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We report the case of a patient in whom oral squamous cell carcinoma and a fatal reactive form of histiocytosis were simultaneously manifested. Our conclusions indicate that such a hematophagocytic syndrome may occur in the setting of oral squamous cell carcinoma as previously described in other malignancies.
A 65-year-old man presented with 4 weeks of partial right visual field loss. A left occipital granular cell tumor was diagnosed via open biopsy. No specific tumoricidal therapy was given, and the patient returned 2 weeks later with fluent dysphasia and mild right hemiparesis, and formed visual hallucinations. A large left parietotemporal mass, separate from the granular cell tumor, was diagnosed as a glioblastoma multiforme by stereotactic biopsy. The histogenesis of cerebral granular cell tumors is controversial; this case supports recent speculation of their possible glial origin.
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Brown Norway (BN) rats carrying a transplantable acute myelocytic leukemia (BNML) were given a supralethal combination of cyclophosphamide (80-100 mg/kg i.p.) and total-body irradiation (9.0 Gy gamma rays or 8.5 Gy X-rays) followed by isologous bone marrow transplantation. Of 110 long-term survivors (greater than 95 days), 40 (45%) died of a secondary malignancy at a median posttreatment age of 450 days. At a comparable age, non-treated control BN rats show a spontaneous tumor incidence of 5% only, which increased to 83% during the aging process. Thus the latency period for the appearance of tumors was impressively shortened. Tumors of neurogenic origin and acute leukemias were the most prominent types, in contrast with non-treated control rats.
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Wistar rats received 2 Gy whole body irradiation followed immediately by 10 mg/kg of ethyl nitrosourea (ENU) on the day of birth. Out of 33 rats which were given ENU alone 14 developed 22 tumours of the nervous system, out of which 15 (68.2%) were gliomas and 7 (31.8%) were Schwannomas. Out of 34 rats which were given both irradiation and ENU 12 were found to harbour 15 neural tumours out of which 14 (93.3%) were gliomas and 1 (7.1%) was a Schwannoma. The pretreatment with irradiation seems to have resulted in selective suppression of Schwannoma induction.
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Ionizing radiation has long been recognized as a weak carcinogen, and the risk of developing a radiation induced neoplasm after exposure to therapeutic radiation has been established. In the case of therapeutic radiation for treatment of existing malignancies, concomitant risk factors for second malignancies can confound the effect of radiation alone. This study presents a model for evaluating the isolated contribution of ionizing radiation to the induction of second malignancies in cancer patients, and presents estimates of the expected number of second malignancies induced in selected sensitive sites by scatter radiation during radiotherapy for cancer. The study focused on the year 1987, during which it was estimated that 192,761 new cancer patients received radiotherapy as part of their initial treatment plan. The model predicted that radiation may induce 63-84 secondary breast cancers, 64-72 secondary thyroid cancers, 94-157 secondary lung cancers, and 489-707 secondary leukemias over the remaining lifetime of this patient population. This represents a lifetime incidence of 0.7% for leukemia, and 0.3% for the solid tumors. This incidence must be placed in perspective with the current concepts of cancer management, such as combined modality therapy that may carry a risk of carcinogenesis greater than either modality alone, and when the alternatives to radiotherapy may be nonexistent or may be cosmetically or functionally undesirable. The information presented may be used in weighing the risks and benefits of alternative treatments for cancer.
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We report two retroperitoneal Castleman's tumors (giant lymph node hyperplasia) of hyaline vascular type. One was a large tumor situated in the pararenal region, the other was located in the pancreas head. On computed tomography (CT), both tumors were solid and moderately enhanced after administration of contrast material. On angiography, both tumors were hypervascular with dilated feeding arteries, and showed capillary blush. In an appropriate clinical setting, a retroperitoneal tumor showing these findings should include Castleman's tumor in the differential diagnosis.
Hybrid tumours are very rare tumour entities which are composed of two different tumour entities, each of which conforms with an exactly defined tumour category. The tumour entities of a hybrid tumour are not separated but have an identical origin within the same topographical area. In contrast, biphasically differentiated tumours are a mixture of two cellular patterns with a corresponding term in the tumour classification. Examples of a biphasic differentiation are: basaloid-squamous carcinoma, adeno-squamous carcinoma or sarcomatoid carcinoma, and epithelial-myoepithelial carcinoma, mucoepidermoid carcinoma or adenoid cystic carcinoma. Hybrid tumours must also be distinguished from the multiple occurrence of salivary gland tumours which can develop syn- or metachronously. In the tissue samples of more than 6600 salivary gland tumours covered by the Salivary Gland Register (Institute of Pathology, University of Hamburg, Germany) only 5 cases of hybrid tumours were recorded between 1965 and 1994. This means less than 0.1% of all registered tumours. Case 1 was a very rare example of a hybrid adenoma with differentiation as a basal cell adenoma and a canalicular adenoma of the parotid gland. The similar cellular origin of both types of adenoma may be an explanation for its development in a hybrid adenoma. Case 2 is a hybrid tumour with a composition of basal cell adenoma and a glandular type of adenoid cystic carcinoma. In both types of tumours the two cell types (duct-lining cells and modified myoepithelial cells) have a similar histogenetic origin. Therefore, the development of the both cell types in a hybrid tumour with two trends of differentiation is possible. Case 3 represents a hybrid adenoma as a mixture of a Warthin tumour and a sebaceous adenoma. Although inclusions of sebaceous cells are observed in Warthin tumours, this hybrid tumour shows a composition of two different epithelial structures in a varied mixture. Case 4 is a very rare and unique hybrid carcinoma with two absolutely different components: acinic cell carcinoma and salivary duct carcinoma. The poor prognosis of this hybrid carcinoma is determined by the salivary duct carcinoma. Case 5 represents a hybrid carcinoma whose two components have a similar histogenetical basis: epithelial-myoepithelial carcinoma and a glandular type of adenoid cystic carcinoma. Both carcinomas are composed of variable proportions of ductlining cells and myoepithelial cells.
Detection of a breast mass accompanied by a contralateral axillary lymphadenopathy presents a dilemma because of the possible presence of an occult breast cancer on the same side as the axillary lymphadenopathy. A patient presented with an axillary lymphadenopathy from an occult breast cancer and a synchronous contralateral breast cancer, for which the differential diagnosis was established through a significant difference in estrogen and progesterone receptor levels. The patient was treated with neoadjuvant chemotherapy followed by bilateral modified radical mastectomy, adjuvant chemotherapy, and adjuvant radiation therapy. She is alive and free of disease 1.5 years after the diagnosis.
PURPOSE: To determine and quantitate the radiological characteristics of tubular carcinoma of the breast, to report clinical and pathologic findings and to define findings at follow-up. MATERIALS AND METHODS: A retrospective review of records of 2872 women who received a diagnosis of breast carcinoma between January 1988 and January 2006 revealed 32 histopathologically proven pure tubular carcinoma of the breast. Analysis included history; findings at physical examination, mammography, and sonography (US) at the time of diagnosis and in postoperative follow-up and histopathological results. RESULTS: Fifty-nine percent of the patients (n=19) presented with a palpable mass. The mammographic findings were a mass in 23 (72%), a mass with microcalcifications in 2 (6%), asymmetric focal density in 1 (3%), architectural distortion in 1 (3%) and negative in 5 (16%) of the 32 patients. Most (96%) masses had spiculated margins. US depicted 30 masses in 29 patients, all of which were hypoechoic, mostly (n=27, 90%) with posterior acoustic shadowing. The cancer was clinically occult in 41% (n=13), mammographically occult in 16% (n=5), and sonographically occult in 6% (n=2) of the patients. Histologically, the tumor was multifocal in 3% (n=1) of the patients. Four (13%) patients developed contralateral breast carcinoma at follow-up. CONCLUSION: Tubular carcinoma has a variety of presentations, but it is mostly seen on mammography as a small spiculated mass, and on sonography as an irregular mass with posterior acoustic shadowing. Although tubular carcinoma is known as a well-differentiated tumor with excellent prognosis, the mammographic follow-up of the contralateral breast is important.
OBJECTIVE: To evaluate existing models for the origin of meta- and synchronous urothelial carcinomas in light of the accumulated genetic data. METHODS: Published studies on the clonal origin and genetic relationships of syn- and metachronous tumors, genetic aberrations in normal and premalignant urothelial lesions, as well as histologic and genetic mapping studies of cystectomized bladder samples are reviewed. RESULTS: The most common models for the origin of syn- and metachronous tumors are found to conform less well to the accumulated genetic data. A new model is proposed, the field-first-tumor-later model, in which aberrant cells with a stem cell, or stem cell-like, origin spread in the urothelium by cellular displacement, creating fields of premalignant cells. Tumor growth is suggested to be initiated by critical genetic events occurring in individual cells in such fields. Hence, recurring tumors are proposed to originate from a shared field of premalignant cells and not from previous overt tumors. CONCLUSIONS: The proposed model can better account for the existing genetic and histological data on syn- and metachronous urothelial carcinomas.
We report the first case of a gliosarcoma arising from an anaplastic ependymoma and the second case of gliosarcoma arising from any type of ependymal neoplasm. The patient was a 48-year-old woman with a solid and cystic, peripherally enhancing, 7-cm right frontal mass lesion. Histologically, the lesion displayed characteristics of anaplastic ependymoma (grade III, World Health Organization scale). The tumor recurred despite multiple cycles of postoperative radiation and chemotherapy. After the fourth recurrence, the tumor displayed a biphasic pattern of differentiation. The first pattern was similar to the original anaplastic ependymoma, whereas there was a second new sarcomatous pattern resembling fibrosarcoma that was admixed with and overrunning the ependymal component. The spectrum of gliosarcoma is therefore expanded to include not only astrocytic and oligodendroglial components but ependymal components as well.
BACKGROUND: There is a high prevalence of skin cancer in World War II servicemen stationed in the Pacific theater as a result of various risk factors such as exposure to ultraviolet radiation and genetic predisposition. OBJECTIVE: We sought to describe whether a possible association exists between basal cell carcinoma (BCC) development and the use of high-voltage cathode ray tube (CRT) oscilloscopes manufactured around 1940 to 1955, which were a source of X-radiation. METHODS: We present a case series of 9 men aged 65 to 93 years who presented with similar head and neck distributions of BCC and a history of extensive use of early CRT oscilloscopes during and shortly after the World War II era. The patients were interviewed and their medical records reviewed to determine CRT exposure times and BCC location, subtype, and treatment. Representative BCC histologic sections were reviewed. RESULTS: A total of 230 BCCs of the head and neck region were identified and mapped. Questionnaires determined a minimum exposure of 600 (range, 624-9600) hours within a 60-cm distance of early CRT screens in all patients. The average number of aggressive histologic subtypes was 23.5%. The average number of Mohs micrographic surgery layers required to obtain negative margins was 1.99 compared with 1.63 in the control group treated by the same Mohs micrographic surgeon (P < .002). CONCLUSION: This descriptive study is the first to suggest that ionizing radiation from early CRT oscilloscopes may be a factor in the development of multiple BCCs of the head and neck with increased subclinical spread.