Sixty-eight patients with thoracic lesions (48 with lung cancer and 20 with benign lesions) underwent color Doppler ultrasound (US) examinations. Of those, 21 patients (13 with lung cancer and eight with benign lesions) also received resections, and the correlation between color Doppler US signals and resected histologic specimens was evaluated. Our results showed that three patterns of color Doppler US signals could be detected and confirmed: pulsatile flow (artery), constant flow, and triphasic flow (pulmonary vein). Among the 48 patients with lung cancer, pulsatile flow, constant flow, and/or triphasic flow were detected in 34 (71%), 24 (50%), and 14 (29%), respectively. Among the 20 patients with benign lesions, only pulsatile flow and/or triphasic flow were detected in nine (45%) and eight (40%), respectively. From the correlation between color Doppler US signals and histologic specimens, constant flow was representative of the true neovascularity of lung cancers, and it was valuable for differentiating lung cancers from benign lesions (p = 0.00008, sensitivity = 0.50, and specificity = 1.0). Although color Doppler US still had some limitations in detecting blood vessels in thoracic lesions, the correlation between the vascularity represented by color Doppler US signals and histologic specimens was excellent. We conclude that color Doppler US is a valuable method for assessing blood flow in thoracic lesions and differentiating lung cancers from intrapulmonary benign lesions.

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A human lung-cancer PC-9 subline with acquired resistance to vincristine (VCR), a chemotherapeutic agent, was established with incremental increases of the drug. The resistant PC-9 subline (PC-9/VCR) shows a 12-fold increase in resistance to VCR and a unique cross-resistance pattern: high cross-resistance to the potent VCR analogue colchicine (6.9-fold) and vinblastine (2.5-fold); lower cross-resistance to actinomycin D (1.8-fold), cisplatin (1.2-fold) and adriamycin (1.3-fold) and a sensitivity to melphalan and VP-16 which is similar to that of the parental cell line. A reduced accumulation of VCR in the resistant cells was demonstrated. Interestingly, the VCR resistance of the PC-9/VCR cell line was partially reversed by ascorbic acid, and the drug uptake was enhanced. In contrast, ascorbic acid had no effect on drug tolerance and drug accumulation was not observed in either PC-9 parental cells or known multidrug-resistant (MDR) cells, suggesting that VCR resistance in PC-9/VCR cells results essentially from reduced drug accumulation. It is worth noting that, whereas reduced drug accumulation in the PC-9/VCR cells was susceptible to modulation by ascorbic acid, the increased efflux rate characteristic of the resistant cells was not. Further, there was a higher efflux rate in resistant cells than in parental cells. DNA Southern- and RNA Northern-blot hybridization analyses indicate that PC-9/VCR cells do not contain amplified mdr genes or overexpress P-glycoprotein. In addition, the calcium-channel blocker verapamil, which acts as a competitive inhibitor of drug binding and efflux, did not affect the resistant phenotype of PC-9/VCR cells. These findings suggest an ascorbic acid-sensitive drug uptake mechanism which is important in mediating VCR resistance per se in human lung-cancer cells; this differs from the P-glycoprotein-mediated MDR mechanism.