Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Obstructing carcinoma of the left side of the colon causes proximal distension of the colon with subsequent thinning of the colonic wall and vascular impairment. Conventional surgical treatment is multi-staged. Each stage carries its own morbidity and mortality. An alternate treatment, extended right hemicolectomy, requires a single surgical procedure. Fifty-six cases of acute obstructing carcinoma of the left colon are presented: 16 in Group I were treated conventionally; 40 in Group II were treated by extended right hemicolectomy. In Group I, four died within one week of surgery. Six survived with a colostomy; all suffered from poor quality of life until death. For the six who received complete treatment, average total hospitalization was 54 days. Group II suffered no peri-operative mortality. Patients were discharged without a colostomy after an average hospitalization of 15.7 days. Advantages of and conditions for treatment by extended right hemicolectomy are discussed.
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PMID:Obstructing carcinoma of the left colon: treatment by extended right hemicolectomy. 193 4

An experimental study of bladder tolerance to intraoperative radiotherapy (IORT) was designed using a large animal model (adult American Foxhounds, weight 25-30 kg) to access acute and late radiation effects. Dogs were subjected to laparotomy where the bladder was mobilized and IORT was delivered using a 5 cm circular cone through a cystotomy incision with 12 MeV electrons. The bladder trigone including both ureteral orifices and the proximal urethra was irradiated in groups of 3 dogs with doses of 0, 20, 25, 30, 35, and 40 Gy. Dogs were followed clinically with repeat urinalysis, intravenous pyelogram (IVP), and cystometrogram at 1 month and then Q6 months for up to 4 years. One dog from each dose group was sacrificed electively at 1 and 2 years, whereas the other dog is being followed clinically for a minimum of 4 years. Complete autopsies were performed with particular attention to genitourinary and pelvic structures. No clinically detectable acute toxicity resulted from IORT to the bladder. Three of 15 IORT dogs (1 each at 25, 35, and 40 Gy) showed obstruction of a ureteral orifice with 2 dogs dying of renal failure secondary to bilateral hydronephrosis within 1-2 years of treatment. The remaining 12 IORT dogs and 3 control dogs have normal repeat IVP's and renal function with up to 4 years of follow-up. Serial cystometry demonstrates no major loss of bladder contractility or volume. At autopsy, histological changes of mucosal thinning and telangiectasia with submucosal fibrosis were confined to the IORT field and appeared dose-related. However, the bladder epithelium remained intact at all doses. The ureterovesical junction in animals receiving 20 Gy showed mild fibrosis of the lamina propria and moderate chronic inflammation. Above 20 Gy, these histological changes at the U-V junction were more pronounced with gross stenosis in 3 animals as predicted by the IVP. We conclude that the bladder trigone will tolerate IORT to 20 Gy without major clinical sequellae. Above 20 Gy, progressive inflammation and fibrosis of the U-V junction resulted in obstructive hydronephrosis in three animals within 1-2 years of IORT. The bladder mucosa remained intact with doses to 40 Gy, although submucosal fibrosis and chronic inflammation were evident and appeared dose-related. However, bladder function as measured by cystometry showed essentially no change with follow-up to 4 years. From this large animal study, IORT for early-stage bladder carcinoma is technically feasible and deserves a careful clinical study.
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PMID:Tolerance of the canine bladder to intraoperative radiation therapy: an experimental study. 312 84

Highly purified antibodies to two ubiquitous components of basement membrane, type IV collagen and laminin, were applied to both fresh-frozen and formalin-fixed tissue sections of a variety of invasive carcinomas, carcinomas in situ, and their "look-alike" benign counterparts. These included lesions of the breast (infiltrating ductal carcinoma, comedocarcinoma, and sclerosing adenosis); lesions of the skin (squamous cell carcinoma, Bowen's disease, and pseudoepitheliomatous hyperplasia); lesions of the pancreas (adenocarcinoma and pancreatitis); lesions of the prostate (adenocarcinoma and benign prostatic hyperplasia); and other epithelial lesions of the invasive, in situ, and benign category. By both immunofluorescence and immunoperoxidase techniques, benign and in situ lesions showed intact basement membranes with linear staining of type IV collagen and laminin. The majority of invasive carcinomas, in contrast, lacked immunoreactivity for both of these basement membrane components. In cases of in situ carcinoma with microinvasion, there was thinning, fragmentation, and disruption of the basement membrane in the foci of microinvasion but not elsewhere. Utilizing antibodies to type IV collagen and laminin aids in both understanding the pathophysiology of the invasive process and the recognition of its presence in tissue sections.
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PMID:Loss of basement membrane components by invasive tumors but not by their benign counterparts. 634 6

Upon autopsy of a 67-year-old male who died of recurrence and metastasis from a carcinoma of the colon, early esophageal carcinoma was found. Diffuse slight thickening and longitudinal linear thinning with brownish discoloration were found in the esophageal mucosa. Upon microscopical examination, the esophageal epithelium showed mild dysplasia, severe dysplasia or intramucosal carcinoma. A diagram of the distribution of these lesions indicated that the carcinoma arose multicentrically in the lower two-third of the esophagus and always within, or adjacent to, the area of severe dysplasia.
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PMID:[A case with intramucosal carcinoma of the esophagus in widely expanding dysplasia--an autopsy case with simultaneous double-cancer of the esophagus and sigmoid colon]. 647 98

Clinical staging is often inaccurate in the evaluation of local extension of cervical carcinoma. In the present study the sensivity of MR imaging in predicting extracervical tumor invasion on the basis of the detection of a thinning of the univolved cervical stromal ring (3 mm or less) was compared to the sensivity achieved by direct visualization of a complete stomal interruption. Fifteen consecutive patients with adenocarcinoma of the uterine cervix (FIGO stage Ib-IIa), were examined with axial and sagittal weighed MR sequences. Pathologic proof after hysterectomy was obtained in all subjects. The sensitivity in predicting extracervical involvement on the basis of the MR Imaging visualization of a thinned stroma was 83%, whereas the sensitivity obtained by detection of a complete stromal interruption was 50%. Among women with a spared cervical stroma of more than 3 mm at MR Imaging, only one had at pathologic examination microscopic metastasis in a parametrial lymphnode, accounting for a negative predictivity value of 87%. The results of our study points out a high concordance between MR Imaging findings and pathologic results, and indicate that the detection of a intact cervical stromal ring exceeding 3 mm at MR imaging is related to a very low risk of extracervical seeding of tumor. On the other side, the detection of a thinned stromal ring is related to a high incidence of parametrial invasion. The information obtained by this imaging technique may therefore be extremely useful in the accurate tailoring of treatment for these patients.
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PMID:[Nuclear Magnetic Resonance Imaging in the staging of adenocarcinoma of the uterine cervix]. 872 Sep 72

A 63-year-old woman with abnormal Q waves in leads II, III, aVF developed ventricular tachycardia after an operation for thyroid carcinoma. Coronary arteriography revealed no organic stenosis, but acetylcholine induced total occlusion of the right coronary artery and severe narrowing of the left coronary artery. Left ventriculography showed inferoposterior and septal akinesis, and echocardiography revealed slight thinning of these affected walls. She had old myocardial infarction due to spasm. One year later, she developed bilateral uveitis and recurrence of tachycardia. Cardiac sarcoidosis was diagnosed by endomyocardial biopsy. In our patient with cardiac sarcoidosis, the presence of multivessel coronary spasm made the diagnosis difficult and may have contributed to cardiac dysfunction. Coronary arteries are rarely involved, but the development of coronary spasm may be linked to sarcoidosis.
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PMID:[Cardiac sarcoidosis complicated by multivessel coronary spasm: a case report]. 1046 90

Skin cancer is the most commonly occurring cancer in humans. Solar keratoses are related benign tumours that are at least ten times commoner than skin cancers and photoageing of the skin is still more common. Descriptive studies show that incidence rates of the main types of skin cancer, basal cell carcinoma, squamous cell carcinoma and melanoma are maximal in populations in which ambient sun exposure is high and skin (epidermal) transmission of solar radiation is high, suggesting strong associations with sun exposure. Analytic epidemiological studies confirm that exposure to the UV component of sunlight is the major environmental determinant of skin cancers and associated skin conditions and evidence of a causal association between cumulative sun exposure and SCC, solar keratoses and photodamage is relatively straightforward. Results for BCC and melanoma are complicated by several factors including the existence of subgroups of these diseases which do not appear to be caused by sun exposure yet have been included in most aetiological studies to date. Complementary to epidemiological data is the molecular evidence of ultraviolet (UV) mechanisms of carcinogenesis such as UV-specific mutations in the DNA of tumour suppressor genes in skin tumours. With increased UV irradiation resulting from thinning of the ozone layer, skin cancer incidence rates have been predicted to increase in the future--unless, as is hoped, human behaviour to reduce sun exposure can offset these predicted rises.
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PMID:Sun exposure, skin cancers and related skin conditions. 1070 45

To clarify the clinicopathological features of an atypical cystic duct (ACD) as defined by Tsuchiya's criteria as a precancerous lesion of the breast, we used 200 whole mammary gland serial sections of breast cancer. Forty-four (22%) of the 200 breast cancer patients had ACD breast lesions. The frequency of patients with ACD increased in premenopausal women (P = 0.001). There was no correlation between the ACD-present group and the ACD-absent group for immunohistochemical status of the estrogen receptor (ER), progesterone receptor (PgR), p53, or c-erbB2; Ki-67 labeling index of cancer tissues; size of tumor, or lymph node metastases. A number of ACD lesions displayed continuity to cancer lesions. In 500 serial sections of a paraffin-embedded tissue of a ACD case at 3 microm intervals, an apparent transition from ACD into ductal carcinoma in situ was observed. Immunohistochemical analysis using alpha-smooth muscle actin showed that myoepithelial cells of ACD stained strongly, and their nuclei and cytoplasm were thinning. In 16 of the 44 (36%) ACD-present patients, carcinoma cells stained positive for p53. Within those 16 cases, 12 cases (75%) were positive for p53 in ACD lesions. There was a significant correlation between the expression of p53 protein in malignant cells and ACD (P = 0.001). All 44 ACD lesions had no staining of c-erbB2, regardless of staining in malignant lesions. The mean Ki-67 labeling index of ACD lesions was low (0.3%), suggesting that ACD had a low proliferative rate. We suggest that ACD is the precancerous breast lesion because of a histologic continuum between ACD and malignancy, and because of p53 protein expression in ACD.
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PMID:Clinicopathological characteristics of atypical cystic duct (ACD) of the breast: assessment of ACD as a precancerous lesion. 1110 51

Bone is one of the most common sites of breast cancer metastasis. Metastases are often associated with bone destruction and are a major cause of morbidity. We examined structural bone changes induced by metastatic tumor in bone biopsies from 33 patients with metastatic breast carcinoma (20 from patients with pathological femoral fracture and 13 with no fracture) and 20 normal controls. In all metastatic biopsies bone remodeling was shown to be tumor volume-dependent. Bone resorption and bone formation were biphasic with both increasing at earlier stages of metastatic bone disease and decreasing later on. A comparison of patients with fracture and no fracture did not reveal statistically significant differences in the extent of bone destruction or trabecular thinning. Bone histomorphometry showed limited ability to explain the higher bone volume loss in fracture patients (decreases of 42% and 25%, respectively, in fracture and nonfracture patients compared with controls). However, changes in bone quality, including increased disconnectivity and decreased connectivity, as evaluated by node-strut analysis, suggested that there were more structural changes in the fracture compared with the nonfracture group. The nonfracture group included six patients with no radiological evidence of bone metastasis (occult metastasis). They showed a higher tumor volume and a twofold lower eroded surface compared with the rest of the group. The decrease in bone volume (14% lower than controls) was below the limit of X-ray detection. Because we observed no increase in osteoclast-related parameters and no correlation between osteoclast surface and eroded surface, we believe that, in occult metastasis, osteoclastic bone resorption is not an important factor in overall bone resorption. Quantitatively, the eroded surface in direct contact with tumor cells was threefold higher than the osteoclast surface in occult metastasis, whereas the rest of the metastatic group (27 of 33) showed predominantly osteoclast-mediated eroded surface. Node-strut analysis on occult metastasis revealed a significant increase in disconnectivity without a concomitant significant decrease in bone volume and trabecular thinning. We conclude that, in occult metastasis, bone resorption may be more osteoclast-independent and other mechanisms involving the tumor cells may be more prevalent.
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PMID:Morphological, histomorphometric, and microstructural alterations in human bone metastasis from breast carcinoma. 1239 51

The carcinogenic potential of muraglitazar, a dual human peroxisome proliferator-activated receptor alpha/gamma agonist, was evaluated in 2-year studies in mice (1, 5, 20, and 40 mg/kg) and rats (1, 5, 30, and 50 mg/kg). Benign gallbladder adenomas occurred at low incidences in male mice at 20 and 40 mg/kg (area under the curve [AUC] exposures > or = 62 times human exposure at 5 mg/day) and were considered drug related due to an increased incidence of gallbladder mucosal hyperplasia at these doses. There was a dose-related increased incidence of transitional cell papilloma and carcinoma of the urinary bladder in male rats at 5, 30, and 50 mg/kg (AUC exposures > or = 8 times human exposure at 5 mg/day). At 30 and 50 mg/kg, the urinary bladder tumors were accompanied by evidence of increased urine solids. Subsequent investigative studies established that the urinary bladder carcinogenic effect was mediated by urolithiasis rather than a direct pharmacologic effect on urothelium. Incidences of subcutaneous liposarcoma in male rats and subcutaneous lipoma in female rats were increased at 50 mg/kg (AUC exposures > or = 48 times human exposure at 5 mg/day) and attributed, in part, to persistent pharmacologic stimulation of preadipocytes. Toxicologically relevant nonneoplastic changes in target tissues included thinning of cortical bone in mice and hyperplastic and metaplastic adipocyte changes in mice and rats. Considering that muraglitazar is nongenotoxic, the observed tumorigenic effects in mice and rats have no established clinical relevance since they occurred at either clinically nonrelevant exposures (gallbladder and adipose tumors) or by a species-specific mechanism (urinary bladder tumors).
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PMID:Rodent carcinogenicity profile of the antidiabetic dual PPAR alpha and gamma agonist muraglitazar. 1742 6


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