PubMed Health⌕ Search

PubMed · 14585231

Malignant spinal cord compression.

Abstract

Malignant spinal cord compression is one of the most dreaded complications of cancer. If untreated, it can lead to worsening neurologic function culminating in paralysis and sphincter incontinence. The most challenging aspect in the management of this complication is early diagnosis because the single most important factor determining outcome is the level of neurologic function at initiation of therapy. Magnetic resonance imaging is the diagnostic modality of choice. Steroids have a proven role in the treatment. Radiation therapy has been the standard of care, with surgery reserved for special cases. A recent randomized trial has proven that in appropriately selected patients initial surgery, followed by radiation, provides better functional and neurologic outcome compared to radiation alone and will likely become the standard of care in the future. Newer modalities, such as transarterial embolization and extracranial stereotactic radiosurgery, are emerging and may be considered in appropriate cases if available.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Madhuri Yalamanchili, Glenn J Lesser. 2003. Malignant spinal cord compression.. https://doi.org/10.1007/s11864-003-0051-6

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Epigenetic mechanisms in breast cancer therapy and resistance.

The majority of breast cancers express the estrogen receptor (ERα) and agents targeting this pathway represent the main treatment modality. Endocrine therapy has proven successful in the treatment of hormone-responsive breast cancer since its early adoption in the 1940s as an ablative therapy. Unfortunately, therapeutic resistance arises, leading to disease recurrence and relapse. Recent studies increased our understanding in how changes to the chromatin landscape and deregulation of epigenetic factors orchestrate the resistant phenotype. Here, we will discuss how the epigenome is an integral determinant in hormone therapy response and why epigenetic factors are promising targets for overcoming clinical resistance.

Antineoplastic Agents, Hormonal↗

Sinus histiocytosis with massive lymphadenopathy (SHML) prednisone resistant but dexamethasone sensitive.

Sinus histiocytosis with massive lymphadenopathy (SHML) is a histiocytic disorder affecting children and adults. It usually presents as markedly enlarged lymph nodes that require surgical biopsy for confirmation. This lesion is usually self-limited but can present in areas that can cause significant morbidity or disfigurement. We report a case that required therapy due to the severe disfigurement but was resistant till treated with dexamethasone. This case illustrates that SHML may be resistant to prednisone but still be sensitive to dexamethasone.

Antineoplastic Agents, Hormonal↗

Interferon-regulatory factor-1 is critical for tamoxifen-mediated apoptosis in human mammary epithelial cells.

Unlike estrogen receptor-positive (ER(+)) breast cancers, normal human mammary epithelial cells (HMECs) typically express low nuclear levels of ER (ER poor). We previously demonstrated that 1.0 microM tamoxifen (Tam) promotes apoptosis in acutely damaged ER-poor HMECs through a rapid, 'nonclassic' signaling pathway. Interferon-regulatory factor-1 (IRF-1), a target of signal transducer and activator of transcription-1 transcriptional regulation, has been shown to promote apoptosis following DNA damage. Here we show that 1.0 microM Tam promotes apoptosis in acutely damaged ER-poor HMECs through IRF-1 induction and caspase-1/3 activation. Treatment of acutely damaged HMEC-E6 cells with 1.0 microM Tam resulted in recruitment of CBP to the gamma-IFN-activated sequence element of the IRF-1 promoter, induction of IRF-1, and sequential activation of caspase-1 and -3. The effects of Tam were blocked by expression of siRNA directed against IRF-1 and caspase-1 inhibitors. These data indicate that Tam induces apoptosis in HMEC-E6 cells through a novel IRF-1-mediated signaling pathway that results in activated caspase-1 and -3.

Antineoplastic Agents, Hormonal↗