Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

[Hypercalcemia and neoplasms: recent advances in pathogenesis].

L Virgolini1, C Gallizia

  • 1Cattedra di Ematologia, Istituto di Scienze mediche, Università, Udine.

Recenti Progressi in Medicina
|October 1, 1990
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Granulocyte colony-stimulating factor (G-CSF) allows the delivery of effective doses of CHOP and CVP regimens in non-Hodgkin lymphomas.

Leukemia & lymphoma·1995
Same author

Laparoscopic splenectomy in idiopathic thrombocytopenic purpura.

Vox sanguinis·1995
Same author

Incidence and diagnosis of EDTA-dependent pseudothrombocytopenia in a consecutive outpatient population referred for isolated thrombocytopenia.

Vox sanguinis·1995
Same author

Laparoscopic splenectomy in the management of hematological diseases.

Haematologica·1995
Same author

The role of granulocyte colony-stimulating factor (filgrastim) in maintaining dose intensity during conventional-dose chemotherapy with ABVD in Hodgkin's disease.

Tumori·1994
Same author

Development of autoimmune thyroid diseases during long-term treatment of hematological malignancies with alpha-interferons.

Haematologica·1994
Same journal

Recenti progressi in medicina·2026
Same journal

Recenti progressi in medicina·2026
Same journal

Recenti progressi in medicina·2026
Same journal

Recenti progressi in medicina·2026
Same journal

Recenti progressi in medicina·2026
Same journal

Recenti progressi in medicina·2026
See all related articles

Paraneoplastic hypercalcemic syndromes have diverse causes, often involving parathyroid hormone-related protein and other factors in malignancy-associated hypercalcemia. Understanding these mechanisms is key for managing cancer-related high calcium levels.

Area of Science:

  • Endocrinology
  • Oncology
  • Molecular Biology

Background:

  • Paraneoplastic hypercalcemic syndromes present with heterogeneous mechanisms.
  • Neoplastic hypercalcemia can occur with or without bone metastatic disease.
  • Humoral hypercalcemia of malignancy involves various growth factors and cytokines.

Purpose of the Study:

  • To elucidate the diverse mechanisms underlying paraneoplastic hypercalcemic syndromes.
  • To identify key mediators of hypercalcemia in different cancer types.
  • To differentiate causes of hypercalcemia in neoplastic disease with and without bone metastases.

Main Methods:

  • Review of literature on humoral hypercalcemia of malignancy.
  • Analysis of the roles of specific proteins, growth factors, and cytokines.

Related Experiment Videos

  • Examination of mechanisms in multiple myeloma and Adult T-cell Leukemia/Lymphoma.
  • Main Results:

    • Parathyroid hormone-related protein is a primary cause of hypercalcemia without bone metastases.
    • Growth transforming factors, platelet-derived growth factor, tumor necrosis factors, and interleukin-1 contribute to humoral hypercalcemia.
    • Prostaglandin E (PGE) is implicated in hypercalcemia associated with bone metastases.
    • Tumor necrosis factors, interleukin-1, and vitamin D3 overproduction are significant in multiple myeloma and Adult T-cell Leukemia/Lymphoma.

    Conclusions:

    • The mechanisms of paraneoplastic hypercalcemia are varied and depend on the underlying malignancy.
    • Parathyroid hormone-related protein, cytokines, and other factors play distinct roles in different hypercalcemic syndromes.
    • Understanding these specific pathways is crucial for effective management of cancer-associated hypercalcemia.