Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0376358 (prostate cancer)
 59,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Beckwith-Wiedemann syndrome, familial atypical multiple mole melanoma syndrome, and hereditary tylosis are bona fide genodermatoses with malignant potential. Each of these conditions is associated with an increased incidence of certain tumors: Wilms' tumor, adrenocortical carcinomas, pancreatoblastomas, and hepatoblastomas in Beckwith-Wiedemann syndrome; intraocular malignant melanoma, pancreatic carcinoma, and noncolorectal gastrointestinal cancers in familial atypical multiple mole melanoma syndrome; and squamous cell carcinoma of the esophagus in hereditary tylosis. Other cancer-related genodermatoses are Birt-Hogg-Dube syndrome (associated with medullary carcinoma of the thyroid and renal cell carcinoma) and its variant, Hornstein-Knickenberg syndrome (associated with colon carcinoma). Kidney tumors (Wilms' tumor and malignant rhabdoid tumor), leukemias (acute myelogenous and acute myelomonocytic), retinoblastoma, and paratesticular rhabdomyosarcoma have been reported recently in children with another genodermatosis-incontinentia pigmenti. Supernumerary nipples (polythelia) may be sporadic or familial in occurrence; their presence has been associated with an increased incidence of renal adenocarcinoma, testicular cancer, prostate cancer, and urinary bladder carcinoma. The general characteristics, mucosal and skin manifestations, and noncutaneous features of all these conditions are reviewed. Also, the associated malignancies of these genodermatoses and other conditions that are characterized by dermatologic manifestations and may be either familial or secondary to an inherited gene defect are summarized.
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PMID:Miscellaneous genodermatoses: Beckwith-Wiedemann syndrome, Birt-Hogg-Dube syndrome, familial atypical multiple mole melanoma syndrome, hereditary tylosis, incontinentia pigmenti, and supernumerary nipples. 771 45

In this retrospective study plain radiographs, radionuclide bone scans, computed tomography (CT) and magnetic resonance (MRT) examinations of 115 patients with metastatic carcinoma of the spine were analyzed. In 32 patients metastases were proven histologically and in the remainder by follow-up studies. Altogether, 513 vertebrae were evaluated. Forty-one patients had histologically proven breast cancer, 14 renal cell carcinoma, 11 prostate cancer, 8 melanoma. 8 tumors of the gastrointestinal system and 7 bronchial carcinoma. Evaluation of the plain films showed that the initial site of metastasis (n = 463) was the vertebral body in 441 cases and the pedicles in 294 cases. In CT scans most of the lesions confined to one part of the vertebral body (36 of 98) were localized in the posterior part. Twelve percent of the metastases were diagnosed with conventional radiography and 17% of those diagnosed with CT were not detected in skeletal scintigraphy. MRI was rarely used in diagnosing occult vertebral metastases (n = 37); 22% of the metastases demonstrated by MRI were not detected in skeletal scintigraphy. We concluded that only in 63.8% was the pedicle sign the initial site of metastasis on plain films. Bone scans and plain films are the most important diagnostic procedures for detecting and monitoring vertebral metastases. CT and MRI are only needed in patients with neurological symptoms and persistent pain.
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PMID:[Spinal metastases. Value of diagnostic procedures in the initial diagnosis and follow-up]. 789 39

Lymph node status in prostate cancer is not only of prognostic but also of tremendous therapeutic relevance. In case of positive lymph nodes (N+), common standards demand the renunciation of local curative therapy (such as radiotherapy or radical prostatectomy) and hormonal withdrawal, or an appropriate adjuvant therapy can be planned (for example, early androgen ablation). But none of the currently available means of radiologic imaging (CT, MRT, PET-CT) provides sufficient identification of lymph node (micro)metastases (< 5 mm). Also, predictive nomograms which are based on data from limited pelvic lymph node dissection (PLND) do not offer a sufficient grade of reliability. However, the limitation of the dissection area results in missing about 50-60% of N+ patients. In addition, the preoperative diagnostics often underestimate the true pathological stage. Presently, it seems that only the histological detection of lymph node metastases by methods with high sensitivity, like sentinel lymph node dissection or extended PLND, are suitable for lymph node staging in prostate cancer. The disadvantages of extended PLND are a high operative effort and increased complication rate. Therefore, sentinel lymph node dissection seems to strike a balance between high sensitivity and low complication rate.
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PMID:Lymphadenectomy in prostate cancer. Radio-guided lymph node mapping: an adequate staging method. 1854 86

3,3'-Diindolylmethane (DIM) and its synthetic halogenated derivatives 4,4'-Br2- and 7,7'-Cl2DIM (ring-DIMs) have recently been shown to induce protective autophagy in human prostate cancer cells. The mechanisms by which DIM and ring-DIMs induce autophagy have not been elucidated. As DIM is a mitochondrial ATP-synthase inhibitor, we hypothesized that DIM and ring-DIMs induce autophagy via alteration of intracellular AMP/ATP ratios and activation of AMP-activated protein kinase (AMPK) signaling in prostate cancer cells. We found that DIM and ring-DIMs induced autophagy was accompanied by increased autophagic vacuole formation and conversion of LC3BI to LC3BII in LNCaP and C42B human prostate cancer cells. DIM and ring-DIMs also induced AMPK, ULK-1 (unc-51-like autophagy activating kinase 1; Atg1) and acetyl-CoA carboxylase (ACC) phosphorylation in a time-dependent manner. DIM and the ring-DIMs time-dependently induced the oncogenic protein astrocyte-elevated gene 1 (AEG-1) in LNCaP and C42B cells. Downregulation of AEG-1 or AMPK inhibited DIM- and ring-DIM-induced autophagy. Pretreatment with ULK1 inhibitor MRT 67307 or siRNAs targeting either AEG-1 or AMPK potentiated the cytotoxicity of DIM and ring-DIMs. Interestingly, downregulation of AEG-1 induced senescence in cells treated with overtly cytotoxic concentrations of DIM or ring-DIMs and inhibited the onset of apoptosis in response to these compounds. In summary, we have identified a novel mechanism for DIM- and ring-DIM-induced protective autophagy, via induction of AEG-1 and subsequent activation of AMPK. Our findings could facilitate the development of novel drug therapies for prostate cancer that include selective autophagy inhibitors as adjuvants.
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PMID:Diindolylmethane and its halogenated derivatives induce protective autophagy in human prostate cancer cells via induction of the oncogenic protein AEG-1 and activation of AMP-activated protein kinase (AMPK). 2892 15