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Glutamate dehydrogenase activity was found to be present at a high level in neoplastic cytosol and microsomes, 3.45 and 9.90 nmoles NADH/min mg protein, respectively. This remains in accordance with the high rate of RNA and protein synthesis in the neoplastic process.
Eleven benign giant cell tumors of bone were studied in the electron microscope, and the fine structural localization of acid phosphatase was elucidated. Three distinct cell types are always present in these tumors: stromal cells type 1; stromal cells type 2; and multinucleated giant cells. Small mononuclear cells may also occur, but are not likely to be actively participating in the neoplastic process. The range of variability in the fine structure of the different cell types constituting this tumor has been established. Variations in appearances include: a) presence of nuclear pseudoinclusions in stromal cells type 1 and multinucleated giant cells; b) aberrations in the structure of the rough surfaced endoplasmic reticulum in the same cell types; c) occurrence of ruffled borders, ectoplasmic layers and cytoplasmic labyrinths containing acid phosphatase in the giant cells. Some giant cells show evidence of marked phagocytic activity and contain large and numerous residual bodies carrying acid phosphatase. The significance of the interrelations between the different cell types are discussed and the possible role of stromal cells type 2 in immunological mechanisms directed against the tumor cells are mentioned.
The authors report on a 43-year-old male with apparent myelomeningeal encephalitis. The most important clinical symptoms included severe lymphocytosis of the CSF, cranial nerve palsies, obstructive hydrocephalus, progressive coma, and presence of an intramedullary mass causing paraplegia. Neither CSF analysis, nor the intraoperative findings gave evidence of a neoplastic process. Regarding the paraclinical data we supposed a CNS inflammatory process, but autopsy revealed the diagnosis of an intraspinal, leptomeningeal gliomatosis.
Heat-induced inhibition of erythrocyte sedimentation (HIES) was examined in 158 cases. HIES is significantly lower in patients with a liver cell damage isolated or due to metastases of a neoplastic process in comparison to that in patients suffering from inflammation or malign tumor not involving the liver. Generally, HIES depends upon the concentration of lysophosphatidyl choline (lysolecithin) which is set free in plasma by lecithin-cholesterol-acyltransferase (LCAT) during incubation. In patients with lever cell damage, LCAT is diminished. HIES is being influenced by several factors: Lysophosphatidyl choline is bound to albumin, and this prevents its reaction on the erythrocyte surface. Lysophospholipase reduces the concentration of lysophosphatidyl choline in the plasma by splitting off its fatty acid in the alpha-position. Specific serum proteins, the so-called agglomerines, which are responsible for the acceleration of erythrocyte sedimentation, are counteracting the HIES. The concentration of albumin and agglomerines in plasma and the activity of lysophospholipase are subject to physiologically and pathologically caused deviations. Thereby, HIES is being influenced individually at varying degrees. This makes it difficult to estimate the LCAT activity which represents the principal cause of HIES. As a consequence, HIES seems not to be suitable for clinical diagnostics.
We investigated the clinicopathological findings in five cases of multicystic mesothelial proliferation (MMP). All masses consisted of multiloculated cysts attached to pelvic organs and sometimes growing into the upper abdominal cavity. The cystic spaces were lined by flattened or cuboidal cells. The stroma showed fibrosis, oedema and chronic inflammation. Immunohistochemistry revealed strong positive staining for cytokeratin and epithelial membrane antigen, and focal positivity for vimentin and carcinoembryonic antigen. The endothelial markers were negative. Electron microscopy showed abundant surface microvilli and well-developed basal lamina. DNA analysis identified euploid cell populations in all cases. All but one case had a previous history of abdominal surgery. Despite the worrying appearance the clinical outcome was favourable in all cases; there was one recurrence. Clinical and pathological data support the hypothesis that MMP represent a reactive mesothelial proliferation and not a neoplastic process.
Cecal diverticulitis is a rare entity and remains a difficult diagnostic problem. A retrospective review was undertaken of 16 patients (11 men, 5 women; average age, 33.2 years) with a pathologic diagnosis of cecal or right colon diverticulosis who received treatment from 1979 to the present. Preoperative symptoms were difficult to distinguish from appendicitis. The majority complained of right lower quadrant pain and tenderness. Diagnostic studies were not helpful. Preoperative diagnosis was appendicitis in 88% (14 of 16) and correct in 1 patient (6%). At exploratory celiotomy, the surgeon was able to make the diagnosis of cecal diverticulitis in 9 (60%) of the 15 patients in whom the correct diagnosis had not been made preoperatively. Neoplasm was suspected in 5 patients, and an appendiceal abscess was suspected in 1. Treatment was colectomy in 9 and local excision in 4 patients. In 3 patients, the inflamed diverticulum was left in situ at initial exploration; all underwent later excision, one of these urgently for sepsis. No patient died; however, one anastomotic leak requiring reoperation occurred. On the basis of this experience, we recommend excisional therapy in all cases in which the intraoperative diagnosis is certain. Suspicion of a neoplastic process continues to prompt colectomy in an emergency setting.
Among the multiple experimental animal models employed for analyzing the various aspects of mammary carcinogenesis, the induction of mammary tumors in rats by chemical carcinogens is one of the models most utilized. Experimentally-induced mammary tumors in rodents have proven to constitute useful tools for the study of the pathogenesis of cancer and of the molecular mechanisms involved in the initiation and progression of the neoplastic process. In vivo experimental animal models provide information not available in human populations; they are adequate for hazard identification, dose-response modeling, exposure assessment, and risk characterization, the four required steps for quantifying the estimated risk of cancer development associated with toxic chemical exposure. Using the DMBA rat mammary model, we have been able to demonstrate that the carcinogen acts on the intermediate cell of the terminal end bud (TEB), and that this structure is the one that evolves to intraductal proliferation, carcinoma in situ, and invasive carcinoma. There are several factors that regulate the susceptibility of the TEB; some of them are: a) topographic location of the mammary gland, b) age of the animal, and c) reproductive history. The understanding of the mechanisms that modulate tumorigenesis will further our knowledge and understanding in the prevention of the disease, as a result of the development of strategies for stopping the progression of the initiated cells.
Short-term cultures of tissue samples from three bilateral prophylactic mastectomies and one in situ ductal carcinoma from four women belonging to a family with hereditary breast cancer were cytogenetically analyzed. Clonal chromosome abnormalities were detected in five of the six prophylactically removed breasts, all of which had the histologic diagnosis epithelial hyperplasia without atypia, and in the in situ carcinoma. The same karyotypic imbalance, a loss of 3p12-14, was detected in the in situ carcinoma as well as in one of the hyperplasias, indicating that these bands may harbor a pathogenetically relevant gene in this breast cancer family. The finding of chromosome aberrations in clonal proportions in the prophylactically removed breasts indicates that a neoplastic process was already present, lending support to the view that prophylactic bilateral mastectomy in these high-risk individuals prevented the development of breast carcinoma.
With the advent of new gray scale imaging techniques, ultrasound plays a major role in the diagnosis of pancreatic lesions. As a noninvasive, nonionizing, accurate, and inexpensive diagnostic modality that directly images the pancreatic gland, ultrasound can be used as a primary screening tool. It is helpful in confirming the diagnosis of acute pancreatitis and in detecting and following pseudocysts and other complications. Neoplasms can be detected with a high rate of accuracy, and by assessing the presence of ascites or metastatic foci in the liver, ultrasound can aid in the staging of the neoplastic process. Bowel gas and obesity remain serious limitations to adequate examination, and in these patients computed tomography offers a complementary modality.
Ultrasound can define masses in the cecum and the cecal bed. In the patient with a prior resection of adenocarcinoma of the cecum, the sonogram fulfills a primary role in the detection of large and ill-defined recurrences not amenable to detection by barium enema because of a right colectomy. Discrete lesions within the cecum whether secondary to inflammatory or neoplastic processes could not be differentiated.
Individuals who are seropositive for the human immunodeficiency virus (HIV) frequently have disorders affecting the anorectum, yet little has been reported on this subject. We reviewed our initial experience with patients with HIV referred to the Division of Colon and Rectal Surgery. Forty patients (age range, 19-45 years; mean, 32.2 years) were seen between 1985 and 1989. The mean duration of symptoms was six months (range, one week to six years). In 25 patients (63 percent), more than one anorectal condition was identified. Condylomata were seen in 21 patients (52 percent), and in 11 these were associated with other pathologies. Fistulas and/or abscesses were identified in 15 patients (37 percent). Three had a "watering-can perineum," all without any identifiable predisposing factors. Nineteen patients had symptomatic hemorrhoids (seven), fissures (17), and/or perianal herpes infections (five), usually in combination with other lesions (89 percent). Three individuals developed neoplastic processes. Rectal disease was discovered in addition in nine patients. This included nonspecific proctitis in four, a rectal mass in four (polyps, two; rectal diverticulum, one; and Kaposi's sarcoma, one), and a nonspecific rectal ulcer in one. Four patients had other symptoms, including diarrhea, incontinence, soiling, frequency, and/or urgency, always in combination with other anal disorders. Seventy-one operative procedures were performed in 31 patients (78 percent). Only six (8 percent) of these were for diagnosis and biopsy alone. Mean follow-up was 15.5 months in the 23 patients followed for greater than one month. Only 6 of 23 (26 percent) had resolution of their problem. Nine (39 percent) developed new perianal conditions. Anorectal disorders are often seen in patients infected with HIV. They may be aggressive, cause significant morbidity, and be difficult to resolve.
The very common hyperplastic polyp is not a neoplasm and is unrelated to either adenoma or carcinoma. Adenomas, which are only one-tenth as common, are true neoplasms. Depending on size, and probably related to a sessile mode of growth, in adenomas one may readily observe intramucosal carcinoma and/or early invasive cancer. Although microscopic examination has been performed on many thousands of minute mucosal lesions (e.g., 5 mm or less), "early" cancer, defined cancer, defined as intramucosal carcinoma with or without microinvasion, does not seem to occur unassociated with adenoma. The apparent nonexistence of small foci of intramucosal carcinoma, with or without microinvasion, in normal mucosa, and their frequency in adenomas, are two fundamental pathologic facts. They seem to disprove the proposition that cancer calls ordinarily arise de novo from the normal cells of the crypt of Lieberkühn without the interposition of a stage in the neoplastic process that we recognize as adenoma.
Pathomorphological examination of large bronchi in patients with occupational diseases, lung cancer, and in subjects exposed to radiation revealed structural and functional heterogeneity of the epithelium: the presence of focal atrophy, metaplasia, hyper- and dysplasia in the same biopsy specimen. This phenomenon was termed as instability of the epithelium. Thickness of the epithelium greatly varied, especially, in neoplastic processes. Atrophy and epithelial instability phenomenon are interpreted as morphological markers of ecological and oncological risk.
Lumbar fusion is practicable by combined operations with dorso-ventral combined procedures. The indication is advisable following degenerative, inflammative, neoplastic processes and fractures of the spine. We operated 125 patients with combined procedures in 10 years. Beside dorsal instrumentation an intervention at the spinal canal is mostly necessary, only in 9 patients we preferred first the ventral part for the correction of a deformity. According to our experience the advantage for delayed dorso-ventral procedure is the preoperative blood donation, perioperative ferrum substitution and intraoperative cell saver system. In contrast to 1 combined procedure, most patients with 2 operations during the same hospital stay do not need homologous blood, the addition of time for 2 delayed procedures is shorter than for a single operation with intraoperative patient turn round in anesthesia, the convalescence was better, complications were seldom and hospital stay shorter. This comes out very clear in the group of lumbar degeneration in high age, who otherwise were bedridden for a long time following frequent complications.
Treatment of cultured HeLa cells with 5 mM sodium butyrate causes an inhibition of growth as well as extensive chemical and morphological differentiation. Lysosomal enzyme activity changes have been associated with both normal and neoplastic growth as well as many aspects of the neoplastic process. The comparative ultrastructural results show that the butyrate-treated cells have a more extensive internal membranous system than the untreated cells, whereas other organelles seem unaffected by the butyrate treatment. Methods for the histochemical localization of lysosomal acid phosphatase show a twofold increase in particulate reaction product in the butyrate-treated HeLa cells. Isolation of lysosomes followed by a comparative enzyme analysis shows a two to three fold increase in acid phosphatase activity per cell after 24 h of butyrate treatment, as well as three to four fold increase in beta-glucuronidase activity. These increases reverse within 24 h of removal of the butyrate from the culture medium. These results as interpreted suggest that butyrate treatment may be preventing sublethal autolysis by arresting the leakage of the lysosomal enzymes from the lysosome into the cytosol and thus allowing the cell to chemically and morphologically differentiate.
Tenascin (Tn) is an extracellular matrix (ECM) glycoprotein strongly and widely expressed during embryogenesis. Tn is decreased in normal adult tissues but is reexpressed in numerous inflammatory, reparative and neoplastic processes. We immunostained samples of fetal and normal adult bladders and samples of bladder tissue from patients with chronic cystitis, detrusor hypertrophy, malakoplakia and transitional cell carcinomas (TCC) of all grades, with a monoclonal antibody (mAb) to Tn 143DB7. Sections of flat in situ carcinomas were also studied. In fetal bladders, strong and ragged Tn reactions were noted at the epithelial-stromal interface; in normal adult bladders, the reaction was delicate and less extensive. In chronic cystitis, Tn reactivity was enhanced particularly around prominent capillary blood vessels. In flat in situ carcinomas, Tn staining was stronger and more extensive than in normal mucosa but was often less extensive than in some examples of cystitis. In TCC I and II, Tn immunoreactivity was strong and predominated in the pericapillary stroma of the papillae; in infiltrating TCC II, comparatively limited Tn staining was noted. In deeply infiltrating grade III TCC with abundant stroma, Tn reaction was invariably strong and extensive, particularly around advancing tumor nests. The strongest Tn reactions were noted in invasive, high-grade TCC with abundant stroma. We conclude that in inflammatory-reactive processes, and in in situ carcinomas as well as in TCC, the extent and intensity of the Tn reaction correlates with the severity of the inflammatory infiltrate and with the extent of the stromal remodelling.
This study examines the behavior of glycogen-storing rat hepatoma (N13) in vitro using cytophotometric techniques. A significant increase in glycogen is observed in these cells after 30 min incubation in a buffered solution containing 0.1 mM glucose, that is 80 times lower than the physiological glucose concentration in rat blood. N13 hepatoma cells grow exponentially in culture using RPMI 1640 tissue culture medium supplemented with 10% fetal bovine serum. During the first day in culture these cells store a large amount of glycogen and this increase is also observed in serum-free cultures. In more prolonged cultures the amount of glycogen per cell gradually becomes lower, although the culturing conditions are maintained. Similar variations of protein are also observed during the initial period of culture. DNA distribution does not show significant changes, although in serum-free cultures an increase in the proportion of cells in S and G2/M phases is observed. The addition of glucagon, epinephrine and cyclic AMP derivatives to serum-free cultures does not impede the storage of glycogen. Nevertheless, addition of either 2 mM N6,O2'-dibutyryl cyclic AMP or 0.1 mM 8-(4-chlorophenylthio)-cyclic AMP blocks the cell cycle at G0/G1 and glycogen content does not decrease after the first day in culture. We believe that this cell line offers an appropriated model to study glycogen metabolism and its involvement in the neoplastic process.
Histogenetic features of lung tumours were studied in Syrian hamsters that had been induced with 6.8 mg N-nitrosomethyl-n-heptylamine/animal by gavage once a week for 35 weeks. At intervals from experimental week 2 until week 46, pulmonary tissues from hamsters were examined by light and electron microscopy. This report describes early hyperplastic lesions associated with terminal bronchioles and the progression of these lesions to bronchioloalveolar tumours. Using immunohistochemical and ultrastructural colloidal gold labelling techniques, hamster Clara cell antigen was found to be localized in Clara cell granules and smooth endoplasmic reticulum of normal cells, in dysplastic Clara cells migrating through basement membrane defects or from the open end of terminal bronchioles, and in hyperplastic peribronchiolar cell foci. The latter progressed to bronchioloalveolar tumours growing out along alveolar basement membranes in a characteristic lace-like, lepidic pattern. Tumours were composed of secretory (Clara), ciliated, mucous, and undifferentiated cells, as well as trapped, non-neoplastic alveolar type II cells. Hyperplastic neuroendocrine cell foci lining airways were immunoreactive for chromogranin, but these cells did not participate in the pre-neoplastic or neoplastic process. It is suggested that bronchioloalveolar carcinomas in hamsters are derived from bronchiolar secretory (Clara) cells growing along alveolar walls, differentiating into other bronchiolar cell types and entrapping resident alveolar type II cells. Due to the migratory capacity of Clara cells, it is also possible for tumours composed of bronchiolar cells to develop at the lung periphery.