A Case of pituitary somatotroph adenoma with concomitant secretion of growth hormone, prolactin, and adrenocorticotropic hormone ? an adenoma derived from primordial stem cell, studied by immunohistochemistry, in situ hybridization, and cell culture

1996 ◽  
Vol 138 (8) ◽  
pp. 1002-1007 ◽  
Author(s):  
A. Matsuno ◽  
T. Sasaki ◽  
T. Mochizuki ◽  
T. Fujimaki ◽  
N. Sanno ◽  
...  
Keyword(s):  
Cell Culture ◽  
Growth Hormone ◽  
Stem Cell ◽  
In Situ Hybridization ◽  
Adrenocorticotropic Hormone ◽  
Somatotroph Adenoma

Pituitary adenoma producing growth hormone and adrenocorticotropin: a histological, immunocytochemical, electron microscopic, and in situ hybridization study

1998 ◽  
Vol 88 (6) ◽  
pp. 1111-1115 ◽  
Author(s):  
Kalman Kovacs ◽  
Eva Horvath ◽  
Lucia Stefaneanu ◽  
Juan Bilbao ◽  
William Singer ◽  
...  
Keyword(s):  
Growth Hormone ◽  
In Situ Hybridization ◽  
Pituitary Adenoma ◽  
Immunoelectron Microscopy ◽  
Secretory Granules ◽  
Cell Types ◽  
Content Type ◽  
Separate Cell ◽  
Fine Print

✓ The authors report on the morphological features of a pituitary adenoma that produced growth hormone (GH) and adrenocorticotropic hormone (ACTH). This hormone combination produced by a single adenoma is extremely rare; a review of the available literature showed that only one previous case has been published. The tumor, which was removed from a 62-year-old man with acromegaly, was studied by histological and immunocytochemical analyses, transmission electron microscopy, immunoelectron microscopy, and in situ hybridization. When the authors used light microscopy, the tumor appeared to be a bimorphous mixed pituitary adenoma composed of two separate cell types: one cell population synthesized GH and the other ACTH. The cytogenesis of pituitary adenomas that produce more than one hormone is obscure. It may be that two separate cells—one somatotroph and one corticotroph—transformed into neoplastic cells, or that the adenoma arose in a common stem cell that differentiated into two separate cell types. In this case immunoelectron microscopy conclusively demonstrated ACTH in the secretory granules of several somatotrophs. This was associated with a change in the morphological characteristics of secretory granules. Thus it is possible that the tumor was originally a somatotropic adenoma that began to produce ACTH as a result of mutations that occurred during tumor progression.

scholarly journals Interleukin-5 is at 5q31 and is deleted in the 5q- syndrome

Blood ◽  
1988 ◽  
Vol 71 (4) ◽  
pp. 1150-1152
Author(s):  
GR Sutherland ◽  
E Baker ◽  
DF Callen ◽  
HD Campbell ◽  
IG Young ◽  
...  
Keyword(s):  
Growth Hormone ◽  
In Situ Hybridization ◽  
Colony Stimulating Factor ◽  
Interleukin 5 ◽  
Viral Oncogene ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor ◽  
Viral Oncogene Homolog

Human interleukin-5 (IL-5) is a selective eosinophilopoietic and eosinophil-activating growth hormone. By in situ hybridization this gene is mapped to chromosome 5q23.3 to 5q32. It is shown to be deleted in two patients with the 5q-syndrome and in one patient previously diagnosed with myelodysplasia whose condition had progressed to acute myeloblastic leukemia. The clustering of other genes involved in hematopoiesis (IL-3, granulocyte-macrophage colony-stimulating factor, feline sarcoma viral oncogene homolog, colony-stimulating factor 1) to the same region as IL-5 suggests a nonrandom localization and raises interesting questions concerning the evolution and regulation of these genes.

In situ hybridization to rat brain and pituitary gland of growth hormone cDNA

1987 ◽  
Vol 79 (3) ◽  
pp. 251-256 ◽  
Author(s):  
Francis Gossard ◽  
Françoise Dihl ◽  
Georges Pelletier ◽  
Paul M. Dubois ◽  
Gérard Morel
Keyword(s):  
Growth Hormone ◽  
In Situ Hybridization ◽  
Pituitary Gland ◽  
Rat Brain

scholarly journals Silent Somatotroph Adenoma, Detected by Catalyzed Signal Amplification and Non-radioisotopic In situ Hybridization

1999 ◽  
Vol 46 (Suppl) ◽  
pp. S81-S84 ◽  
Author(s):  
AKIRA MATSUNO ◽  
NAOKO SANNO ◽  
SHIGEYUKI TAHARA ◽  
AKIRA TERAMOTO ◽  
R. YOSHIYUKI OSAMURA ◽  
...  
Keyword(s):  
In Situ Hybridization ◽  
Signal Amplification ◽  
Somatotroph Adenoma

Immature CD34+CD19− progenitor/stem cells in TEL/AML1-positive acute lymphoblastic leukemia are genetically and functionally normal

Blood ◽  
2002 ◽  
Vol 100 (2) ◽  
pp. 640-646 ◽  
Author(s):  
Marc Hotfilder ◽  
Silja Röttgers ◽  
Annegret Rosemann ◽  
Heribert Jürgens ◽  
Jochen Harbott ◽  
...  
Keyword(s):  
Stem Cell ◽  
In Situ Hybridization ◽  
Acute Lymphoblastic Leukemia ◽  
Cell Clone ◽  
Lymphoblastic Leukemia ◽  
Leukemic Cell ◽  
Leukemic Cells ◽  
Cell Fraction ◽  
Rt Pcr

Abstract One important question in stem cell biology of childhood acute lymphoblastic leukemia (ALL) is whether immature CD34+CD19− cells are part of the leukemic cell clone. CD34+CD19− cells from the bone marrow of 9 children with TEL/AML1-positive ALL were purified by flow sorting and subjected to reverse transcriptase–polymerase chain reaction (RT-PCR), fluorescence in situ hybridization, and methylcellulose cultures. In 3 of 8 patients analyzed by RT-PCR, noTEL/AML1-positive cells could be detected in the CD34+CD19− cell fraction. Altogether, the percentage of TEL/AML1-positive cells was low: 1.6% (n = 8; SD 2.2%) by nested real-time RT-PCR and 2.5% (n = 5; SD 2.6%) by fluorescence in situ hybridization. This correlated with the percentage of contaminating CD19+ leukemic cells in the CD34+CD19− cell fraction in 6 control sorts (mean 4.6%, SD 3.6%), indicating that the low levels of leukemic cells detected in the CD34+CD19− cell fraction could be attributed to sorter errors. Methylcellulose cultures in 3 patients provided further evidence that CD34+CD19− cells represent a candidate normal cell population. The clonogenicity of the CD34+CD19− cell fraction was similar to normal progenitors, including growth of primitive granulocyte, erythroid, macrophage, megakaryocyte colony-forming units. Each of 92 colonies from cultures with CD34+CD19− cells tested negative for TEL/AML1. In conclusion, our data support the hypothesis that the leukemia inTEL/AML1-positive childhood ALL originates in a CD19+ lymphoid progenitor. This has many therapeutic implications, eg, for purging of autologous stem cell products, flow cytometric monitoring of minimal residual disease, and targeting immunotherapy against the leukemic cell clone.

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