The S-phase fraction (SPF) measured by flow cytometry of DNA and the thymidine labeling index (TLI) measured autoradiographically indicate the proportion of carcinoma cells currently synthesizing DNA and reflect the rate of proliferation. The TLI and SPF are lognormally distributed. The median TLI performed to maximize precursor uptake is near 5% (5 labeled carcinoma cells per 100), the mean near 7%, and the range from less than 1% to near 40%. Corresponding values for the SPF measured by DNA flow cytometry are slightly higher when appropriate measures are taken to reduce background debris counts and other artefacts. Residual elevation of SPF above TLI may result from S-phase arrested cells. Flow cytometric histograms show that clearly aneuploid cell lines exist in 50–80% of primary breast carcinomas. Aneuploid breast carcinomas have higher mean TLI than diploid breast carcinomas, and therefore proliferate more rapidly. They also more frequently lack estrogen receptor (ER). Carcinomas with minimal nuclear anaplasia, particularly those of tubular, mucinous, infiltrating lobular and adenocystic types have low TLI and SPF, whereas carcinomas with highly anaplastic nuclei, including medullary carcinomas, have high TLI and SPF. TLI and SPF correlate inversely with ER and PgR content, have no relationship to axillary lymph nodal status, and have a weak positive correlation with tumor size and a weak negative correlation with age. High TLI predicts a high risk of early relapse after primary therapy for both node-negative and node-positive carcinomas. Carcinomas that produce brain metastases have particularly high TLI. Current evidence suggests that high SPF and aneuploidy may prove to have prognostic significance like TLI.

The thymidine labeling index (TLI) was measured in vitro in 278 primary breast carcinomas. In 227 operable women treated by radical mastectomy, TLI's below the median of 4.55% carried a probability of relapse of 20% at four years, in contrast to 52% for TLI's above the median (P = 0.0001). The probability of relapse was significantly related to the TLI independent of TNM pathologic stage, axillary lymph nodal status alone, estrogen receptor (ER) content, or menopausal status. The abilities of the TLI and nodal status to predict early relapse were equally strong and independent, whereas other variables tested had less or no independent predictive capacity. The predictive value of the ER content depended largely on its relationship to the TLI, and ER was related to the probability of relapse in the below median TLI group only. The TLI can select a subgroup of node-negative patients with a relapse-expectancy of approximately 50% at four years.

Juvenile laryngeal papillomas, solitary laryngeal papillomas of the adult, and cylindric cell papillomas of the nose and sinuses were examined for the presence of papillomavirus antigens by means of immunocytochemistry. By using an antiserum capable of recognizing a common group antigen that reacts with papillomavirus antigens of different species, it was found that half of the juvenile laryngeal papillomas studied contained cells staining for papillomavirus antigens. No positive cells were found in adult solitary papillomas or cylindric cell papillomas. These results strongly implicate a human papillomavirus as the causative agent of juvenile multiple laryngeal papillomas.

Juvenile nasopharyngeal angiofibromas (JNA) are rare. They have been frequently treated with estrogens, either solely or as an adjuvant therapy prior to surgery or irradiation. Clinical trials have proveded no evidence to explain the objective respose to estrogens observed in some tumors. Since the mechanism of steroid hormone action is mediated via specific receptors, we analyzed 8 JNA for tumor cytosol estrogen receptors. None were positive for estrogen receptors. Additionally, all were also negative for progesterone receptors. Nasopharyngeal angiofibromas occur predominantly in adolescent boys at a time when there is a gradual change in androgen availability. Therefore, three latter angiofibromas were also analyzed for the presence of cytosol androgen receptor. Specific testosterone and dihydrotestosterone binding components in the tumor cytosol were detected. This observation raises for the first time the possibility that JNA may be an androgen-dependent tumor. Estrogen may act as an antiandrogen on these tumors, an action similar to that on prostate cancer.

Verrucous carcinomas of the rectum, plantar surface of the foot, and oral cavity were studied by means of light and electron microscopy, and autoradiographic and immunofluorescent techniques. Histologic examination showed that each tumor was composed mainly of mature squamous epithelium, and each had foci of slight cellular atypia. The cells in S-phase consistently were situated near the basal layer. Immunofluorescent examination with antibasement membrane antibody showed areas of marked focal thickening and other areas where basement membrane was absent. Ultrastructural examination showed reduplicated as well as normal basal lamina. Numerous interdigitating microvilli and well developed desmosomes characterized the cells above the basal layer. A proliferative basal zone underlying a thick layer of well differentiated nonproliferating keratinocytes and reduplicated basal lamina were seen in all tumors, regardless of location. These consistent findings constitute evidence that verrucous carcinoma is a morphologic and cytokinetic entity that may occur in multiple anatomic sites.

A breast tumor is described which presented as an exophytic mass, and which by both light and electron microscopic examination had a biphasic histologic composition. In the superficial area adjacent to the epidermis, it showed tubular differentiation similar to a cutaneous tubular apocrine adenoma and salivary basal cell adenoma, and, in the deeper portion, it had the characteristic features of adenoid cystic carcinoma. Their possible interrelationships are discussed, and mammary adenoid cystic carcinoma is briefly reviewed.

38 specimens of benign breast tissue from young women and 92 primary breast carcinomas were evaluated for tritiated thymidine ([ 3 H] TdR) labeling index (TLI) by in vitro pulse labeling. The TLI on non‐neoplastic, terminal breast ducts was significantly higher during the latter half than during the first half of the menstrual cycle (P < 0.001), and a geometric mean TLI of 1.5 during the latter half of the cycle is consistent with approximately 47% turnover of these cells during the menstrual cycle. Ducts of fibroadenomas showed similar menstrual variation TLI. The range of TLI observed in the carcinomas was 0.04‐18.6, arithmetic mean 3.7, geometric mean 2.1. The TLI of carcinomas was not significantly correlated with size of the tumor, but tended to be higher in women less than 50 yr old than in women older than 50 yr (P < 0.05), and in the presence of two or more metastatic axillary lymph nodes than when fewer than two nodes were involved (P < 0.02).

Nine patients with primary adenocarcinoma of the larynx representing 0.1 per cent of 888 patients with primary laryngeal malignancy treated between 1955 and 1971 are reported. Following surgical therapy, four patients are alive without disease and five patients are dead due to their disease. Survival time was not related to histopathologic type, stage of disease, or mode of therapy. We cautiously advocate the use of the most conservative surgery feasible as the primary treatment of this poorly understood and highly fatal disease.

In a classic paper published in 1952, Altmann et al4first drew attention to a series of patients with carcinoma of the larynx in whom the malignant changes were largely limited to the mucosa. Carcinoma in situ or intraepithelial carcinoma of the larynx and pharynx is now widely recognized, and with few minor variations there is general agreement as to the histologic requirements for the diagnosis.5-9These requirements have been spelled out best for lesions of the uterine cervix10; we employ them for laryngopharyngeal lesions essentially without change. The characteristics include replacement of the full thickness of the epithelium by cells with the cytologic characteristics of malignancy, a lack of maturation or differentiation, and an absence of invasion. These essential features are depicted in Fig 3. It is generally recognized that the superficial cell layer may show some flattening and minimal piling up of cells, and also

Journal Article Technical Note Paraphenylenediamine Staining of Osmium-Fixed, Plastic-Embedded Tissue for Light and Phase Microscopy Get access Juan F. Estable-Puig, M.D., Juan F. Estable-Puig, M.D. Washington, D. C. ‡UCP Fellow on leave of absence from Facultad de Medicina, Montevideo, Uruguay; Present Address: Experimental Pathology Branch, Ames Research Center, NASA, Moffett Field, California. Search for other works by this author on: Oxford Academic PubMed Google Scholar Walter C. Bauer, Capt., M.C., USA., Walter C. Bauer, Capt., M.C., USA. Washington, D. C. §Present Address is Washington University School of Medicine, St. Louis, Missouri. Search for other works by this author on: Oxford Academic PubMed Google Scholar J. M. Blumberg, Brig., Gen., M.C., USA. J. M. Blumberg, Brig., Gen., M.C., USA. Washington, D. C. Search for other works by this author on: Oxford Academic PubMed Google Scholar Journal of Neuropathology & Experimental Neurology, Volume 24, Issue 3, July 1965, Pages 531–535, https://doi.org/10.1097/00005072-196507000-00012 Published: 01 July 1965

Radioautographs of tissue from the thyroid gland prepared 24 hours after the administration of iodine-125 showed that the concentration of radioactivity in intracellular colloid droplets was the same as that in the follicular colloid. This observation indicates that colloid droplets are due to phagocytosis of small portions of follicular colloid.

CancerVolume 15, Issue 2 p. 263-270 ArticleFree Access A critical analysis of laryngectomy in the treatment of epidermoid carcinoma of the larynx Walter C. Bauer M.D., Walter C. Bauer M.D. Department of Surgery, Division of Surgical Pathology, Washington University School of Medicine, and McMillan, Barnes, Barnard Free Skin and Cancer hospitals, 600 S. Kingshighway, St. Louis 10, Mo.Search for more papers by this authorDavid L. Edwards M.D., David L. Edwards M.D. Department of Surgery, Division of Surgical Pathology, Washington University School of Medicine, and McMillan, Barnes, Barnard Free Skin and Cancer hospitals, 600 S. Kingshighway, St. Louis 10, Mo. Clinical Fellow (950) of the American Cancer Society, Inc., 1959–1960.Search for more papers by this authorMalcolm H. McGavran M.D., Malcolm H. McGavran M.D. Department of Surgery, Division of Surgical Pathology, Washington University School of Medicine, and McMillan, Barnes, Barnard Free Skin and Cancer hospitals, 600 S. Kingshighway, St. Louis 10, Mo.Search for more papers by this author Walter C. Bauer M.D., Walter C. Bauer M.D. Department of Surgery, Division of Surgical Pathology, Washington University School of Medicine, and McMillan, Barnes, Barnard Free Skin and Cancer hospitals, 600 S. Kingshighway, St. Louis 10, Mo.Search for more papers by this authorDavid L. Edwards M.D., David L. Edwards M.D. Department of Surgery, Division of Surgical Pathology, Washington University School of Medicine, and McMillan, Barnes, Barnard Free Skin and Cancer hospitals, 600 S. Kingshighway, St. Louis 10, Mo. Clinical Fellow (950) of the American Cancer Society, Inc., 1959–1960.Search for more papers by this authorMalcolm H. McGavran M.D., Malcolm H. McGavran M.D. Department of Surgery, Division of Surgical Pathology, Washington University School of Medicine, and McMillan, Barnes, Barnard Free Skin and Cancer hospitals, 600 S. Kingshighway, St. Louis 10, Mo.Search for more papers by this author First published: March/April 1962 https://doi.org/10.1002/1097-0142(196203/04)15:2<263::AID-CNCR2820150209>3.0.CO;2-3Citations: 34 AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume15, Issue2March/April 1962Pages 263-270 ReferencesRelatedInformation

CancerVolume 14, Issue 1 p. 55-66 ArticleFree Access The incidence of cervical lymph node metastases from epidermoid carcinoma of the larynx and their relationship to certain characteristics of the primary tumor. A study based on the clinical and pathological findings for 96 patients treated by primary en bloc laryngectomy and radical neck dissection Malcolm H. McGavran M.D., Malcolm H. McGavran M.D. Department of Surgery, Division of Surgical Pathology, and the Department of Oto-Rhino-Laryngology, Washington University School of Medicine, Barnes Hospital, McMillan Hospital, and the Barnard Free Skin and Cancer Hospital, St. Louis, Mo.Search for more papers by this authorWalter C. Bauer M.D., Walter C. Bauer M.D. Department of Surgery, Division of Surgical Pathology, and the Department of Oto-Rhino-Laryngology, Washington University School of Medicine, Barnes Hospital, McMillan Hospital, and the Barnard Free Skin and Cancer Hospital, St. Louis, Mo.Search for more papers by this authorJoseph H. Ogura M.D., Joseph H. Ogura M.D. Department of Surgery, Division of Surgical Pathology, and the Department of Oto-Rhino-Laryngology, Washington University School of Medicine, Barnes Hospital, McMillan Hospital, and the Barnard Free Skin and Cancer Hospital, St. Louis, Mo.Search for more papers by this author Malcolm H. McGavran M.D., Malcolm H. McGavran M.D. Department of Surgery, Division of Surgical Pathology, and the Department of Oto-Rhino-Laryngology, Washington University School of Medicine, Barnes Hospital, McMillan Hospital, and the Barnard Free Skin and Cancer Hospital, St. Louis, Mo.Search for more papers by this authorWalter C. Bauer M.D., Walter C. Bauer M.D. Department of Surgery, Division of Surgical Pathology, and the Department of Oto-Rhino-Laryngology, Washington University School of Medicine, Barnes Hospital, McMillan Hospital, and the Barnard Free Skin and Cancer Hospital, St. Louis, Mo.Search for more papers by this authorJoseph H. Ogura M.D., Joseph H. Ogura M.D. Department of Surgery, Division of Surgical Pathology, and the Department of Oto-Rhino-Laryngology, Washington University School of Medicine, Barnes Hospital, McMillan Hospital, and the Barnard Free Skin and Cancer Hospital, St. Louis, Mo.Search for more papers by this author First published: January/February 1961 https://doi.org/10.1002/1097-0142(196101/02)14:1<55::AID-CNCR2820140109>3.0.CO;2-2Citations: 207AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume14, Issue1January/February 1961Pages 55-66 ReferencesRelatedInformation

CancerVolume 13, Issue 6 p. 1185-1187 ArticleFree Access Sebaceous lymphadenoma of the parotid salivary gland Malcolm H. McGavran M.D., Malcolm H. McGavran M.D. Department of Surgery, Division of Surgical Pathology, Washington University School of Medicine, St. Louis, Mo., and the Ellis Fischel Memorial State Cancer Hospital, Columbia, Mo.Search for more papers by this authorWalter C. Bauer M.D., Walter C. Bauer M.D. Department of Surgery, Division of Surgical Pathology, Washington University School of Medicine, St. Louis, Mo., and the Ellis Fischel Memorial State Cancer Hospital, Columbia, Mo.Search for more papers by this authorLauren V. Ackerman M.D., Lauren V. Ackerman M.D. Department of Surgery, Division of Surgical Pathology, Washington University School of Medicine, St. Louis, Mo., and the Ellis Fischel Memorial State Cancer Hospital, Columbia, Mo.Search for more papers by this author Malcolm H. McGavran M.D., Malcolm H. McGavran M.D. Department of Surgery, Division of Surgical Pathology, Washington University School of Medicine, St. Louis, Mo., and the Ellis Fischel Memorial State Cancer Hospital, Columbia, Mo.Search for more papers by this authorWalter C. Bauer M.D., Walter C. Bauer M.D. Department of Surgery, Division of Surgical Pathology, Washington University School of Medicine, St. Louis, Mo., and the Ellis Fischel Memorial State Cancer Hospital, Columbia, Mo.Search for more papers by this authorLauren V. Ackerman M.D., Lauren V. Ackerman M.D. Department of Surgery, Division of Surgical Pathology, Washington University School of Medicine, St. Louis, Mo., and the Ellis Fischel Memorial State Cancer Hospital, Columbia, Mo.Search for more papers by this author First published: November/December 1960 https://doi.org/10.1002/1097-0142(196011/12)13:6<1185::AID-CNCR2820130605>3.0.CO;2-PCitations: 41AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL No abstract is available for this article. References 1. Foote, F. W., Jr., and Frazell, E. L.: Tumors of major salivary glands. Cancer 6: 1065– 1133, 1953. 2. Hartz, P. H.: Development of sebaceous glands from intralobular ducts of parotid gland. Arch. Path. 41: 651– 654, 1946. 3. Lee, C. M., Jr.: Intraparotid sebaceous glands. Ann. Surg. 129: 152– 155, 1949. 4. Meza-Chavéz, L.: Sebaceous glands in normal and neoplastic parotid glands; possible significance of sebaceous glands in respect to origin of tumors of salivary glands. Am. J. Path. 25: 627– 645, 1949. 5. Rawson, A. J., and Horn, R. C., Jr.: Sebaceous glands and sebaceous gland-containing tumors of parotid salivary gland, with consideration of histogensis of papillary cystadenoma lymphomatosum. Surgery 27: 93– 101, 1950. 6. Thompson, A. S., and Bryant, H. C., Jr.: Histogenesis of papillary cystadenoma lymphomatosum (Warthin's tumor) of parotid salivary gland. Am. J. Path. 26: 807– 849, 1950. Citing Literature Volume13, Issue6November/December 1960Pages 1185-1187 ReferencesRelatedInformation