Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 66-yr-old female was admitted with a 3-yr history of generalized bone pain and nasal obstruction. CT and MRI of the head revealed a large nasal mass. A whole-body bone scan revealed multifocal lesions of increased activity. Surgical removal of the nasal tumor revealed hemangiopericytoma. The patient improved clinically and a repeat bone scan 10 mo after surgery revealed markedly improved findings.
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PMID:Bone scan in tumor-induced osteomalacia. 783 Jan 24

A total of 295 patients with lytic bone metastases from breast cancer were randomized to receive chemotherapy or chemotherapy plus pamidronate (Aredia) 45 mg intravenously every 3 weeks. Primary endpoints were time to progressive bone disease (evaluated by blind extramural review), and improvement in pain (according to a 6-point self-assessment scale). Secondary endpoints included incidence of bone-related complications (pathological fractures, tumor-induced hypercalcemia, need for radiotherapy), sclerotic response of lytic lesions, WHO performance status, and analgesic score. Median time to bone progression was 249 days and 168 days in the pamidronate and control groups respectively (p = 0.02). Marked improvement in bone pain was observed in 44% of patients receiving pamidronate compared to 30% in controls (p = 0.025). With respect to secondary endpoints, pamidronate reduced the need for radiotherapy (66 times vs. 82 times in controls), and median time to radiotherapy was 697 days with pamidronate, 571 in the control arm. No severe adverse reactions or worsening of chemotherapy-induced toxicities were observed during 1598 pamidronate infusions. We conclude that intravenous pamidronate is well tolerated, significantly prolongs time to progressive bone disease, and significantly improves bone pain in patients with osteolytic metastases from breast cancer.
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PMID:Delayed progression of bone metastases with pamidronate therapy in breast cancer patients: a randomized, multicenter phase III trial. 787 61

The development of bone metastases is a selective process in which the hematogenous dissemination of tumor cells into the bone marrow does not play a decisive role. In addition to the peculiarities of blood flow within the marrow sinuses, leading to an accumulation of circulating tumor cells, host organ specific factors (adhesion molecules, chemotactic signals, cytokines and growth factors) are pathogenetically involved. These factors are liberated from the bone matrix by osteoclasts, which are activated by a variety of osteotropic tumor factors. Thereby a tumor osteopathy develops, which by osteolytic bone destruction and tumor-enhanced remodelling may cause bone pain, pathological fractures and hypercalcemia of malignancy. So far only the late stage of macrometastases and the concomitant osteopathy can be diagnosed. Using immunocytological methods, tumor cells can now be detected in bone marrow aspirates during the early subclinical stage of tumor cell shedding. Tumor cell-positive bone marrow aspirates in general mean a worsening of the prognosis and may in breast cancer indicate those patients who are threatened by the development of bone metastases.
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PMID:[Pathogenesis of bone metastasis and tumor osteopathies]. 789 37

Pancreatic polypeptidioma, a pancreatic endocrine tumor, is an extremely uncommon disease and its clinical features and responses to therapy are not well known. We present a 33-year-old woman with disseminated pancreatic polypeptidioma, who subsequently showed various signs and symptoms of metastases, including bone pain, cranial nerve palsy, spinal block, and hematuria, and died 22 months after the presentation. Responses to various therapeutic regimens including hepatic arterial embolization, radiation therapy, systemic chemotherapy, and administration of interferon-alpha or somatostatin analogue, are discussed. Particular note in this case is a prompt response of bone metastases to the radiotherapy.
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PMID:Disseminated pancreatic polypeptidioma. 814 81

Tumor-induced hypercalcemia (TIH) and tumor-induced osteolysis (TIO) are essentially due to a marked increase in osteoclast-mediated bone resorption. Parathyroid-hormone-like protein plays an essential role in TIH, and maybe in TIO, but other substances, such as growth factors or cytokines, could contribute to the osteoclast activation and osteoblast inhibition secondary to the neoplastic infiltration of the skeleton. Treatment of TIH essentially consists of volume repletion and administration of potent anti-osteolytic drugs. Intravenous administration of the bisphosphonate clodronate or pamidronate is particularly useful for this. Pamidronate at a dose of 1.0-1.5 mg/kg as a single 4- to 24-h infusion can normalize serum calcium in about 90% of hypercalcemic cancer patients. The apparently low response rate of bone metastases to systemic antineoplastic therapy seems essentially to reflect the relative insensitivity of our current methods for assessing response in TIO. Quantitative evaluation of pain and of newly developed biochemical markers of bone turnover could be particularly useful for early assessment of response. Prolonged administration of oral pamidronate could reduce by almost one-half the complications of TIO, and iterative bisphosphonate infusions could induce a dramatic relief of bone pain in one-third and a sclerosis of lytic lesions in one-fourth of the cases. These data must, however, be confirmed in randomized blind trials and many questions remain unanswered concerning the optimal therapeutic schemes. Despite these limitations, medical therapy of TIO by non-cytotoxic means has already become a reality.
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PMID:Medical treatment of tumor-induced hypercalcemia and tumor-induced osteolysis: challenges for future research. 814 98

Thirty patients were examined initially because of neurologic problems and later were diagnosed as having systemic malignant disorders. Acute leukemia was the most common malignancy (36.6%), followed by neuroblastoma (33.3%), non-Hodgkin lymphoma (13.3%), rhabdomyosarcoma (10%), Ewing tumor (3.3%), and Hodgkin lymphoma (3.3%). Four of the 11 acute leukemia patients had nervous system involvement due to meningeal, orbital, or cerebellar infiltration. The complaints of the remaining patients included back pain, weakness, and difficulty in walking, all of which were caused by anemia or bone pain. Neurologic involvement in systemic malignancies, other than acute leukemia, mainly appeared as spinal cord compression (7 with neuroblastoma, 3 non-Hodgkin lymphoma, 1 rhabdomyosarcoma, 1 Ewing tumor), orbital or cavernous sinus infiltration (3 with acute leukemia, 1 rhabdomyosarcoma), and VIIth cranial nerve involvement (2 with rhabdomyosarcoma). One patient had skull infiltration without any neurologic deficit. Cerebellar signs were caused by the remote effects of cancer. It is concluded that acute leukemia is the first and neuroblastoma is the second most common malignancy among childhood systemic malignancies presenting with neurologic involvement; however, neuroblastoma is the most common cause of spinal cord compression.
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PMID:Neurologic features as initial presentations of childhood malignancies. 819 71

To determine the changes in bone metabolism in response to combined chemotherapy in patients with bone metastases (BM), we examined osteocalcin (BGP), alkaline-phosphatase (ALP), hydroxyproline (HYP), pyridinoline (PYR), and/or deoxypyridinoline (D-PYR) in 25 cancer patients. In patients without BM, serum BGP was normal and not affected by chemotherapy. In patients with BM, however, BGP was often abnormally high or low, and some patients reacted to chemotherapy with a BGP increase at 4 weeks after initiation of therapy. Such an increase was observed in the group of patients who responded favorably to therapy as judged by a decrease in bone pain and tumor-associated biochemical markers. Urine HYP, PYR, and D-PYR were high in patients with BM before therapy; D-PYR decreased transiently at 2 weeks and increased thereafter. We assume that increased bone-resorption markers along with increased bone formation markers after therapy would indicate recovery of coupled bone metabolism, as the deranged bone remodeling is improved by tumor-regression. This study suggests that BGP and D-PYR can be useful early markers to predict favorable bone response to chemotherapy in patients with BM.
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PMID:Changes of bone metabolic markers in patients with bone metastases: clinical significance in assessing bone response to chemotherapy. 831 57

A 71-year-old man who had undergone a total cystectomy and a transureterocutaneostomy more than a year earlier was admitted to our hospital on February, 1992 because of the chief complaints of anorexia and systemic bone pain due to multiple bone metastases of bladder cancer. At two weeks after the admission, he had a sudden attack of dyspnea. His chest reontgenogram revealed no significant abnormalities. He had repeated attacks and died of respiratory failure two days after the first attack. An autopsy disclosed diffuse microscopic pulmonary tumor emboli in the pulmonary arteries and arterioles of bilateral lungs, but there was no parenchymal metastasis. The metastatic lesions in the sinusoids of the liver were also occupied by numerous tumor emboli, suggesting that the tumor emboli in the lungs had derived from those in the sinusoids. Microembolization of the whole lung area must be considered as a cause of clinically unexplained dyspnea.
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PMID:[Acute respiratory failure resulting from diffuse microscopic pulmonary tumor emboli by bladder cancer: a case diagnosed at autopsy]. 832 32

The principal pathophysiologic alteration in severe hypercalcemia accompanying hyperparathyroidism and malignancy is enhanced osteoclastic bone resorption. Hypercalcemia impairs renal mechanisms that lead to sodium and calcium excretion; PTH and PTHrP acting on renal tubules enhance further calcium reabsorption. Although rehydration is often necessary as an initial therapy of hypercalcemia, the cornerstone of therapy is to inhibit osteoclastic bone resorption. The bisphosphonates, plicamycin, gallium, and calcitonin all inhibit osteoclastic bone resorption. Calcitonin is the most rapidly acting agent. Toxicities of calcitonin are minimal, yet its therapeutic efficacy is limited by lack of potency and tachyphylaxis. The second-generation bisphosphonates such as pamidronate represent a class of compounds that are extremely effective in inhibiting the metabolic function of the osteoclast. Given in a single infusion, a significant majority of patients will have normalization of corrected serum calcium lasting, on average, 1-2 weeks. Therapeutic benefit will be of greater duration because most patients remain only minimally symptomatic until corrected serum calcium rises above 11.5 mg/dL. Side effects of low-grade fever, hypophosphatemia, hypomagnesemia, and hypocalcemia may occur. Gallium nitrate is a potent inhibitor of bone resorption and may be of increased clinical value when more efficient administration protocols can be developed. Plicamycin, available for two decades, has cumulative toxicities and is less potent than the aminobisphosphonates. Renal insufficiency often accompanies severe hypercalcemia. The nephrotoxicity of gallium nitrate and plicamycin should preclude their use when there is moderate impairment of renal function, and amino bisphosphonates become the treatment of choice in these patients. Although several authors have advocated individualized approaches to the management of hypercalcemia, the potency and duration of action of the aminobisphosphonates make them a reasonable treatment choice for most patients with symptomatic hypercalcemia. Most importantly, the most effective therapy for hypercalcemia is to recognize and treat the underlying disease. Acute primary hyperparathyroidism requires surgery. The effective treatment of hypercalcemia of malignancy allows the introduction of tumor-specific therapy, limits morbidity, and shortens and deintensifies hospitalization. At times, the most appropriate and compassionate decision (particularly in patients with malignancy who have exhausted all therapeutic options and have relentless bone pain) is to withhold therapy for hypercalcemia. Future therapies directed at the osteoclast, such as more potent later-generation bisphosphonates; inhibitors of osteoclast attachments and inhibitors of peptides, which stimulate osteoclastic bone resorption, may permit safe, easily administered, outpatient therapies that will improve the quality of life for hypercalcemic patients.
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PMID:Pathophysiology and management of severe hypercalcemia. 832 91

Oncology applications in nuclear medicine include both the staging of tumors, e.g., bone scanning, and monitoring response to therapy with tumor-specific radionuclides such as 67Ga-citrate and 201Tl-chloride. An increasing role for positron emission tomography and monoclonal antibody studies in oncology is emerging, and therapeutic applications in thyroid cancer and in the treatment of metastatic bone pain are achieving impressive results. This area is likely to become the fastest growing component of nuclear medicine practice over the next decade.
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PMID:Tumor imaging and therapy. 833 72


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