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Identification of breast cancer tumor associated antigens

ABSTRACT: Four prototypic situations, corresponding to progressive stages of mammary carcinogenesis, were analyzed. Total RNA from whole-mount for 10, 15, 19 and 22 weeks old BALB-neuT animals was extracted. Differential expression between the various prototypic conditions indicates the presence of changing in level of mRNAs due to the increment in the tumor mass (Astolfi et al. Cancer Immunol Immunother 2005, 54:599-610). Since the same amount of RNA is hybridized on all arrays the change in composition of mRNA species associated to the increment of the tumor cellular population allows the tagging as “putative tumor associated antigens” (Cavallo et al. BMC Bioinformatics 2005 6(Suppl 4):S7) for all transcripts progressively up-modulated as the age of the animals increases. Keywords: Disease state analysis

ORGANISM(S): Mus musculus

PROVIDER: GSE7395 | GEO | 2007/04/19

SECONDARY ACCESSION(S): PRJNA97883

REPOSITORIES: GEO

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Project description:Toll like receptor 4 (TLR4), an innate immunity gene, is involved in responses to several pulmonary agonists including endotoxin (LPS; Poltorak et al.,1998), ozone (O3 ,Kleeberger et. al., 2001), Pseudomonas aeruginosa (Faure et al, 2004), and hyperoxia (Zhang et al, 2005). TLR4 appears to partially mediate the response to LPS- and O3-induced lung injury, however, TLR4 is protective for prevention of injury in Pseudomonas aeruginosa infection and against acute lung injury (hyperoxia). The mechanism behind this protection is unclear. We previously demonstrated that TLR4 was also protective against BHT-induced chronic inflammation and tumor promotion (Bauer et al, 2005). C.C3H-Tlr4Lps-d (BALBLps-d) mice, congenic for a 10 cM region of C3H/HeJ chromosome 4 that contains Tlr4 (Vogel et al, 1994), have a missence mutation that renders TLR4 dysfunctional. The Tlr4 mutation likely abrogates signaling by disrupting a direct point of contact with other signaling molecules (Akira S, Takeda K. Toll-like receptor signalling. Nat Rev Immunol 2004;4(7):499-511.). Bronchoalveolar lavage fluid (BALF) alveolar macrophages, lymphocytes, and total protein content were significantly elevated in BALBLps-d mice compared to BALB/c (BALB; Tlr4 sufficient) mice following chronic BHT (Bauer et al., 2005). BALBLps-d mice also had a significant increase in tumor multiplicity (60%) over that of BALB mice in response to an MCA/BHT tumor promotion protocol. While this was the first model to demonstrate a protective role for TLR4 in chronic lung inflammation and tumorigenesis, the downstream mechanism regulating this protective response remains unknown. Using Affymetrix microarray analysis followed by GeneSpring and Ingenuity pathway analyses, we herein identified known and novel downstream pathways and their interactions that may be involved in the protective mechanism elicited by TLR4. We therefore hypothesize that these pathways and interactions amongst the genes identified during the tumor promotion/chronic inflammation stage are in part influencing the differential strain response observed during tumorigenesis. Keywords: time course, tumor study

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Identification of breast cancer tumor associated antigens

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