse B16(F10) melanoma model

100%

Smolarczyk R., Cichoń T., Graja K., Hucz J., Sochanik A., Szala S.

Acta Biochimica Polonica

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2006

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vol. 53

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issue 4

801-805

EN

Vasculature targeting agents have been tested as cancer therapeutics for the past few years. Such therapy could be accomplished using, for example, bifunctional (two-domain) peptides. RGD-4C-GG-D(KLAKLAK)2, a peptide designed by Ellerby and coworkers (1999) (full sequence: ACDCRGDCFCGGKLAKLAKKLAKLAK), binds selectively to αVβ3 integrin receptors expressed in tumor neovasculature and, after internalization, effectively induces apoptosis of endothelial cells. The aim of this study was to examine if RGD-4C-GG-D(KLAKLAK)2 would efficiently target cells, among them B16(F10), that overexpress αVβ3 receptors, and whether it would be suitable for therapeutic treatment of primary B16(F10) murine melanoma tumors. Thus, the peptide would target two distinct tumor compartments: that formed by endothelium of blood vessels and that made up of neoplastic cells. The therapeutic peptide was recognized and did induce apoptosis in B16(F10) cell line. Tumor growth inhibition was observed following direct intratumoral administration. However, cessation of peptide administration led to rapid tumor growth and death of the animals.

2

Direct and indirect control of cancer populations

88%

Świerniak A.

Bulletin of the Polish Academy of Sciences: Technical Sciences

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2008

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vol. 56

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issue 4

3

Vasostatin increases oxygenation of B16-F10 melanoma tumors and raises therapeutic efficacy of cyclophosphamide

88%

Cichoń T., Jarosz M., Smolarczyk R., Ogórek B., Matuszczak S., Wagner M., Mitrus I., Sochanik A., Jazowiecka-Rakus J., Szala S.

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EN

One of the preconditions of effective anticancer therapy is efficient transfer of the therapeutic agent (chemotherapeutic) to tumor cells. Fundamental barriers making drug delivery and action difficult include underoxygenation, elevated interstitial pressure, poor and abnormal tumor blood vascular network and acidic tumor milieu. In this study we aimed at developing an optimized scheme of administering a combination of an angiogenesis-inhibiting drug (vasostatin) and a chemotherapeutic (cyclophosphamide) in the therapeutic treatment of mice bearing experimental B16-F10 melanoma tumors. We report that the strongest tumor growth inhibition was observed in mice that received two, three or four vasostatin doses in combination with one injection of cyclophosphamide (i.e., V2 + CTX, V3 + CTX or V4 + CTX schemes). Double administration of vasostatin increases oxygenation of B16-F10 tumors. On the other hand, its five-fold administration lowers tumor oxygenation, breaks down tumor vascular network (increasing hypoxia) and leads in consequence to death of cancer cells and appearance of necrotic areas in the tumor. A decreased cyclophosphamide dose in combination with two doses of vasostatin (V2 + CTX scheme) inhibits tumor growth similarly to a larger dose of cyclophosphamide alone.

4

Przeciwciała monoklonalne w regulacji transdukcji sygnału receptora naskórkowego czynnika wzrostu (EGFR) w komórkach nowotworowych

63%

Kampa R. P., Sypniewski D., Bednarek I.

Annales Academiae Medicae Silesiensis

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2018

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issue 72

12-20

EN

In recent years intensive research has been dedicated to the Epidermal Growth Factor Receptor (EGFR) due to its significant role in the pathogenesis of malignant tumors. In many types of cancers intracellular pathways modulated by EGFR have been identified as crucial factors influencing tumor survival and development. On the other hand, EGFR has also been shown to be a promising molecular target for potential therapeutic agents. Attempts to modify the signal transduction exerted by EGF have been made either by blocking the activity of certain elements of the EGFR pathway or by direct inhibition of the EGF receptor itself. It has also been demonstrated that the use of monoclonal antibodies to block the EGF receptor increases the effectiveness of conventional anticancer agents such as cisplatin. Thus, many anticancer therapies based on inhibitors of the selected components of the EGFR signaling pathway have been established, and many of them apply monoclonal antibodies.

PL

Receptor naskórkowego czynnika wzrostu EGFR (Epidermal Growth Factor Receptor), ze względu na jego ważny udział w patogenezie nowotworów złośliwych, jest obiektem intensywnych badań naukowych ostatnich lat. W wielu typach nowotworów wewnątrzkomórkowe szlaki sygnalizacyjne pobudzane przez EGFR mają wręcz kluczowe znaczenie w ich rozwoju. Z drugiej strony wykazano, iż EGFR może stanowić bardzo obiecujący punkt uchwytu dla czynników terapeutycznych. Podjęto próby modyfikacji transdukcji sygnału przekazywanego przez aktywny EGFR wewnątrz komórek poprzez blokowanie aktywności elementów tego szlaku bądź samego receptora. Wykazano też, że blokowanie receptora EGFR przez przeciwciała monoklonalne podwyższa efektywność stosowanych w terapii kon-wencjonalnych czynników przeciwnowotworowych, np. cisplatyny. Dodatkowo opracowano wiele terapii przeciwno-wotworowych opierając się na zastosowaniu inhibitorów wybranych, kluczowych składowych szlaku sygnalizacyj-nego EGFR, z których wiele bazuje na zastosowaniu przeciwciał monoklonalnych.

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Antitumor effect of RGD-4C-GG-D(KLAKLAK)2 peptide in mouse B16(F10) melanoma model

Direct and indirect control of cancer populations

Vasostatin increases oxygenation of B16-F10 melanoma tumors and raises therapeutic efficacy of cyclophosphamide

Przeciwciała monoklonalne w regulacji transdukcji sygnału receptora naskórkowego czynnika wzrostu (EGFR) w komórkach nowotworowych