Measuring tumor growth

It is imperative to depend on sensitive and precise marker assays. Guess [38] tried to address this problem by use of splines or line segments to average all PSA-DT values in an attempt to better detect therapy-induced changes of PSA-DT. Unfortunately, this computerized technique is cumbrous for most to apply.

The accurate and reproducible measurement of tumor diameters from imaging studies is critical. Keep in mind that occasionally plain radiographs of larger lesions are preferred because CT imaging may slice through a lesion at variable levels producing aberrant results for elliptical lesions.

A closer look at differences between DT and SGR.

The mathematical relationship between DT and SGR as revealed by the exponential growth model is important because as displayed in Figure 10, sole use of tumor volume doubling time (TV-DT) or tumor marker doubling time (PSA-DT) rather than tumor or marker specific growth rate as a measure of treatment outcome may be destined for failure depending on the magnitude of differences in the clinical study. Applying the exponential model of tumor growth to published studies reporting only DT as displayed here Table 1,2 and Figures 11,12 reveals discordant conclusions from those using SGR. Note that the DT is mathematically logarithmically related to the inverse of the exponential growth constant (SGR): SGR = ln(2)/DT.

The opposite results using SGR compared to those obtained with DT are critical since prostate cancer research is steeped in the use of the PSA-DT to predict survival, tumor dissemination, relapse, and tumor response to drugs and hormones and to radiation efficacy. In the prostate cancer literature use of DT as a parameter of response is established canon.

Mehrara reveals that DT is not normally symmetrically distributed (non-Gaussian distribution) and its use as an indicator of treatment response could yield inaccurate conclusions. Changes in DT over-predict drug effects in slow growing tumors while they under-predict in rapidly growing tumors and DT is essentially of no value for tumor volumes (or markers) that show no change in value (stable disease) where DT approaches infinity see Figure 10.

Work by others confirms the importance of the tumor or marker-specific growth rate. Stein et al. [46] studied a combination of equations that simultaneously modeled both tumor/ PSA regression and tumor/PSA exponential growth. They found that only the exponential growth equation with its specific growth rate constant (PSA-SGR) predicted a statistically significant high mortality hazard ratio of 5.14 (95% confidence interval, 3.10 - 8.52) in his study group of patients with prostate cancer. The disease regression formula was unable to predict patient mortality.

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