Influence of surgical trauma on experimental metastasis in healing wounds is investigated using a transplantable murine mammary carcinoma cell line, TA3Ha. Intravenous injection of 10(5), 10(6), and 2 x 10(6) TA3Ha cells into syngeneic Strain A mice led to liver or kidney tumor development in none of the 96, ten, and ten mice tested, respectively. In contrast, injection of 10(5) cells into mice immediately after hepatic wedge resection performed using milliwatt carbon dioxide laser and electrocautery resulted in tumor formation at the site of trauma in 21/37 (57%) and 25/52 (48%) mice, (P less than 0.001) respectively. Similar results were obtained in mice subjected to partial nephrectomy using the laser (nine of 18) and electrocautery (eight of 13). These results clearly demonstrate that surgical trauma renders a nonprivileged organ susceptible to experimental metastasis formation, and that at least in this model both laser and electrocautery have similar effects. Tumor cell injection 1, 7, and 10 days posthepatic surgery resulted in 36%, 20%, and 0% tumor formation, respectively, indicating that the earlier events in wound healing support tumor implantation and/or growth better than those later on. Frequency of tumor formation at sites of trauma in the peritoneum induced by scalpel blade, laser, and electrocautery were 28%, 50% and 82%, respectively. Peritoneal tumors were seen in 33% of the nonsurgical mice. Skin incisions induced with the three above probes had little influence on experimental metastasis formation. Thus the influence of trauma on tumor formation is not uniform in every organ.

Background. This study examined the association between cigarette smoking status and the development of lung metastases in a group of 835 women diagnosed with primary malignant unilateral breast cancer. Method. Female patients with breast cancer diagnosed between 1982 and 1991 at Roswell Park Cancer Institute (RPCI) in Buffalo, New York, who provided information on their cigarette smoking history at the time of their diagnosis were included. The subsequent disease status of patients was monitored by the RPCI Tumor Registry. The Cox regression model was used to estimate the relationship between smoking status and the development of lung metastases, adjusting for the patient's age, stage of disease at diagnosis, and body weight. Results. Of those patients who developed lung metastases, 8.7% were nonsmokers, 14.1% were former smokers, and 14.3% were current smokers. Tests showed that nonsmokers had significantly fewer lung metastases than either of the two smoking groups (P < 0.01). The estimated relative rates of lung metastases developing adjusting for age, stage, and body weight in women who smoked less than 10,000, between 10,001 and 20,000, and more than 20,000 packs over their lifetimes compared with non–smokers were 1.06 (95% CI, 0.51‐2.20), 3.10 (95% CI, 1.5‐6.3), and 3.73 (95% CI, 1.6‐8.9) respectively. The Cox regression model showed that every 1000 packs of cigarettes consumed over a lifetime increased a woman's risk of developing lung metastases by about 3% to 7% (P < 0.001). Conclusion. This study found a significant association between cigarette smoking history and risk of lung metastases developing in women diagnosed with primary invasive unilateral breast cancer. The risk of lung metastases developing increased as the number of cigarettes smoked in a lifetime increased. Cancer 1995;75:2693–9.

Tn antigen is the immediate precursor of the carcinoma (CA)‐associated T antigen; both are masked in non‐CA tissues. Tn antigen was detected by absorption of human anti‐Tn antibody in 46 of 50 primary breast CAs and in all 6 metastases originating from Tn‐positive primary CAs. Thirteen of 25 (52%) anaplastic CAs, but only 2 of 15 (13%) well differentiated CAs had more Tn than T; 1 anaplastic CA had neither antigen. Eighteen of 20 benign breast lesions had no Tn; the 2 positive lesions were premalignant. All 19 breast CAs, studied immunohistochemically, reacted strongly with human polyclonal anti‐Tn; benign or normal glandular tissues had minimal or no reactivity. Among live cancer cell lines, the most malignant sublines had more Tn than T on their cell surfaces. Preliminary studies with rodent monoclonal anti‐Tn and anti‐T antibodies gave immunohistochemical reactivity patterns similar to those of the polyclonal antibodies, but the former were less sensitive in absorption tests. Tn is a CA marker that promises to be useful in tumor detection.

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We report here sensitive and specific measurement of immune responses of patients with certain kinds of carcinoma toward the physically and chemically well defined T antigen isolated from healthy human erythrocytes. Over 90% of adenocarcinoma tissues tested possess T-specific immunoreactive structures as determined with human antisera, in contrast to healthy tissues and benign lesions. Adenocarcinoma patients recognize the carcinoma-associated T antigen as foreign. Delayed-type skin hypersensitivity reaction to T antigen (DTHR-T) was positive in all 25 lung adenocarcinoma patients tested, in 88% of 101 patients with ductal, in 43% of 30 patients with lobular or tubular breast carcinoma and in 9/9 patients with adenocarcinoma of body cavities. Patients of all Stages reacted positively. All 7 patients with small cell lung carcinoma and 3/5 with malignant melanoma had a positive DTHR-T. None of 17 patients with malignant brain tumors, leukemia or Hodgkin's disease, sarcoma or thyroid carcinoma reacted. The DTHR-T was specific in that all 77 healthy persons and 48/49 with other diseases, including 23/24 with non-cancer lung disease were negative; one patient with organizing interstitial pneumonitis was positive. This points to a possible source of false positive reactions. 91% of 149 patients with histologically benign breast disease had a negative DTHR-T; the histology of some of the positive ones was reexamined, 2 proved to have carcinoma in situ.

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Taken together, A47 blocks E2/EGF-induced activation of EGFR and therefore interferes with the proximal EGFR signaling pathway. A47 also arrests the cells at the G1-S transition of the cell cycle and induces cell death by apoptosis. Thus, a growth factor RTK may be useful in blocking hormone-dependent tumor growth in an elevated E2 environment.

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