. Author manuscript; available in PMC: 2024 Sep 2.

Published in final edited form as: Toxicol Pathol. 2023 Apr 3;51(1-2):39–55. doi: 10.1177/01926233231157322

Table 5.

Most significantly altered canonical molecular pathways in alveolar/bronchiolar carcinomas (ABCs) due to chronic AT-exposure in B6C3F1/N mice as determined by Ingenuity Pathway Analysis (IPA).

Canonical Pathways	log(p-value)	Ratio^*


Cell Cycle Control of Chromosomal Replication	3.52	26/37 (0.703)
Ovarian Cancer Signaling	3.13	77/141 (0.546)
Pancreatic Adenocarcinoma Signaling	2.97	64/115 (0.557)
Ephrin Receptor Signaling	2.86	90/171 (0.526)
Phospholipase C Signaling	2.79	110/215 (0.512)
Signaling by Rho Family GTPases	2.58	118/235 (0.502)
Mouse Embryonic Stem Cell Pluripotency	2.51	57/104 (0.548)
Paxillin Signaling	2.27	57/106 (0.538)
Mismatch Repair in Eukaryotes	2.20	12/16 (0.750)
Purine Nucleotides De Novo Biosynthesis II	2.14	9/11 (0.818)
Adipogenesis pathway	2.08	65/125 (0.520)
ILK Signaling	2.06	91/182 (0.500)
Glioma Signaling	2.05	57/108 (0.528)

Note: Statistical Significance is set at p < .01 by Fisher’s exact test.

Ratio indicates the number of genes from that particular canonical pathway present in the differentially expressed gene data set compared to the total number of genes in that particular canonical pathway curated in the IPA database.