Retroviral gene transfer of interferon‐inducible protein 10 inhibits growth of human melanoma xenografts

Feldman, Andrew L.; Friedl, Josef; Lans, Titia E.; Libutti, Steven K.; Lorang, Dominique; Miller, Misha D.; Turner, Ewa M.; Hewitt, Stephen M.; Alexander, H. Richard

doi:10.1002/ijc.10292

Cited by 80 publications

(52 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has been reported that the intratumor injection of CXCL10 proteins or CXCL10-transduced cells led to reduced tumor growth and the potent inhibition of angiogenesis in a mouse models of lung cancer or melanoma (22,24). We also found that the intratumoral administration of CXCL10 have recruited apparent mononuclear cells and profoundly inhibited angiogenesis, compared with systemic administration of CXCL10 (data not shown).…”

Section: Discussionsupporting

confidence: 51%

Improved Therapeutic Effectiveness by Combining Recombinant CXC Chemokine Ligand 10 with Cisplatin in Solid Tumors

Tian

Hou

et al. 2005

Clinical Cancer Research

View full text Add to dashboard Cite

Purpose: CXC chemokine ligand 10 (CXCL10) is a potent inhibitor of angiogenesis.We wonder whether the combination of CXCL10 with cisplatin would improve the therapeutic antitumor efficacy. Experiment Design: We evaluated the antitumor activity of the combination therapy in the immunocompetent C57BL/6 and BALB/c mice bearing LL/2 Lewis lung cancer and CT26 colon adenocarcinoma , respectively. Mice were treated with either CXCL10 s.c. at 25 Mg per kg per day once daily for 30 days, cisplatin cycled twice (5 mg/kg i.p. on days 14 and 21 after the initiation of CXCL10), or both agents together. Tumor volume and survival time were observed. Antiangiogenesis of CXCL10 in vivo were determined by alginate capsule models and CD31 immunohistochemistry. Histologic analysis and assessment of apoptotic cells were also conducted in tumor tissues. Results: CXCL10 + cisplatin reduced tumor growth in LL/2 and CT26 tumor model, respectively, more effectively, although cisplatin or CXCL10 individually resulted in suppression of tumor growth and improved survival time of tumor-bearing mice. CXCL10 successfully inhibited angiogenesis as assessed by alginate model and CD31 (P < 0.05). Histologic analysis of tumors exhibited that CXCL10 in combination with cisplatin led to the increased rate of apoptosis, tumor necrosis, and elevated lymphocyte infiltration. Conclusions: Our data suggest that the combination of CXCL10, a well-tolerated angiogenesis inhibitor, with cisplatin can enhance the antitumor activity. The present findings may be of importance to the further exploration of the potential application of this combined approach in the treatment of lung and colon carcinoma.

show abstract

Section: Discussionsupporting

confidence: 51%

Improved Therapeutic Effectiveness by Combining Recombinant CXC Chemokine Ligand 10 with Cisplatin in Solid Tumors

Tian

Hou

et al. 2005

Clinical Cancer Research

View full text Add to dashboard Cite

show abstract

“…21 Several candidate genes, such as Thrombospondin-1, 22 Interleukin (IL)-12, 23 CXC chemokines platelet factor-4 (PF4), 24 Interferon-inducible protein-10 (IP-10), have been tested in preclincal trails. 25 MIG, monokine induced by IFN-g, belongs to the CXC chemokine subfamily. The absence of the ELR motif in MIG is the source of its potent angiostatic and antineoplasm properties in mouse tumor models.…”

Section: Discussionmentioning

confidence: 99%

Combination of MIG (CXCL9) chemokine gene therapy with low-dose cisplatin improves therapeutic efficacy against murine carcinoma

Zhang

Tian

et al. 2006

Gene Ther

View full text Add to dashboard Cite

MIG (monokine induced by interferon-g) is a CXC chemokine ligand (CXCL9) that can potently inhibit angiogenesis, and displays thymus-dependent antitumor effects. The effectiveness of a treatment combining gene therapy with plasmid-borne MIG (pORF-MIG) and low-dose cisplatin chemotherapy was determined using colon carcinoma (CT26) and Lewis lung carcinoma (LL/2c) murine models. The program was carried out via intramuscular delivery of pORF-MIG at 100 mg/mouse twice a week for 4 weeks, and/or intraperitoneal delivery of cisplatin at 0.6 mg/kg/ mouse every 3 days for 48 days. Tumor volume and survival time were evaluated after treatment. CD31 immunohistochemical staining in tumor tissues and alginate capsule models in vivo was used to evaluate angiogenesis. Induction of apoptosis and cytotoxic T-lymphocyte (CTL) activity were also assessed. The combination of pORF-MIG and low-dose cisplatin produced significant antitumor activity, with complete tumor regression in 4/10 of CT26 colon carcinomas and 3/10 of LL/2c lung carcinomas, low vascularity, in alginate capsules, apparently degraded tumor microvessel density, and increased induction of apoptotic and CTL activities compared with either treatment alone. This study suggests that the combination of pORF-MIG plus cisplatin augments the inhibition of angiogenesis and the induction of apoptosis or CTL activity, all of which enhance antitumor activity. These findings may prove useful in further explorations of the application of combinatorial approaches to the treatment of solid tumors.

show abstract

“…Interferon-g-inducible protein 10 is expressed in some diseases in association with VEGF. It is reported that VEGF may also play a major role to augment the expression of IP-10 in T cells (Feldman et al, 2002). Interferon-g-inducible protein 10 also inhibits the proliferation of vascular ECs via IP-10 receptor CXCR3 expressed in ECs (Lasagni et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

“…Vascular endothelial growth factor augments the effect of IFN-g on the induction of IP-10 mRNA and protein expression in ECs, and Chinese hamster ovary cells designed to secrete VEGF were injected subcutaneously into the skin of nude mice and found to mediate a time-dependent increase in IP-10 mRNA (Feldman et al, 2002). Therefore, angiogenic factors specific to IP-10 might be IL-8, bFGF and VEGF.…”

Section: Ip-10mentioning

confidence: 99%

See 1 more Smart Citation

Expression of IP-10 related to angiogenesis in uterine cervical cancers

et al. 2007

View full text Add to dashboard Cite

Angiogenesis is essential for development, growth and advancement of solid tumours. Interferon-g-inducible protein 10 (IP-10) regulates lymphocyte chemotaxis, mediates vascular pericyte proliferation and acts as an angiostatic agent, thus inhibiting tumour growth. This prompted us to study the clinical implications of IP-10 expression related to angiogenesis in uterine cervical cancers. The levels of IP-10 decreased with advancement, and the prognosis of the 30 patients with low IP-10 expression in uterine cervical cancers was poor (66%), whereas the 24-month survival rate of the other patients with high IP-10 expression was 90%. Furthermore, IP-10 levels significantly reverse-correlated with vascular endothelial growth factor (VEGF) levels in uterine cervical cancers. Interferon-g-inducible protein 10 might work on suppression of angiogenesis associated with VEGF in advancement, and can be recognised as a prognostic indicator. Furthermore, IP-10 activation might be effective on the suppression of regrowth or recurrence after intensive treatment for advanced cervical cancers.

show abstract

Retroviral gene transfer of interferon‐inducible protein 10 inhibits growth of human melanoma xenografts

Cited by 80 publications

References 19 publications

Improved Therapeutic Effectiveness by Combining Recombinant CXC Chemokine Ligand 10 with Cisplatin in Solid Tumors

Improved Therapeutic Effectiveness by Combining Recombinant CXC Chemokine Ligand 10 with Cisplatin in Solid Tumors

Combination of MIG (CXCL9) chemokine gene therapy with low-dose cisplatin improves therapeutic efficacy against murine carcinoma

Expression of IP-10 related to angiogenesis in uterine cervical cancers

Contact Info

Product

Resources

About