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Percutaneous biopsy of abdominal masses under ultrasound
Notes
424 carrying EPOR cDNA. We found that a single point mutation within the exoplasmic domain of the EPOR enables it to induce hormone-independent cell growth and oncogenicity after its introduction into nontumorigenic, IL3-dependent cell growth and oncogenicity after its introduction into nontumorigenic IL3-dependent cells. We also found that the carboxyterminal truncation of the EPOR renders the receptor hyperresponsive to EPO, but is insufficient to induce hormone-independent growth. These are the first examples of mutational aCtiVatiOn and hypersensitization in the cytokine receptor family and quite reminiscent to the activation of cellular oncogenes. Such mutations may be related to human erythroleukemia and polycythemia Vera. our findings also raise a new possibility that mutational activation of the cytokine receptors as well as EPOR might be a mechanism for overriding normal hormonal control of proliferation of hematopoietic cells. Recent cloning of the myeloproliferative leukemia virus oncogene (a fusion gene between env gene and cellular-derived unknown cytokine receptor gene) (Souyri et al 1990, Cell. 63, I 137-I 147) also encourages this hypothesis.
A Yoshimura(I) WhiteheadInstitutefor Biomedical Research, Cambridge,MA 02142, USA Percutaneous biopsy of abdominal masses under ultrasound The authors describe application of a recently developed percutaneous needle biopsy technique to the histological diagnosis of abdominal masses detected clinically or by previous imaging procedures. The technique has the advantages of requiring only local anaesthesia for percutaneous biopsy which is performed under continuous ultrasound scanning which enables accurate targeting and immediate confirmation that the mass has been biopsied. This is achieved by using an automated firing device to activate the biopsy needle (Biopsy gun) and provides histologica! rather than cytological samples. In 108 consecutive patients, biopsy failed in 4; there were 3 complications and no mortality as a result of the procedure. Masses biopsied were situated in a wide variety of organs including liver, pancreas, kidneys and adrenal glands as well as lymph0 nodes and retroperitoneal masses. Whilst biopsy merely confirmed the clinical suspicion of malignancy in 70 out of 84 patients, it additionally demonstrated dissemination in 26 of these patients. Furthermore, in 10 patients an altered primary tumor was demonstrated and in a further 12 patients the diagnosis of malignancy was refuted. Conversely, 7 out of 24 patients considered to have benign disease proved to have an unsuspected neoplasm. There were 4 false negative results but no false Positive diagnoses in these series. It is concluded that ( t ) h’urure (LondJ ( 1990) 348, 647
this technique is safe and accurate and the results obtained have a considerable effect on clinical management. CJ Mitchell (2) ScarboroughHospital, Scarborough,North Yorks, YO 12 6QL, UK Alzbeimer’s disease and amyloid p Scientists may be closer to identifying the triggering events that cause the nerve degeneration of Alzheimer’s disease (AD). NIA grantee BA Yankner and colleagues at the Harvard Medical School and the Children’s Hospital in Boston have found that a common brain protein, amyloid p, may damage mature cells in the central nervous system and lead to the type of cell death associated with AD. Paradoxically, the same protein has been found to promote cell growth in young brain cells. The investigators studied the effects of p amyloid, a specific portion of amyloid 0, in both high and low concentrations in laboratory cultures containing hyppocampal cells from the rats brain. The hippocampus area of the brain is essential for learning and memory and its function is severely affected in people with AD. The researchers found that the most destructive effect of amyloid p occurred in older cell cultures at high concentrations where the protein caused an almost complete collapse of nerve growth and cell function. While conducting these studies, the researchers recognized a similarity between the active sequence of the amyloid p protein and a family of neuropeptides called tachykinins. The area of greatest similarity is in the part of the protein chain where most of the biological activity occurs. When tachykinins and amyloid p were placed together in dishes of cultured hippocampal cells, the destructive effects of amyloid were reversed. This exciting finding has led Dr Yankner to speculate that the tachykinins naturally occurring in the brain may have the opposite effect of amyloid p. Thus, if the destructiveness of amyloid p protein proves to be related to Alzheimer’s disease, tachykinins could be the key to finding a treatment. BA Yankner (3) HarvardMedical School, Boston MA 02 115,USA A model experiment on muscular dystrophy During the last years, one of the most successful applications of DNA technology to the analysis of human disease has been the molecular identification and characterisation of the Duchenne/Becker muscular dystrophy gene on the X chromosome, and of its product, the submembraneous cytoskeletal protein dystrophin. Dystrophin deficient muscle cells in Duchenne/Becker (2) EMJ (1990) 301, 1186 (3) Science (1990) 250. 280
424 carrying EPOR cDNA. We found that a single point mutation within the exoplasmic domain of the EPOR enables it to induce hormone-independent cell growth and oncogenicity after its introduction into nontumorigenic, IL3-dependent cell growth and oncogenicity after its introduction into nontumorigenic IL3-dependent cells. We also found that the carboxyterminal truncation of the EPOR renders the receptor hyperresponsive to EPO, but is insufficient to induce hormone-independent growth. These are the first examples of mutational aCtiVatiOn and hypersensitization in the cytokine receptor family and quite reminiscent to the activation of cellular oncogenes. Such mutations may be related to human erythroleukemia and polycythemia Vera. our findings also raise a new possibility that mutational activation of the cytokine receptors as well as EPOR might be a mechanism for overriding normal hormonal control of proliferation of hematopoietic cells. Recent cloning of the myeloproliferative leukemia virus oncogene (a fusion gene between env gene and cellular-derived unknown cytokine receptor gene) (Souyri et al 1990, Cell. 63, I 137-I 147) also encourages this hypothesis.
A Yoshimura(I) WhiteheadInstitutefor Biomedical Research, Cambridge,MA 02142, USA Percutaneous biopsy of abdominal masses under ultrasound The authors describe application of a recently developed percutaneous needle biopsy technique to the histological diagnosis of abdominal masses detected clinically or by previous imaging procedures. The technique has the advantages of requiring only local anaesthesia for percutaneous biopsy which is performed under continuous ultrasound scanning which enables accurate targeting and immediate confirmation that the mass has been biopsied. This is achieved by using an automated firing device to activate the biopsy needle (Biopsy gun) and provides histologica! rather than cytological samples. In 108 consecutive patients, biopsy failed in 4; there were 3 complications and no mortality as a result of the procedure. Masses biopsied were situated in a wide variety of organs including liver, pancreas, kidneys and adrenal glands as well as lymph0 nodes and retroperitoneal masses. Whilst biopsy merely confirmed the clinical suspicion of malignancy in 70 out of 84 patients, it additionally demonstrated dissemination in 26 of these patients. Furthermore, in 10 patients an altered primary tumor was demonstrated and in a further 12 patients the diagnosis of malignancy was refuted. Conversely, 7 out of 24 patients considered to have benign disease proved to have an unsuspected neoplasm. There were 4 false negative results but no false Positive diagnoses in these series. It is concluded that ( t ) h’urure (LondJ ( 1990) 348, 647
this technique is safe and accurate and the results obtained have a considerable effect on clinical management. CJ Mitchell (2) ScarboroughHospital, Scarborough,North Yorks, YO 12 6QL, UK Alzbeimer’s disease and amyloid p Scientists may be closer to identifying the triggering events that cause the nerve degeneration of Alzheimer’s disease (AD). NIA grantee BA Yankner and colleagues at the Harvard Medical School and the Children’s Hospital in Boston have found that a common brain protein, amyloid p, may damage mature cells in the central nervous system and lead to the type of cell death associated with AD. Paradoxically, the same protein has been found to promote cell growth in young brain cells. The investigators studied the effects of p amyloid, a specific portion of amyloid 0, in both high and low concentrations in laboratory cultures containing hyppocampal cells from the rats brain. The hippocampus area of the brain is essential for learning and memory and its function is severely affected in people with AD. The researchers found that the most destructive effect of amyloid p occurred in older cell cultures at high concentrations where the protein caused an almost complete collapse of nerve growth and cell function. While conducting these studies, the researchers recognized a similarity between the active sequence of the amyloid p protein and a family of neuropeptides called tachykinins. The area of greatest similarity is in the part of the protein chain where most of the biological activity occurs. When tachykinins and amyloid p were placed together in dishes of cultured hippocampal cells, the destructive effects of amyloid were reversed. This exciting finding has led Dr Yankner to speculate that the tachykinins naturally occurring in the brain may have the opposite effect of amyloid p. Thus, if the destructiveness of amyloid p protein proves to be related to Alzheimer’s disease, tachykinins could be the key to finding a treatment. BA Yankner (3) HarvardMedical School, Boston MA 02 115,USA A model experiment on muscular dystrophy During the last years, one of the most successful applications of DNA technology to the analysis of human disease has been the molecular identification and characterisation of the Duchenne/Becker muscular dystrophy gene on the X chromosome, and of its product, the submembraneous cytoskeletal protein dystrophin. Dystrophin deficient muscle cells in Duchenne/Becker (2) EMJ (1990) 301, 1186 (3) Science (1990) 250. 280