Interleukin-6 and new strategies for the treatment of cancer, hyperproliferative diseases and paraneoplastic syndromes

Barton, Beverly E.

doi:10.1517/14728222.9.4.737

Cited by 63 publications

(37 citation statements)

References 132 publications

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“…These conflicting data might be a result of subject selection. In patients with chronic inflammation, the pathophysiology of low BMD is related in part to increased bone resorption resulting from the action of inflammatory cytokines such as TNF-a and IL-6 [28][29][30][31][32][33][34][35]. Inflammatory cytokines are similarly elevated in patients with SCD and could play a part in the pathophysiology of low BMD [21][22][23].…”

Section: Discussionmentioning

confidence: 99%

Sickle cell bone disease: Response to vitamin D and calcium

Adewoye

Chen

et al. 2007

American J Hematol

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Bone disease with osteoporosis and osteomalacia are common in sickle cell disease (SCD). Some patients have vitamin D deficiency and low bone mineral density (BMD). The role of vitamin D and calcium supplementation to restore bone health in SCD has not been well studied. In 14 adults with SCD, we measured 25(OH)D (25-hydroxyvitamin D) and BMD at the femoral neck, lumbar spine, and distal third of the ulna plus radius, along with markers of bone resorption (CTx; C-terminal component of pro-collagen type I) and bone formation (osteocalcin) before and after 12 months of vitamin D 2 and calcium carbonate treatment. Pretreatment, all patients were vitamin D deficient with a mean 25(OH)D level of 10.7 ± 4.7 ng/ml, had low BMD at the lumbar spine (L-spine), 0.87 ± 0.11 g/cm 2 (mean Z-score of -2.6 3 ± 0.71 SD and T score of -2.31 ± 0.75 SD), femoral neck, 0.8 ± 0.18 g/cm 2 (mean Z-score -1.36 ± 0.84, T-score -1.14 ± 0.75), and the distal radius and ulna, 0.6 ± 0.17 g/cm 2 (mean Z-score -1.18 ± 0.79, T-score -1.01 ± 0.74) and had elevated CTx (0.87 ± 0.5 ng/ml) and osteocalcin levels (12.3 ± 3.7 ng/ll). After treatment, all patients corrected their 25(OH)D level (38.8 ± 13.9 ng/ml) (P < 0.001) with a 3.6% ± 3.9% increase in BMD at the L-spine (P 5 0.009), 4.6% ± 8.5% increase at the femoral neck (P 5 0.05) and 6.5% ± 12.6% increase at the distal radius plus ulna (P 5 0.09). CTx, osteocalcin, and PTH(i) levels were unchanged. Treatment of adult SCD with vitamin D and calcium can restore 25(OH)D levels to normal and improve BMD, but, markers of bone resorption remained unchanged. Screening for vitamin D deficiency and BMD in SCD patients seems warranted. Am. J. Hematol. 83:271-274, 2008. V

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Section: Discussionmentioning

confidence: 99%

Sickle cell bone disease: Response to vitamin D and calcium

Adewoye

Chen

et al. 2007

American J Hematol

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“…These include therapeutic strategies intended to inhibit the production, expression, or action of cytokines, NO and polyamines, which would be very beneficial in the treatment of cancer and in the amelioration of cachexia. 40 …”

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confidence: 99%

Production of cachexia mediators by Walker 256 cells from ascitic tumors

Rebeca

Bracht

Noleto

et al. 2008

Cell Biochemistry & Function

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In neoplasic cachexia, chemical mediators seem to act as initiators or perpetuators of this process. Walker 256 cells, whose metabolic properties have so far been little studied with respect to cancer cachexia, are used as a model for the study of this syndrome. The main objective of this research was to pinpoint the substances secreted by these cells that may contribute to the progression of the cachectic state. Since inflammatory mediators seem to be involved in the manifestation of this syndrome, the in vitro production of nitric oxide (NO), cytokines (tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6)), and prostaglandin E2 (PGE2) was evaluated in Walker 256 cells isolated from ascitic tumors. After 4 or 5 h, a significant increase in NO production was observed (2.55 +/- 1.56 and 4.05 +/- 1.99 nmol NO per 10(7) cells, respectively). When isolated from a 6-day-old tumor, a significantly lower production of IL-6 and higher production of TNF-alpha than in cells from a 4-day-old tumor were observed, indicating a relationship between the production of cytokines and the time of tumor development after implantation. Considerable production of PGE(2) by Walker 256 cells isolated from the 6-day-old tumor was also observed. Polyamines were also determined in Walker 256 cells. Levels of putrescine, spermidine, and spermine did not show significant differences in tumors developed during 4 or 6 days. Direct evidence of the release of proinflammatory cytokines and PGE2 by Walker 256 cells suggests that these mediators can drive the cachectic syndrome in the host, the effect being dependent on tumor development time.

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“…IL-6 is found to be involved in the growth of many solid tumours like prostate cancer and renal cancer. Pathogenesis of Kaposi sarcoma has been proven to be due to the secretion of IL-6 [22][23][24]. IL-6 is also involved in the growth of many haematological malignancies.…”

Section: Interleukin -6mentioning

confidence: 99%