Case reports of the metastatic spread of cancer to the psoas muscle, though rare, date back over a century, including one case from a pancreas primary published by Flexner in 1894 (4). There are only a few cases in the literature reporting direct hematogenous metastasis of lung cancer to the psoas muscle. Ampil et al. describe seven cases of metastatic tumors involving the psoas muscle, including one from a lung primary (5). In two patients, RT to the psoas metastasis provided effective palliation of pain. Nash et al. reported on a single case of a biopsy proven psoas metastasis from an adenocarcinoma of the lung (6). Damron et al. presented 30 cases of cancer metastatic to soft tissue; this series included one patient with small cell lung cancer metastatic to the psoas muscle (7). Sudo et al. described a case of adenocarcinoma of the lung metastatic to the psoas muscle in a patient presenting with pain on hip extension (8). Kenny et al. described 25 cases of psoas muscle invasion by malignancy including one adenocarcinoma of a lung primary (9). Of these cases only two represented hematogenous metastasis. Lenchik et al. reported on 44 cases of CT identified psoas abnormalities of which 15 were malignancies, two from a primary lung cancer (10). These published series are summarized in Table 1.

Published reports on the use of CT or MRI also suggest that anatomic imaging cannot accurately identif y psoas muscle pathology (10,11,12). Cases of metastatic disease masquerading as benign processes such as psoas abscesses have been reported (13,14). While it is possible that these findings could be explained by benign processes or synchronous primary malignancies, this possibility is remote. The three psoas lesions described in this series are unlikely to represent any other disease process except hematogenous metastatis of lung cancer. This contention is supported by several findings: the absence of preceding trauma, the absence of the stigmata of infection, the appearance of psoas masses on CT scans (in two patients), correlated hypermetabolic activity on FDG-PET (in three patients), the resolution of these radiographic findings after RT, and the clinical setting of advanced NSCLC. Given the expense and possible morbidity of surgical biopsy balanced against the high likelihood that these lesions represented metastatic NSCLC, the risks of pathologic confirmation were not deemed to be justified.

Based on the relative paucity of published reports, it appears that very few psoas metastases become radiographically apparent or clinically symptomatic. By contrast, autopsy studies suggest that metastatic infiltration of the psoas muscles is far more common. In one Spanish study, 194 patients with known malignancy underwent postmortem examination (15). At autopsy, 50 were found to have involvement of skeletal muscle with cancer, 16 by direct extension, 34 by metastastic spread. The muscle groups most often involved were the diaphragm (23 patients) and the iliopsoas (10 patients), although this distribution may, in part, represent a sampling bias since these muscle groups were sectioned more often than others. Adenocarcinoma appeared to metastasize to skeletal muscle more frequently than other cancer histologies. Another study of patients with a diagnosis of malignancy found metastases in skeletal muscle in six out of 38 autopsies (16). In four of these cases, cancer was found in the iliopsoas muscles.

It is not known how to reconcile the discrepancy between the rarity of clinically apparent psoas metastases and the high incidence of detection on autopsy, however, the “seed and soil” hypothesis may provide some insight. Paget postulated that the formation of metastases depends on the interaction of specially adapted tumor cells (seeds) and a permissive organ milieu (soil) (17). In more recent formulations of this theory, tumor cells must accumulate specific genetic mutations endowing them with the metastatic phenotype. Once tumor cells acquire the ability to intravasate into the vasculature, they disseminate hematogenously and enter the parenchyma of target organs. Tumor cells then face diverse cellular microenvironments that range from permissive to hostile. Only those cells that are well suited to overcoming obstacles to growth, and find themselves in a suitable milieu, will develop into metastases. Tumor cells in less permissive environments may die or grow in a more indolent fashion (18). It is this set of complex interactions between tumor cells and distant organs that underlies disease specific patterns of distant failure.

The “seed and soil” hypothesis has two impor tant implications for the observations in the present study. First, it explains the finding, universal to all malignant processes, that distant metastases tend to be unevenly distributed throughout the body (19). In the case of lung cancer, clinically evident psoas metastases are extremely rare because the cellular environment of skeletal muscle is less hospitable than other organs. Thus, the interactions between tumor cells and target tissues lead to the preferential development of metastatic disease in more permissive tissue such as the brain, bone and adrenal glands. Second, the “seed and soil” hypothesis may account for the seemingly contradictory observations that metastases to the psoas muscle are rarely identified clinically but are commonly found on autopsy. Due to the resistance of skeletal muscle to tumor implantation, psoas metastases may progress more slowly than tumor deposits elsewhere in the body or present later in the course of disease. The advent of PET imaging may reveal psoas metastases that would have otherwise gone undetected. If true, then the frequency of the detection of psoas metastases in NSCLC may increase in the future.