Ferritin concentration was measured in cytosol extracts of 44 mammary carcinomas and 14 benign breast tissues. A six‐fold difference was observed (mean, 364.6 ± 223.3 ng/mcp in malignant tissue versus mean, 60.2 ± 42.1 ng/mcp in benign tissue P < 0.001). Thirty‐five malignant tissue specimens were reviewed independently by a pathologist without knowledge of their ferritin contents. Higher concentrations of ferritin were present in malignancies with greater degrees of epithelial proliferation and plemorphism suggesting the malignant epithelium as the major site of the increased ferritin. There was no correlation between desmoplastic reaction within the tumors or inflammation within or adjacent to the tumors and ferritin concentration. Ferritin in breast tissue may be important as a marker of neoplasia, a source of elevated serum ferritin, an indicator of clinical prognosis or an immunosuppressive substance.
Seven year follow-up data were available on 36 of 40 breast carcinoma patients in whom breast tissue ferritin concentrations at the time of surgery were known. 18 patients were alive and free of recurrence or second tumor (Group 1) and 11 died with breast cancer (Group 2). Patients with lower tissue ferritin concentrations defined as less than 319 ng/mcp (nanograms of ferritin/milligram of cytosol protein) were at reduced risk: 86% of patients with low tissue ferritin concentration survived free of recurrence or second tumor vs. 40% of patients with high tissue ferritin concentration (P = 0.0056). Mean breast carcinoma tissue ferritin concentration was 295 +/- 52 ng/mcp in Group 1 and 444 +/- 55 ng/mcp in Group 2 (P = 0.036). Lymph node involvement was predictive of mortality from breast carcinoma (P = 0.0003), but did not correlate with mean tissue ferritin concentration (P = 0.082). 10/10 (100%) patients who had both low tissue ferritin concentration and absence of lymph node involvement were in Group 1. The correlation of breast tissue ferritin concentration with histopathologic dedifferentiation and with prognosis suggests tumor tissue ferritin as a marker of malignant potential.
Tumor tissue samples from 25 patients with adenocarcinoma of the colon, twelve related samples of normal colons as well as five serum specimens from the same patients were analyzed for ferritin. The average ferritin content of the tumor tissue was 788 ng/mcp with a range of 47-1,745 ng/mcp. The average ferritin content of normal colon mucosa was 115 ng/mcp with a range of 32-230 ng/mcp. Two specimens of metastatic colon cancer taken from the retroperitoneal space and liver, respectively, contained 3,867 and 2,827 ng/mcp of ferritin. The ferritin content of the tumor tissue was higher than that of the normal colon in 8 of 9 patients who had specimens obtained from both sites. The amount of ferritin found in tumor tissue was independent of sex, age, and the site of the original tumor. This study shows that the ferritin content of colon neoplasms is elevated and indicates that the tumor tissue may be the direct source of elevated serum levels of ferritin previously observed in cancer patients.
Ovarian metastasis from a primary thyroid carcinoma is rare. In this report we describe a woman who manifested the unusual occurrence of metastases of papillary thyroid carcinoma to the ovary. Both clinically and pathologically, such a presentation can be difficult to distinguish from benign cystic neoplasms of the ovary or cystic struma ovarii.
To determine if there is a familial component to susceptibility to radiation-induced thyroid neoplasms, we studied 572 individuals who were members of 286 sibpairs who received childhood radiation treatment and for whom follow-up information was obtained. Of these 572 individuals, 240 (42.0%) had thyroid neoplasms (benign and malignant), and 75 (13.1%) had surgically confirmed thyroid cancer. To test the null hypothesis, that neoplasm occurred without regard to family membership, it was necessary to take into account each individual's years at risk and known risk factors. These risk factors, analyzed by the proportional hazards model of Cox, were sex, age at time of radiation treatment, and treatment dose. For each individual, we calculated the cumulative hazard that a neoplasm would occur from that individual's specific risk factors and years at risk. Each individual was also assigned an indicator, D = 1 or 0, according to whether a neoplasm had occurred. Finally, for each individual we computed a residual, D minus the cumulative hazard. In the absence of familial effects, positive and negative residuals would be distributed without regard to family membership, whereas residuals would tend to have concordant signs and magnitudes within families if familial effects were present. Permutational methods, therefore, were used to determine whether the sum among families of the products of residuals within sibpairs was too large, compared to random pairing. For all thyroid neoplasms (both benign and malignant), within-family concordance was significant (P = 0.05, the observed sum among families of the products of residuals was larger than 9468 of 9999 permutations). For thyroid cancer considered alone, the same analysis did not demonstrate familial concordance conclusively, but the results were suggestive (P = 0.18). We conclude that in addition to the previously described risk factors of female sex, younger age at radiation exposure, and higher dose, it is likely that there are independent familial risk factors for developing thyroid neoplasms. Whether these are genetic or environmental factors remains to be determined.
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