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The effect of altered Toll-like receptor 4 signaling on cancer cachexia.

Publication ,  Conference
Cannon, TY; Guttridge, D; Dahlman, J; George, JR; Lai, V; Shores, C; Buzková, P; Couch, ME
Published in: Arch Otolaryngol Head Neck Surg
December 2007

OBJECTIVE: To determine whether mice unable to mount an intact inflammatory response because of a Toll-like receptor (TLR) pathway defect will develop less severe cancer cachexia. DESIGN: Prospective animal study. SETTING: Academic research center. SUBJECTS: Six- to eight-week-old, female C3H/HeJ mice (17-18 g) and age-, weight-, and sex-matched wild-type C3H/HeN mice, differing in that the HeJ mice have nonfunctional TLR4 due to a TLR4 double mutation (TLR4(d/d)). INTERVENTION: The mice were inoculated with equal numbers of SCCF-VII cells and housed in individual cages. MAIN OUTCOME MEASURES: Food intake, body weight, pretumor and posttumor body composition, circulating cytokines, and levels of a marker of muscle atrophy were analyzed. RESULTS: The wild-type HeN mice weighed less on average than the TLR4(d/d) mice (2.6 g vs 4.9 g) (P = .01). They consumed more food, had smaller tumors, and had less lean body mass and fat mass than the TLR4(d/d) mice. Interleukin 1beta level was significantly elevated in the tumor-bearing HeN mice (mean gain of 259 pg/mL) but not in the TLR4(d/d) mice (P = .03). Both mouse strains had evidence of muscle atrophy. CONCLUSIONS: In spite of increased food intake and smaller tumors, the wild-type HeN mice had more severe cachexia than the TLR4(d/d) mice. The impaired ability to secrete proinflammatory cytokines such as interleukin 1beta may protect these animals from developing severe cancer cachexia. This animal model represents a novel system in which the host contributions to cachexia may be further studied.

Duke Scholars

Published In

Arch Otolaryngol Head Neck Surg

DOI

ISSN

0886-4470

Publication Date

December 2007

Volume

133

Issue

12

Start / End Page

1263 / 1269

Location

United States

Related Subject Headings

  • Tumor Cells, Cultured
  • Toll-Like Receptor 4
  • Signal Transduction
  • Prospective Studies
  • Otorhinolaryngology
  • Mice, Inbred C3H
  • Mice
  • Head and Neck Neoplasms
  • Female
  • Disease Progression
 

Citation

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Cannon, T. Y., Guttridge, D., Dahlman, J., George, J. R., Lai, V., Shores, C., … Couch, M. E. (2007). The effect of altered Toll-like receptor 4 signaling on cancer cachexia. In Arch Otolaryngol Head Neck Surg (Vol. 133, pp. 1263–1269). United States. https://doi.org/10.1001/archotol.133.12.1263
Cannon, Trinitia Y., Denis Guttridge, Jason Dahlman, Jonathan R. George, Victor Lai, Carol Shores, Petra Buzková, and Marion E. Couch. “The effect of altered Toll-like receptor 4 signaling on cancer cachexia.” In Arch Otolaryngol Head Neck Surg, 133:1263–69, 2007. https://doi.org/10.1001/archotol.133.12.1263.
Cannon TY, Guttridge D, Dahlman J, George JR, Lai V, Shores C, et al. The effect of altered Toll-like receptor 4 signaling on cancer cachexia. In: Arch Otolaryngol Head Neck Surg. 2007. p. 1263–9.
Cannon, Trinitia Y., et al. “The effect of altered Toll-like receptor 4 signaling on cancer cachexia.Arch Otolaryngol Head Neck Surg, vol. 133, no. 12, 2007, pp. 1263–69. Pubmed, doi:10.1001/archotol.133.12.1263.
Cannon TY, Guttridge D, Dahlman J, George JR, Lai V, Shores C, Buzková P, Couch ME. The effect of altered Toll-like receptor 4 signaling on cancer cachexia. Arch Otolaryngol Head Neck Surg. 2007. p. 1263–1269.

Published In

Arch Otolaryngol Head Neck Surg

DOI

ISSN

0886-4470

Publication Date

December 2007

Volume

133

Issue

12

Start / End Page

1263 / 1269

Location

United States

Related Subject Headings

  • Tumor Cells, Cultured
  • Toll-Like Receptor 4
  • Signal Transduction
  • Prospective Studies
  • Otorhinolaryngology
  • Mice, Inbred C3H
  • Mice
  • Head and Neck Neoplasms
  • Female
  • Disease Progression