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This is a distinctly British textbook that will provide little competition to the three leading textbooks in the field of clinical oncology available in the United States. Although it is presented as a comprehensive and up-to-date text with the intent of providing authoritative help on how best to manage an individual patient, it is in fact neither comprehensive nor authoritative but provides instead superficial information that is frequently outdated or incomplete, and the treatment orientation is extraordinarily unbalanced in the direction of radiation therapy. The book is divided into three sections: "Principles," "Clinical Practice," and "Common Problems." Four of the 13 chapters in the first section are devoted to radiation therapy, reflecting the orientation of the whole text. The second section includes 25 chapters that are unbalanced with regard to comprehensive detail. For example, 20 pages are devoted to breast cancer, a common condition, and 42 pages are devoted to

There were two cases of fatal interstitial pneumonia secondary to bleomycin sulfate administration. Although bleomycin pulmonary toxicity is generally thought to be dose-related and occurs infrequently with a total cumulative dose less than 300 to 400 units, the two reactions reported here occurred with doses of 105 and 165 units. Fatal bleomycin-induced pneumonia has been previously reported at these low dosages, and physicians should be aware that this toxic reaction may occur as an idiosyncratic response. Previous thoracic irradiation may be a predisposing factor. Patients receiving bleomycin should be meticulously monitored by interrogation for cough, dyspnea, and chest pain; by auscultation for rales; by serial chest roentgenograms; and by determinations of vital capacity and single-breath carbon monoxide diffusing capacity. (JAMA235:1253-1255, 1976)

In Reply.— Dr. Davidson's comments are appropriate in that judicious venography can be performed safely in most patients. However, the major issue is whether venography contributes substantially to the diagnosis and potential treatment. Our position is that the diagnosis of SVCS is a clinical one, and that treatment is not determined in most circumstances by the venogram. Furthermore, the potential complication, which is primarily hemorrhage from the venapuncture site, though of a low order of incidence, does not justify routine venography. Dr. Johnston's comments with regard to a controlled trial of radiation therapy do not seem appropriate. Clearly, radiation therapy is an effective palliative measure in the majority of patients with SVCS, whether or not one demonstrates relief of venous obstruction objectively. Additional measures, such as fluid restriction and diuretic therapy, could and should be employed. However, these measures are clearly not focusing on the specific pathophysiology of the syndrome.

HYPERCALCEMIA with or without secondary clinical manifestations develops in up to 10% of patients with malignant disease—most commonly in patients with lung and breast cancer, but also in association with prostate cancer, multiple myeloma, and renal cell tumors. The development of hypercalcemia in malignant lymphomas of the Hodgkin's and non-Hodgkin's type is rare.1,2The mechanism of the hypercalcemia is not established, but may be associated with the ectopic secretion of a parathormone-like substance or other substances, such as prostaglandin or osteoclast-activating factor, that induce bone resorption. This report of a patient with malignant lymphoma and associated hypercalcemia 17 years following complete surgical parathyroidectomy indicates that the hypercalcemia is not mediated through the parathyroid axis involving endogenous parathormone. Report of a Case A 70-year-old woman was admitted to the New England Deaconess Hospital, Boston, for evaluation and treatment of hypercalcemia. In 1961, she had undergone total thyroidectomy for what was

† Superior vena cava syndrome (SVCS) is an acute or subacute oncologic emergency with typical clinical features. The syndrome is almost invariably secondary to a malignant process. The treatment of choice is irradiation, but in resistant cases or in those instances in which radiation tolerance is achieved, either surgery or chemotherapy, or both, may play a crucial role. The major pitfalls in management relate to attempts to establish the site of obstruction and to obtain specific tissue diagnosis. ( JAMA 231:58-61, 1975)

Central nervous system (CNS) metastases are a common clinical problem, and management spans the three major therapeutic disciplines in oncology. Surgery, radiotherapy, and chemotherapy are employed alone, in combination, or sequentially and are based on four local factors—the number, size, site, and depth of the lesions; and three tumor factors—the natural or biologic history of the primary tumor, the quantitative host tumor burden, and the tumor responsiveness to individual therapeutic modalities. The median survival of patients with CNS metastasis is 3 to 12 months and is not necessarily compromised by the CNS lesions, if the diagnosis is established and therapy promptly instituted. (JAMA234:748-751, 1975)

Of all the mysteries of cancer biology, surely the role of hormones in treatment is one of the most complex and intriguing enigmas. In almost a century since oophorectomy was first used for the treatment of advanced breast cancer, we have developed an enormous background of observation with little understanding of the process. In the last decade, the identification of receptor proteins has generated the capacity to study biologic events at the cellular level, and new agents, specifically the antiestrogens and adrenal blockers, have changed the hormonal management of cancer for the first time in three decades or more. These developments have prompted Basil Stoll to develop a second-generation text from that previously published in 1972,Endocrine Therapy in Malignant Disease. The need for a comprehensive text on endocrine aspects of malignancy has been obvious, and the vacuum has existed in part because of our ignorance but also because of

MESOTHELIOMA is primarily an occupational disease of asbestos workers, but the neoplasm may also develop after intense exposure to asbestos outside the workplace. 1 This report of pleural mesotheliomas in the wife and a daughter of an asbestos handler suggests that gross asbestos contamination of the home can be a serious health hazard. Report of Cases Patient 1 (Figure), the father, worked as a pipe insulator at a shipyard for approximately 25 years (1940 to 1965). Pulmonary asbestosis was diagnosed at age 60 years in 1966. He also smoked one to two packs of cigarettes daily for several decades. In 1977, metastatic adenocarcinoma in the left upper lobe of the lung developed and the patient died. Findings from an autopsy demonstrated severe pulmonary asbestosis and lung cancer. Patient 2, the mother, was in good health until a right pleural effusion developed in 1967 at age 50 years. A right thoracotomy

Six of 18 patients with sarcomatous tumors metastatic to the lung had hypertrophic pulmonary osteoarthropathy (HPO), and, in three patients in whom tumor regression was achieved by cytotoxic chemotherapy or surgery, the clinical and radiologic changes of HPO were reversed. All six patients had large mass lesions (greater than 5 cm) that impinged on the pleural surface, and the pathophysiologic mechanism resulting in the clinical syndrome of HPO may be related to the anatomic relationship of the tumor and the pleura. The use of radionuclide scanning to detect HPO in the absence of roentgenographic signs or clinical symptoms is discussed. (JAMA238:37-39, 1977)

Nephrotic syndrome in association with Hodgkin disease may be caused by the deposition of immune complexes within the kidney. A patient with Hodgkin disease is reported in whom the nephrotic syndrome developed. Immunoglobulin deposits and electron-dense accumulations were demonstrated in the glomerular basement membranes. A clinical remission was achieved with therapy that was specifically directed at the Hodgkin disease. The hypothesis is proposed that Hodgkin disease tumor-specific antigens may compose a portion of the deposited immune complexes.

The accumulation of fluid in the potential space between serosal membranes may develop in 5% to 50% of patients with disseminated malignant disease.1Malignant pericardial effusion is particularly important because of its insidious clinical expression and the life-threatening potential of cardiac tamponade. Two mechanisms for the production of pericardial effusion that have been suggested are (1) tumor implantation on serosal surfaces leading to exudation of fluid, and (2) obstruction to lymphatic flow by mediastinal or hilar neoplastic infiltration causing transudation of fluid within the pericardial sac.2In the experimental model, lymph flow proceeds from the endocardial to the epicardial surface, and pericardial effusion is an accumulation of fluid exuding from the visceral pericardium (epicardium). Mere obstruction of the mediastinal lymphatic system draining the heart is inadequate to produce pericardial effusion, and additional ligation of the coronary sinus and the anterior coronary veins is essential. These studies have two