Pediatric brain tumors

Pediatric brain tumors differ from adult brain tumors in several major ways. First, the types of tumors encountered in children are uncommon in adults, and vice versa. Second, tumors of the posterior fossa comprise a far greater percentage of tumors in children as compared to adults. Third, the value of extensive tumor resection, which is controversial for malignant brain tumors in adults, has been confirmed for a variety of childhood brain tumors. Fourth, chemotherapy has been shown to be effective in improving overall outcome in several childhood brain tumors, but has yet to be demonstrated to have a major benefit for adult tumors. In addition, to avoid the morbidity of irradiation on the developing nervous system, chemotherapy is increasingly used to delay or avoid using radiotherapy in children younger than 3 years of age with high-grade and incompletely resected low-grade tumors. Fifth, the prognosis for histologically similar tumors is often more favorable in children than adults. A review of general principles in the clinical presentation, diagnostic evaluation, and treatment of childhood brain tumors is followed by discussion of surgical management, adjuvant therapy, and outcome of the more common types of tumors.     

Pressor effects elicited by stimulation within the medullary raphe nuclei of the guinea pig (Cavia porcellus)

A series of 120 pathologically verified intraspinal tumors was analyzed for the relative incidence and location of the tumors as well as the distribution of age and sex. These data were compared to series from Taiwan, mainland China, Thailand, Korea, Japan, Iran, India, and countries in the West. The ratio of brain to intraspinal tumors was about 5:1 in Taiwan, higher than those reported in China, Korea, and in the West. The male to female ratio is about six to five. For most tumors, male predominance is noted except for meningioma. The incidence of intraspinal tumors in the order of frequency is nerve sheath cell tumor(NSCT), metastatic tumors, meningioma, glioma, congenital tumors, and vascular tumors. In the East, the incidence of NSCT is about 40%, and meningioma is about 10%. In the West, they are both about 20%. Congenital tumors accounted for only 3.3%. In China, it was about 12% and this is the highest incidence of dysembryoplastic tumors in the world. Glioma has similar incidence (about 10%) in Taiwan, China, Thailand, Japan, and Iran (about 10%), whereas it is about 15% in the West and India. Korea has the highest incidence of glioma, (32.3%). Low incidences of metastatic intraspinal tumors (4.6-5.5%) were noted in China and Japan, but a higher incidence (14.2-24.2%) was seen in Taiwan, Iran, and the West. The most common metastatic tumors in the order of frequency is tumors of unknown origin, lung cancer metastasis, hepatoma, and breast cancer. The high percentage of unknown origin of metastasis may have resulted from loss of follow-up and lack of postmortem studies.     

Inhibin A is a sensitive and specific marker for testicular sex cord-stromal tumors

We compared the expression of inhibin A, chromogranin, synaptophysin, S-100 protein, cytokeratins AE1/AE3, 7, and 20, and estrogen and progesterone receptors in testicular sex cord-stromal tumors: 11 Sertoli cell tumors, 3 Sertoli cell adenomas (nodules), 26 benign Leydig cell tumors, 7 malignant Leydig cell tumors (defined clinically by metastatic behavior), and a variety of germ cell tumors. Inhibin was the most sensitive marker, expressed in 91% of the Sertoli cell tumors and 100% of the Sertoli cell adenomas and Leydig cell tumors. The non-neoplastic Sertoli and Leydig cells invariably stained for inhibin. Conversely, no germ cell tumors were immunoreactive. One testicular tumor of the adrenogenital syndrome was immunoreactive. Neuroendocrine marker immunoreactivity was variable. Chromogranin was expressed in the non-neoplastic Sertoli and Leydig cells, 82% of the Sertoli cell tumors, 92% of the benign Leydig cell tumors, and 43% of the malignant Leydig cell tumors. Synaptophysin was expressed in the non-neoplastic Sertoli and Leydig cells, 45% of the Sertoll cell tumors, and 70% of the Leydig cell tumors, in approximately similar proportions between the benign and malignant Leydig cell tumors. S-100 protein was expressed in 64% of the Sertoli cell tumors, 8% of the benign Leydig cell tumors, and none of the malignant Leydig cell tumors. Cytokeratins AE1/AE3 were expressed in 64% of the Sertoli cell tumors and 42% of the Leydig cell tumors, with similar proportions in the benign and malignant cases. Estrogen and progesterone receptor expression were identified in 24 and 39% of benign and malignant Leydig cell tumors, respectively. We conclude that inhibin is a characteristic marker for Sertoli and Leydig cells and that it serves to differentiate testicular sex cord-stromal tumors from germ cell tumors.     

Mutation of the MENIN gene in sporadic pancreatic endocrine tumors

Pancreatic endocrine tumors occur both sporadically and as part of the multiple endocrine neoplasia type 1 (MEN1) syndrome. MEN1 is an autosomal dominant disease characterized by parathyroid hyperplasia, pancreatic endocrine tumors, and pituitary adenomas. The MEN1 gene called MENIN maps to chromosome 11q13 and is thought to function as a tumor suppressor gene. We previously demonstrated loss of heterozygosity (LOH) at 11q13 in approximately 40% of sporadic pancreatic endocrine tumors and hypothesize that MENIN is involved in the development of these tumors. Thirty-one sporadic pancreatic endocrine tumors were analyzed for mutation of MENIN by nonradioactive single-stranded conformation polymorphism. Twelve mutations were detected in 31 sporadic pancreatic endocrine tumors (34%). Twelve of these 31 tumors previously demonstrated loss of heterozygosity at 11q13. Of the tumors with LOH, seven contained mutations of the MENIN gene (58%). The majority of the MENIN mutations occurred within exon 2. Two independent mutations in MENIN were detected in a gastrinoma that also revealed LOH, leading to the possibility of another tumor suppressor gene locus at 11q13. Mutations were present in both benign and malignant pancreatic endocrine tumors, suggesting that a MENIN gene mutation is a frequent and early event in the tumorigenesis. The high incidence of truncating mutations in tumors with LOH at 11q13 support the hypothesis that MENIN is a tumor suppressor gene.     

Amyloid in polypeptide hormone-producing tumors

The hormone content of 72 endocrine tumors was determined by immunofluorescence and their amyloid content was investigated. Seventeen of the 72 tumors contained amyloid. Amyloid was frequently found in tumors producing calcitonin, insulin, or growth hormone, but was rarely found in other tumors. Thus, there is a relationship between the occurrence of amyloid in an endocrine tumor and the type of hormone it produces. The reason for this is not known, but there is evidence that the amyloid fibrils contain proteins related to the hormone produced by the tumors.     

Inhibin expression in ovarian tumors and tumor-like lesions: an immunohistochemical study

We investigated 203 ovarian tumors and tumor-like lesions for inhibin expression using a monoclonal anti-inhibin alpha antibody. Inhibin was present in the tumor cells in all 14 primary adult granulosa cell tumors (4 luteinized) plus 3 metastatic, all 10 primary juvenile granulosa cell tumors plus 1 metastatic, 10 of 11 thecomas, 3 of 11 fibromas, 4 of 11 sclerosing stromal tumors, 6 of 11 Sertoli cell tumors (1 oxyphilic), 7 of 11 Sertoli-Leydig cell tumors, 1 gynandroblastoma, 10 primary ovarian sex cord tumors with annular tubules plus 2 metastatic, 8 of 9 steroid cell tumors, both pregnancy luteomas, 1 of 2 unclassified sex cord tumors, 2 of 5 gonadoblastomas, 9 of 10 female adnexal tumors of probable wolffian origin, and in the non-neoplastic stroma of many carcinomas and germ cell tumors. The tumor cells were inhibin-negative in 10 fibrosarcomas, 12 small cell carcinomas of hypercalcemic type, 24 germ cell tumors (except for a focus of inhibin-positive syncytiotrophoblast in one case), and 17 ovarian carcinomas. Two of the three inhibin-positive fibromas showed diffuse immunostaining and were associated with evidence of estrogenic activity. Among nine Sertoli-Leydig cell tumors with available clinical data, four that were more than minimally inhibin-positive were accompanied by androgenic manifestations; five inhibin-negative or only minimally positive tumors lacked such evidence. Inhibin immunostaining may be useful in the differential diagnosis of inhibin-positive sex cord tumors versus histologically similar inhibin-negative neoplasms, but inhibin negativity does not preclude a diagnosis of sex cord tumor. The unexpected, common inhibin positivity of female adnexal tumors of probable wolffian origin indicates that inhibin staining cannot be used to differentiate these tumors from Sertoli cell tumors. Inhibin immunostaining is also helpful in identifying potential steroid hormone-secreting cells in the non-neoplastic stromal component of epithelial, germ cell, and other ovarian tumors.     

Immunohistologic analysis of gastrointestinal and pulmonary carcinoid tumors

Carcinoid tumors are potentially malignant neoplasms that arise in various body sites, including the lung and gastrointestinal tract. Those that appear cytologically atypical are more likely to behave aggressively than more typical carcinoid tumors. However, in the absence of cytological atypia or large tumor size, it is difficult to predict the biology of an individual tumor, because some lesions metastasize, whereas others do not. This study had four aims: (1) To study the expression pattern of p53, Ki-67, NCAM, and S-100 in carcinoid tumors and to relate these expression patterns to classical histopathologic features and to tumor location. (2) To identify nonhistological markers that might more accurately predict the early behavior of carcinoid tumors. (3) To determine whether sustentacular cells are present in carcinoid tumors arising in tissues derived from different embryological derivatives. (4) To determine the synaptophysin and chromogranin immunoreactivity in neuroendocrine tumors arising in various locations. The immunostaining reactions were quantitatively scored by three observers. Only 3 of the 39 tumors (all histologically atypical) were strongly positive for Ki-67; two of these were also strongly p53 immunoreactive. NCAM immunostaining differed according to the site of origin: 76.5% of foregut lesions, 58% of the midgut lesions, and 20% of hindgut lesions were positive. S-100 immunostaining ranged from 41% in foregut lesions to 50% in both the hindgut- and midgut-derived tumors. S-100-positive sustentacular cells were present in 20.5% of carcinoid tumors. All tumors stained with antibodies against synaptophysin. In contrast, 100% of midgut, 60% of hindgut, and 88% of foregut tumors were chromogranin positive. Carcinoid tumors tend to have low proliferative rates. p53 immunostaining tends to be strongly positive in tumors that are histologically atypical, but it is negative in typical carcinoid tumors arising in the gastrointestinal tract and lungs. Immunostaining reactions with antibodies to NCAM, S-100, and chromogranin differ depending on the site of origin. Synaptophysin stains 100% of carcinoid tumors regardless of their site of origin. In contrast, antibodies to chromogranin fail to stain 40% of hindgut tumors and 12% of foregut carcinoid tumors. S-100-positive sustentacular cells are present in foregut and midgut tumors but not in hindgut tumors.     

Anti-macrophage monoclonal antibody D-11 in the diagnosis of histiocytic tumors

Anti-macrophage monoclonal antibody (Mab) D-11 was tested in surgical material and biopsies of non-epithelial tumors and tumor-like lesions from 181 patients in order to assess possibility of using this Mab for diagnosis of histiocytic tumors, malignant fibrous histiocytoma in particular. The study was performed in parallel on cryostat sections and smears by immuno-peroxidase method. It is established that D-11 reacts positively with both histiocytic tumors and tumors of other genesis this being a limiting factor in differential diagnosis of histiocytic tumors. However, taking into consideration 100% of positive results with histiocytic tumors only, this antibody can be used for exclusion of tumors studied from the group of histiocytomas in cases of negative reaction.     

Pediatric liver tumors

An infant or child who presents with a large intrahepatic mass will most likely have a malignant tumor. In children, benign tumors constitute only 30% of liver tumors and most are vascular in origin. Treatment of benign vascular tumors is conservative and seldom surgical. Hepatoblastoma is the most common malignant tumor followed by hepatocellular carcinoma. Treatment of malignant tumors is based on a combination of surgery and chemotherapy. Children with hepatic malignancies that can be resected have an excellent prognosis. Other rare benign and malignant tumors of the liver do occur and surgery plays a critical role in management.     

Fetal welfare: midwives'' perspectives in Australia

The potential NMR-tomography in detecting and staging of renal carcinoma was elucidated in a group of 41 patients with 42 renal tumors. The diagnosis was verified intraoperatively (34 patients) or at autopsy (7 patients). NMR discovered 41 tumors of 42 (98% all 36 tumors of 3 cm in a diameter and of larger size, visualized 5 of 6 tumors less than 3 cm in size. Staging was possible in 85% of all the lesions. Four cases were overestimated in terms of stage, 2 cases underestimated. NMR-tomography is not perfect as a screening test for renal tumors because in small tumors its sensitivity is limited, but it may provide additional to TC information and is able to clarify doubtful cases, is useful in patients with iodine contrast media intolerance, in those with chronic renal insufficiency, pronounced tumor invasion and in deciding on the variant of surgical intervention.     

Immunoreactivity and expression of amylin in gastroenteropancreatic endocrine tumors

Amylin was isolated from human insulinomas, but there has been only preliminary data regarding whether this peptide can also be detected in other types of gastroenteropancreatic endocrine tumors. In the present study, immunohistochemical staining of 87 gastroenteropancreatic endocrine tumors demonstrated amylin immunoreactivity in 21.8% of the neoplasmas. Thirteen of 15 insulinomas, three of 21 gastrinomas, two of 29 nonfunctioning tumors, and one of 18 carcinoids were amylin-immunoreactive. Seventeen of the 19 amylin-immunoreactive tumors were primarily located in the pancreas, but two tumors were found in the intestine. Measurements of amylin messenger RNA expression in a few tumors revealed amylin synthesis in these tumors. Amylin immunoreactivity did not correlate with invasion and metastasis. However, the rate of curative resections was significantly higher in amylin-immunoreactive tumors. These results demonstrate for the first time that amylin immunoreactivity is not restricted to insulinomas and can also occur rarely in endocrine tumors of the intestine.     

Tumor selective delivery of 5-fluorouracil by capecitabine, a new oral fluoropyrimidine carbamate, in human cancer xenografts

Capecitabine (N4-pentyloxycarbonyl-5'-deoxy-5-fluorocytidine) is a novel fluoropyrimidine carbamate that is converted to 5-fluorouracil (5-FUra) by three enzymes located in the liver and tumors; the final step is the conversion of 5'-deoxy-5-fluorouridine (5'-dFUrd) to 5-FUra by thymidine phosphorylase in tumors. The present study compared the efficacy of capecitabine and 5-FUra at their maximum tolerated doses in CXF280, HCT116, COLO205, and WiDr human colon cancer xenograft models, and measured subsequent 5-FUra and 5'-dFUrd levels in tumors and in the plasma and muscle. Capecitabine was effective in the first three models, whereas 5-FUra was effective only in CXF280, which is a cell line highly susceptible to fluoropyrimidines. In the three susceptible models, 5-FUra AUCs in tumors after capecitabine administration were 210 to 303 nmol x hr/g, whereas those after 5-FUra administration were 8.54 to 13.1 nmol x hr/g. In addition, capecitabine gave higher levels of 5-FUra AUC in tumors than in plasma (114- to 209-fold higher) and muscle (21.6-fold higher), whereas 5-FUra was not selectively distributed to tumors. In the refractory model, WiDr, 5-FUra AUC in tumors after capecitabine administration was only 62.8 nmol x hr/g, although the level of the intermediate metabolite 5'-dFUrd was high (AUC: 695 nmol x hr/g). The ratio of 5-FUra/5'-dFUrd levels in the WiDr tumors was 0.09, which was 23.8-fold lower than that in the HCT116 tumors. The mechanism of resistance would be the inefficient conversion of 5'-dFUrd to 5-FUra by thymidine phosphorylase in tumors. Thus, capecitabine might show its high efficacy as a result of delivering high levels of 5-FUra selectively to the tumors.     

Surgically excised primary mediastinal tumors and cysts: a report of 43 cases

Forty-three primary mediastinal tumors or cysts were surgically treated in 41 patients during a 10-year period. These tumors consisted of 20 thymic tumors, 10 neurogenic tumors, 5 teratomas, 3 lymphoid tumors, 2 congenital cysts, 2 mediastinal thyroid tumors, and 1 chondroma. There were 16 male and 25 female patients. The mean age was 44 years with a range of 6 to 79 years. Sixteen patients (39%) were symptomatic. There were 20 thymic tumors including 13 thymomas, 5 thymic cysts, and 2 hyperplasia with myastenia. Additional radiation therapy was recommended for all but stage I thymomas. Only 1 of the 10 neurogenic tumors was malignant. Eight teratomas were all cystic and matured. Early operative intervention is mandatory in these cases.     

Genetic testings for cancer: the surgeon's critical role. Familial colon cancer

We examined 18 atypical teratoid and rhabdoid tumors of the brain and 7 renal and 4 extrarenal rhabdoid tumors for mutations in the candidate rhabdoid tumor suppressor gene, INI1. Fifteen tumors had homozygous deletions of one or more exons of the INI1 gene, and the other 14 tumors demonstrated mutations. Germ-line mutations of INI1 were identified in four children, one with an atypical teratoid tumor of the brain and three with renal rhabdoid tumors. These studies suggest that INI1 is a tumor suppressor gene involved in rhabdoid tumors of the brain, kidney, and other extrarenal sites.     

Oncogene expression in carotid body tumors

BACKGROUND: The genetic etiology of carotid body tumors is suggested by the familial occurrence of the neoplasm. Environmental influences are also implied by the fact that the tumor is more common in those living at high altitudes. However, the development of sporadic tumors occurring at sea level, which account for the majority of cases, remains unknown. METHODS: The clinical and pathologic features of 13 carotid body tumors excised in 13 patients were reviewed. Two patients had bilateral tumors, one with a strong family history, and two patients had recurrent carotid body tumors. All tumors were benign except for one that had local lymph gland metastases. All patients were followed up for a period ranging from 1 to 17 years. Each tumor was examined for the oncoproteins c-myc, bcl-2 c-erbB-2, c-erbB-3 and c-jun and for the proliferating cell nuclear antigen (PCNA) by immunohistochemistry. RESULTS: c-myc immunoreactivity was observed in all tumors and, in 12 of 13 cases, was present in more than 10% of tumor cells, bcl-2 immunoreactivity was found in 11 cases with 6 tumors exhibiting more than 10% immunopositive cells, c-jun expression was found in 5 cases with 3 tumors containing more than 10% immunopositive cells. Only two tumors were positive for c-erb-B2 immunoreactivity with a cytoplasmic staining pattern. One tumor was positive for c-erb-B3. CONCLUSIONS: The oncogenes c-myc, bcl-2 and c-jun, are abnormally expressed in some carotid body tumors. Their expression may contribute to the genesis of carotid body tumors.     

The lack of a role for p53 in astrocytomas in pediatric patients

Mutations in the p53 gene, which codes for a cell division regulatory protein, have been identified in approximately one-third of adult astrocytomas. We evaluated 35 astrocytic tumors (17 pilocytic, 4 diffuse low grade, 12 anaplastic, and 2 glioblastoma) in pediatric patients for p53 mutations, using polymerase chain reaction-single-stranded conformation polymorphism analysis as a screening technique. Additionally, those tumors identified with homozygosity in the area of the p53 gene on chromosome 17 by Southern blotting were sequenced to look for p53 mutations. No tumors were identified with polymerase chain reaction-single-stranded conformation polymorphism analysis shifts indicative of mutations in the p53 gene. Five of 21 tumors were homozygous in the region of the p53 gene on chromosome 17; no mutations in exons 5 to 8 were found in any of these tumors. The frequency of p53 mutation in pediatric astrocytomas is significantly less than the frequency for adult tumors, regardless of tumor grade. Furthermore, the frequency of p53 mutations in high-grade astrocytomas is significantly lower in pediatric tumors than in adult tumors. These results suggest that p53 is not important in the oncogenesis of pediatric astrocytomas. Oncogenesis in pediatric astrocytomas may occur by different mechanisms than those of similar tumors in adults.     

Telomerase activity in gastrointestinal stromal tumors

BACKGROUND: Telomerase activity has been observed in 80-90% of carcinomas derived from various organs. However, to the authors' knowledge this report is the first assessment of telomerase activity in gastrointestinal stromal tumors (GISTs). METHODS: Telomerase activity was analyzed by the telomerase repeat amplification protocol assay in 29 tumors from 26 patients (23 primary tumors from 22 patients, 1 pair of primary and metastatic tumors from 1 patient, and 4 metastatic tumors from 3 patients). Phenotypes, tumor cell proliferation, and overexpression of p53 protein were evaluated immunohistochemically. RESULTS: Seven of 24 primary tumors (29%) and 5 of 5 metastatic tumors (100%) showed telomerase activity. Telomerase activity positive (+) GISTs were significantly larger (P < 0.05) and showed a significantly higher rate of proliferation than telomerase activity negative (-) tumors (P < 0.0001). All telomerase activity (+) GISTs were classified histologically as high risk tumors. Conversely, 15 of the 17 telomerase (-) GISTs were classified histologically as low risk tumors (P < 0.0001). With regard to p53 immunoreactivity, two and seven telomerase activity (+) tumors showed diffuse and sporadic positivity, respectively, whereas only five telomerase activity (-) tumors showed only focal or sporadic positivity. Telomerase activity was correlated significantly with poor prognosis (P < 0.05) in the patients in whom the primary GISTs were evaluated (n = 23). CONCLUSIONS: Telomerase activity may be a useful marker for evaluating the malignant potential of GIST. A distinct subgroup of GISTs is a target for therapy with a telomerase inhibitor.     

In memoriam: Widukind Lenz, 1919-1995

To determine whether microsatellite instability is involved in the development of transitional cell carcinoma (TCC) of the urinary tract, a microsatellite instability assay was carried out using PCR with 9 microsatellite loci. Thirty-eight TCC samples (30 patients with bladder cancer, 5 with renal pelvic tumors and 3 with ureteral tumors) and 1 lymph node with metastasis were examined. Microsatellite instability was found in 8 of 38 tumors examined, and 3 showed alterations in more than 2 microsatellite loci. All 8 tumors were beyond grade 2 and stage pT2 advanced tumors. Stages pT1-2 and pT3-4 patients differed significantly. Microsatellite instability was greater in smokers than non-smokers, but the differences were not significant. Microsatellite instability in TCC of the urinary tract is rare in superficial tumors but more common in invasive tumors. Microsatellite alterations would thus appear to occur, and possibly be importantly involved, in the tumorigenesis of urinary tract TCC.     

Estrogen receptor, progesterone receptor, and HER-2/neu protein in breast cancers from pregnant patients

BACKGROUND: Because the occurrence of breast cancer during pregnancy is uncommon and because the high levels of estrogens and progestins associated with pregnancy could cause false-negative results from ligand binding assays (LBA), the actual incidence of steroid hormone receptor positivity in tumors from this subset of women is unclear. METHODS: Estrogen receptor (ER) and progesterone receptor (PgR) were determined using LBA methods in 15 tumors from 15 pregnant patients with breast cancer. In addition, immunohistochemistry was done for ER, PgR, pS2, heat shock protein 27 (hsp27), and HER-2/neu on 12 of the 15 tumors. RESULTS: Five of 15 (33%) tumors were positive for ER by LBA, compared with 52% of tumors from age-matched nonpregnant patients. Six of 12 (50%) were ER-positive by immunohistochemistry. For PgR, 7 of 15 (47%) tumors were positive by LBA, compared with 42% of tumors from nonpregnant patients. Ten of 12 (83%) stained positive for PgR. By LBA, 67% of tumors studied were positive for ER or PgR or both, as opposed to 57% of tumors from the nonpregnant comparison group. Two other estrogen receptor-mediated proteins, pS2 and hsp27, were present by staining in 8 of 12 (67%) and 10 of 12 (83%) of tumors, respectively. Seven of 12 tumors (58%) had positive staining for HER-2/neu, whereas only 16% of age-matched nonpregnant patients had positive-staining tumors. CONCLUSION: By LBA, the incidence of ER and PgR in breast tumors from pregnant women was not significantly different from that of tumors from nonpregnant age-matched patients. Some ER-negative tumors were PgR, pS2, or hsp27 positive, indicating that an intact estrogen response system was operative although ER was not detectable by standard LBA.     

Studies on intraocular inflammation produced by intravitreal human interleukins in rabbits

Preoperative evaluation of stenotic rectal tumors is important since they often involve adjacent organs and thus may require additional therapy. Previous reports on endosonographic staging have excluded stenotic tumors because they could not be fully visualized with the available equipment. In this study, we have evaluated the role of endosonography in staging stenotic rectal tumors, with special attention to the use of forward-looking endoprobes. Preoperative staging was performed in 28 patients with stenotic rectal tumors. Tumor extension was evaluated according to the TNM classification, and the results were compared with surgical and histopathologic findings. Endosonography accurately assessed tumor extension in two T2 tumors, 14 T3 tumors, and seven T4 tumors. Three T2 tumors were overstaged, and two T4 tumors were staged as T3. The accuracy was 82 percent. Twenty-two tumors were subject to histopathologic evaluation of lymph nodes. Lymph nodes larger than 1 cm had been seen by endosonography in eight patients, five of whom had nodal metastases. Lymph nodes smaller than 1 cm or no lymph nodes were found in 14 patients, four of whom had nodal metastases. In conclusion, full sonographic visualization of stenotic rectal tumors and thus evaluation of tumor extension can be achieved by using forward-looking endoprobes.