1) 31(67.4) 3(6.5) 36.29 <0.0005 21(45.7) 18(39.1) 7(15.2) 15.05

0.001   Cancerous 96 14(14.6) 25(26) 57(59.4) 20(20.8) 32(33.3) 44(45.8) Matched                           Normal 24 7(29.17) 15(62.5) 2(8.33) 17.524 <0.0005 13(54.2) 7(29.2) 4(16.7) 7.577 0.023   Cancerous 24 2(8.3) 6(25) 16(66.7)     4(16.7) 11(45.8) 9(37.5)     Figure 1 IHC analysis of Hsp90-beta and selleck inhibitor annexin A1 in lung cancer and normal lung tissues (IHC × 400). (A) Low staining of Hsp90-beta in normal tissues; (B) moderate staining of Hsp90-beta in moderately differentiated LAC; (C) high staining of Hsp90-beta in poorly differentiated LAC; (D) moderate staining of Hsp90-beta in moderately differentiated LSCC; (E) high staining of Hsp90-beta in poorly differentiated LSCC; (F) high staining of annexin Eltanexor A1 in LCLC; (G) low staining of annexin A1 in well-differentiated LAC; (H) moderate staining selleck compound of annexin A1 in moderately differentiated LAC; (I) high staining of annexin A1 in poorly differentiated LAC;

(J) high staining of annexin A1 in SCLC; (K) moderate staining of annexin A1 in moderately differentiated LSCC; (L) high staining of annexin A1 in poorly differentiated LSCC; LAC, adenocarcinoma of the lung; LSCC, squamous cell carcinoma of the lung; SCLC, small cell lung cancer; LCLC, large cell lung cancer. Correlation between the expressions of Hsp90-beta and annexin A1 and clinicopathologic factors The association of several clinicopathologic factors with Hsp90-beta and annexin A1 expression is illustrated in Table 4. High expression levels of Hsp90-beta and annexin A1 were found in poorly differentiated lung cancer tissues (80.8% and 84.6%, respectively) compared with well-differentiated tissues (22.7% and 31.8%, respectively) (p < 0.0005) (Figures 2A and B). High expression levels of Hsp90-beta and annexin A1 in lung cancer cases without lymph node metastasis were both Masitinib (AB1010) 26.8%, which is lower than what was noted

in lung cancer cases with lymph node metastases as follows: N1, 85% and 60%; N2, 81.8% and 81.82%; and N3, 100% and 100%, respectively (p < 0.0005) (Figures 2C and D). Annexin A1 was significantly associated with the histological type, and was highly expressed in LAC (23/39, 59%) and SCLC (7/11, 63.6%), but lowly expressed in LSCC (12/41, 29.3%) (p < 0.05). Hsp90-beta exhibited a higher expression in SCLC (9/11, 81.82%) than in LAC (22/39, 56.4%) and LSCC (23/41, 56.1%) (p < 0.05). The expression levels of Hsp90-beta and annexin A1 in lung cancer cases of T3 to T4 were 85.7% (24/28) and 71.4% (20/28), which is higher than what was observed in lung cancer cases of T1 to T2, respectively (p = 0.001). Moreover, Hsp90-beta and annexin A1 were highly expressed in stages III (82% and 68%) and IV (100% and 75%) compared with stages I (both 0%) and II (45.3% and 32.

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