Size doesn't matter: It is difficult to evaluate the efficacy of anticancer drugs when the tumor shrinks

Drug source analysis

The main goal of anticancer drugs is to prolong the patient's OS, but the drug response rate and response time of most tumors are very weakly correlated with OS
.
For example, a recent large-scale study of the effects of antibodies and targeted therapy drugs on OS and PFS compared with chemotherapy showed that 20% of drugs that prolong PFS shortened OS, and 12% of drugs that shortened PFS actually prolonged OS (doi: 10.

Tumor size is not the main cause of death.
Benign tumors usually do not threaten the lives of patients even if they grow large
.
The degree of malignancy is a more important indicator.

There may be several reasons for prolonging PFS but shortening OS
.
The most obvious reason is that while killing tumors, it also severely damages healthy tissues, that is, the toxic side effects are too great, killing 800 enemies, and self-inflicting 1,000

Another possibility is that although the tumors were severely killed, they were all made cannon fodder by the less malignant ones, and those clones with the most malignant levels were not affected
.
These relatively benign tumors are cleared to make room for the heinous clones to grow, leading to drug resistance and recurrence, thus accelerating the death of patients

For antibodies and targeted drugs, the elimination of target expression clones makes clones that do not rely on these targets become the new king, and these targeted drugs are only effective on tumor cells that rely on the target due to the requirements of molecular mechanisms
.
These drug-resistant clones may be more malignant than the primary tumor, leading to shortening of OS

PFS is not profitable, but OS is significantly prolonged, which may be the opposite
.
One is that although tumor shrinkage is not obvious or the shrinkage does not last long, it is the elite troops of the tumor that kills and wounds, and the re-growth of the tumor is just a straggler

Although our understanding of the molecular mechanisms of tumor treatment continues to deepen, the early drug evaluation system still needs a lot of work to improve the prediction of OS, the most critical therapeutic target
.
Increasing the diversity of tumor killing mechanisms before this knowledge is discovered may be the most practical strategy