The Mantoux response was evaluated in 2 groups of patients with carcinoma. In 47 patients with primary carcinoma of the gastrointestinal tract, breast, and prostate, the Mantoux responses were depressed before primary tumor resection, compared with 25 patients tested after resection and with 62 normal controls. Fifty-nine patients with bronchial carcinoma had normal or stronger reactionsthan controls. Old Tuberculin 1:1000 and later Purified Protein Derivative 1:5000 were used. The Mantoux response increased 2–6 weeks after primary tumor resection in 6 of 7 patients with colon and rectal cancer, in 16 of 24 with bronchial cancer, and in 2 after estrogen treatment for prostate cancer. This increase in response appeared to be a “release” of preexisting sensitivity, suppressed in the presence of the tumor, rather than a conversion from an “intrinsic” negativity to positivity. Mantoux release indicated a change in immunologic status after treatment and did not necessarily indicate curative surgery. The suppression of response was associated with a circulating immunosuppressive factor in 11 of 16 patients examined: Serum suppressed tuberculin-induced lymphocyte DNA synthesis, but in higher dilution DNA synthesis was stimulated. This appeared to be one cause of Mantoux depression, and changing titer following tumor resection appeared to be one cause of Mantoux release. This clinical picture may resemblethe nonspecific immunosuppression seen in mice during experimental tumor induction, but a more specific relationship cannot be discounted.