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PubMed1977

Acute dermatomyositis-polymyositis and malignancy.

A partial review of selected published case reports of AD-P associated with malignancy has been enhanced by the presentation of pertinent data on 15 unreported examples of the association. It is noteworthy that the first case in current literature of AD-P associated with a malignancy was described in 1916. The brief clinical report of a patient with proximal muscle weakness and skin lesions, with the obvious association with a malignancy (adenocarcinoma of the stomach), describes an example that has been repeated many times with different types of tumors but with essentially no variations in the clinical findings. In 1959 Williams identified 590 cases of AD with an overall tumor rate of 15%, and recently Barnes identified 258 cases of AD associated with a malignancy. The original designation, dermatomyositis or AD, has now been expanded to include proximal muscle polymyositis with systemic involvement, which syndrome at the current state of the art is indistinguishable clinically and pathologically from AD except for the lack of skin lesions. It may be that at some future time one or more immunologic features may differnetiate the clinical entity polymyositis from AD and further subdivide each of these entitites from similar clinical syndromes associated with a malignancy. However, the problem in management in either AD or polymyositis is similar. A number of patients with a malignancy and muscle weakness or neuropathy have been reported. These associations have been mentioned briefly, but insufficient data are available to determine whether these should be considered as a variant of AD-P or only casually related conditions with certain clinical features in common. Most of the patients described in the literature of AD-P with an associated malignancy have had skin lesions; a minority only have lacked this feature. However, unless a patient is followed carefully, it is possible for a transient or evanescent erythema or insignificant skin lesions to be present and not recorded in the case record.

Acute Disease↗
PubMed2002

Thymic basaloid carcinoma with hepatic metastasis.

A thymic basaloid carcinoma is rare, as is an unusual case with extra-thoracic metastasis. We report on a 41-year-old woman who had a thymic basaloid carcinoma with liver metastases. The patient underwent resection of the thymic basaloid carcinoma followed by curative partial hepatectomy. At 1 year later, another metastatic lesion developed in the residual liver, which was also curatively resected. The postoperative course was uneventful, and the patient is surviving without recurrence for 12 months, to date.

Adult↗
PubMed2001

Endoscopic findings of radiation esophagitis in concurrent chemoradiotherapy for intrathoracic malignancies.

BACKGROUND AND PURPOSE: The incidence and extent of radiation esophagitis were assessed endoscopically in patients treated with concurrent chemoradiotherapy. PATIENTS AND METHODS: Eighty-two patients who received thoracic radiotherapy for lung, thymic, or esophageal cancer were investigated endoscopically from July 1991 to the end of 1997. Among them, 23 esophageal cancer patients were treated with radiation alone, and the others were treated with concurrent chemoradiotherapy. Esophageal endoscopy was performed during or just after radiotherapy. The presence of radiation esophagitis was assessed and assigned an endoscopic score (i.e. grade 0 for normal, 1 for erythema, 2 for erosion or sloughing, 3 for ulcer, hemorrhage, or stricture). The symptomatic grade was assessed using the RTOG (Radiation Therapy Oncology Group) acute radiation morbidity score. RESULTS: A correlation was seen between endoscopic and RTOG scores. However, even some patients with RTOG grade 0 to 1 had endoscopic grade 3 esophagitis. Endoscopic grade 3 was observed in 16 (27.1%) patients in the concurrent chemoradiotherapy group, whereas it did not occur in any patient in the radiation alone group (P=0.004). CONCLUSIONS: Our results suggest that (1) RTOG score correlates closely to esophageal mucosal damage, and (2) more severe esophagitis occurs in those undergoing concurrent chemoradiotherapy than those undergoing radiotherapy alone [corrected].

Adult↗
PubMed2000

Lack of susceptibility of transgenic mice carrying the human c-Ha-ras proto-oncogene (rasH2 mice) to phenolphthalein in a 6-month carcinogenicity study.

Phenolphthalein has carcinogenic activity, causing malignant lymphomas in B6C3F1 mice at a dietary dose of 3000 ppm in a 2-year carcinogenicity study and in heterozygous p53-deficient female mice at the same dose in a 6-month study. To examine whether phenolphthalein carcinogenic potential can be detected in male and female transgenic (Tg) mice carrying the human c-Ha-ras gene (rasH2 mice) and their wild-type littermates (non-Tg mice), a diet containing 3000, 6000 or 12000 ppm was given for 6 months. Unequivocal induction of neoplastic lesions was not apparent, suggesting that rasH2 mice are resistant to the induction of malignant lymphomas by the treatment of phenolphthalein.

Adenoma, Liver Cell↗
PubMed2001

Somatic activation of the K-ras oncogene causes early onset lung cancer in mice.

About 30% of human tumours carry ras gene mutations. Of the three genes in this family (composed of K-ras, N-ras and H-ras), K-ras is the most frequently mutated member in human tumours, including adenocarcinomas of the pancreas ( approximately 70-90% incidence), colon ( approximately 50%) and lung ( approximately 25-50%). To construct mouse tumour models involving K-ras, we used a new gene targeting procedure to create mouse strains carrying oncogenic alleles of K-ras that can be activated only on a spontaneous recombination event in the whole animal. Here we show that mice carrying these mutations were highly predisposed to a range of tumour types, predominantly early onset lung cancer. This model was further characterized by examining the effects of germline mutations in the tumour suppressor gene p53, which is known to be mutated along with K-ras in human tumours. This approach has several advantages over traditional transgenic strategies, including that it more closely recapitulates spontaneous oncogene activation as seen in human cancers.

Alleles↗
PubMed1971

Growth of metastases from P-388 sarcoma in the rat followig whole body irradiation.

The growth of an allogeneic rapidly growing and metastasizing sarcoma (P-388) in the rat is described. Quantitative and kinetic data are provided concerning the growth of individual metastases produced in three principal regional lymph node drainage groups, and are compared with growth of the primary tumour of origin in muscle; the incidence of pulmonary metastases is also given. The effects on growth of metastases and primaries produced by sublethal whole body irradiation (WBI) before inoculations of 10-10(8) tumour cells are described.Growth of P-388 sarcoma in unirradiated recipients (ED(50) ≃ 5 × 10(3) cells) obeyed the linear growth law proposed by the Mayneord model for tumour growth, but in irradiated recipients (ED(50) < 10 cells) early growth of primaries and metastases approximated more closely to an exponential rate of growth.The ratio M/P of weight of metastases (M) to weight of primary tumour of origin (P) increased at a linear rate with age (t) of tumour, and gave the same slope namely, 0·029 for pelvic node metastases) in unirradiated rats inoculated with a large (10(6)-10(7)) number of cells as in irradiated rats. The slope was decreased to 0·014 for pelvic node metastases in unirradiated rats challenged with fewer (10(4)) cells but not in irradiated recipients. It is postulated that the effects of WBI on growth of metastases are confined to causing a suppression of immunity, and that WBI does not affect tumour spread significantly through other mechanisms.In immunologically competent rats the phenomena of sequestrated progressive growth of isolated metastases in lymph nodes and of a chronic nonprogressive enlargement of nodes in which persistent tumour growth and destruction occurred side by side are described, and effects on prognoses and clinical behaviour, are discussed.The P-388 tumour is considered of value in quantitative and kinetic experimental studies of metastases, and particularly those in which the role of immunity needs to be assessed and measured to avoid confusion with other factors or agents which might affect the spread and growth of metastases.

Animals↗
PubMed1998

Comparative studies on the expression of somatostatin receptor subtypes, outcome of octreotide scintigraphy and response to octreotide treatment in patients with carcinoid tumours.

We have compared the expression of somatostatin receptor (sstr) subtypes with the outcome of somatostatin receptor scintigraphy and the effect of somatostatin receptor activation in patients with disseminated carcinoid tumours. Tumour tissues from nine patients with midgut carcinoids (ileal) and three patients with foregut carcinoids (gastric, thymic) were analysed using Northern blotting. Expression of somatostatin receptors was demonstrated in all tumours (12 out of 12), with all five receptor subtypes present in 9 out of 12 tumours. Somatostatin receptor scintigraphy using [111In]DTPA-D-Phe1-octreotide visualized tumours in all patients (12 out of 12). The 111In activity concentrations in tumour tissue (T) and blood (B) were determined in three tumours 1-7 days after injection of the radionuclide. The T/B 111In activity concentration ratios ranged between 32 and 651. Clinically, treatment with the long-acting somatostatin analogue octreotide resulted in marked symptom relief accompanied by a significant reduction in tumour markers, for example urinary-5-HIAA levels (28-71% reduction). Incubation of midgut carcinoid tumours in primary culture with octreotide (10 microM) resulted in a reduction in spontaneously secreted serotonin (45-71% reduction) and 5-HIAA (41-94% reduction). The results demonstrate that carcinoid tumours possess multiple somatostatin receptor subtypes and that somatostatin analogues such as octreotide, which preferentially bind to somatostatin receptor subtype 2 and 5, can be used in the diagnosis and medical treatment of these tumours. In the future, novel somatostatin analogues with subtype specific receptor profiles may prove to be of value for individualizing the treatment of disseminated carcinoid tumour disease.

Aged↗
PubMed1997

Pim-2 transgene induces lymphoid tumors, exhibiting potent synergy with c-myc.

Evidence from proviral tagging experiments has suggested that pim-2 is similar in oncogenic behavior to its well characterized relative pim-1. While the basal expression in tissues differs, both genes are highly expressed in mitogenically stimulated hematopoietic cells and their transcription is induced in response to the same cytokines. Expression of a pim-2 transgene in lymphoid cells predisposed mice to T-cell lymphomas like those promoted by pim-1 transgenes. Moreover, strong collaboration with an E mu-myc transgene was manifested as pre-B cell leukemia in neonate bi-transgenic animals. Remarkably, this collaboration was attenuated but not prevented by X-inactivation of one of the transgenes. The addition of pim-2 to the fold increases the prominence of the pim proto-oncogene family in tumorigenesis.

Age Factors↗
PubMed2003

Mapping of genetic modifiers of thymic lymphoma development in p53-knockout mice.

The strain dependency of the spectrum and latency of tumors has been reported in p53-deficient (KO) mice, suggesting the presence of modifiers for the outcome of the p53 deficiency. The modifiers provide clues to the oncogenic pathway in cells lacking p53, the most frequently mutated gene in a wide variety of human cancers. To search the modifiers, we induced 160 lymphomas and 69 skin tumors by gamma-irradiation of p53(KO/+) backcross mice between BALB/c and MSM strains and performed genome scan. BALB/c-derived alleles at three loci on chromosome 19, Mp53D1 (modifier of p53-deficiency) at D19Mit5, Mp53D2 at D19Mit90 and Mp53D3 at D19Mit123, extended the latency of thymic lymphoma development (P values in Mantel-Cox test were 0.0007, 0.0007 and 0.0003, respectively). Mp53D3 also increased the latency of skin tumors (P value, 0.0008). The linkage of Mp53D2 was confirmed by the experiment using 94 p53-KO mice consomic for chromosome 19, providing a significant linkage. However, the linkage was not confirmed for Mp53D1 or Mp53D3, suggesting epistasis of genes involved in the tumorigenesis.

Alleles↗
PubMed1999

MEN1 gene mutations in sporadic neuroendocrine tumors of foregut derivation.

Foregut-derived neuroendocrine (NE) tumors occur sporadically or in association with multiple endocrine neoplasia type 1 (MEN1) syndrome. Thirty-nine sporadic NE tumors of foregut derivation (six thymic, 21 bronchial, three gastric, and nine pancreatic tumors) as well as two hindgut-derived rectal carcinoids for somatic MEN1 gene mutation were analyzed by direct sequencing analysis. Five tumors showed mutations: nonsense mutations (Q393X and R98X) in thymic and pancreatic NE tumors, respectively, a 4 b.p. deletion (357del4) in a gastric NE carcinoma, and missense mutations (D172Y and S178Y) in pancreatic NE tumors. No mutation was identified in pulmonary or rectal NE tumors. In a patient with a pancreatic NE tumor (D172Y), the corresponding germline DNA showed the same mutation, suggesting that sporadic MEN1 syndrome was masked in this case. Somatic MEN1 gene mutations and deletions may play a crucial role in the tumorigenesis of a subset of foregut-derived NE tumors. Sporadic MEN1 syndrome may occur as a sporadic NE tumor of the pancreas.

Adult↗
PubMed2000

Thymohemangiolipoma, a rare histologic variant of thymolipoma: a case report and review of the literature.

We report a case of a thymic neoplasm in an 18-year-old woman who presented with chest discomfort and an anterior mediastinal mass. The surgically resected tumor showed abundant adipose tissue admixed with thymic tissue and numerous medium-caliber blood vessels. We consider this tumor a rare variant of thymolipoma and designate it as thymohemangiolipoma. Because of its benign nature, it should be distinguished from other mediastinal lesions.

Adolescent↗
PubMed1989

[CT morphology and clinical diagnosis of thoracic space-occupying lesions in patients under 40 years of age].

83 patients with thoracic masses and aged under 40 years, who had been seen in a chest clinic, were examined by CT. They were classified according to their diagnosis and typical CT findings were analysed. Bronchial carcinomas showed predominantly radial extensions and air trapping. Malignant lymphomas and benign tumours usually showed smooth outlines and evidence of some fat content. Malignant mediastinal or neurogenic tumours frequently contained liquid portions and calcification. The CT diagnosis of lymphomas (seven cases), metastases (28 cases) and benign tumours (13 cases) presented no problems in view of the typical appearance and position of the tumours; classification of malignant mediastinal or neurogenic tumours (seven cases) was difficult. Inflammatory masses (14 cases) and bronchial carcinomas (14 cases) showed similar CT appearances.

Adult↗