Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The interferons are natural glycoproteins secreted in response to various stimuli, including viral infection. They have antiviral, antiproliferative and immunomodulatory effects on different target cell populations. Since recombinant human interferons have become available, they have been tested in a wide range of malignancies. They are well established in the treatment of hairy cell leukaemia, chronic myelogenous leukaemia and multiple myeloma. Although they have documented activity against lymphoma, melanoma, renal cell cancer and carcinoid tumours, their role in the treatment of these tumours is less clear. In the common solid tumours, such as lung cancer and colorectal cancer, the use of interferons remains experimental. Here we will summarise their practice applications in oncology, using randomised studies where available to establish their place in multi-modality treatment. We will not discuss their use as antiviral or immunomodulating agents in viral and autoimmune diseases, multiple sclerosis or after organ transplantation.
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PMID:Interferons in oncology. 915 55

Kidney tumors represent a wide scale of histological observations. However, only angiomyolipoma can be recognised preoperatively from results of the graphical examination. Other types can be recognised only on the bases of histological examination. Completely benign tumor is oncocytoma (it represents about 5% of all kidney tumors). Angiomyolipoma (2%) is also benign, though some case reports describing its malign transformation has been published. Angiomyolipoma under 4 cm can be only monitored, the larger tumors should be resected or selectively embolised the arterial blood supply to prevent spontaneous rupture. From the group of benign tumors only cystic nephroma can be diagnosed more often (up to 1%). One of the criteria for diagnosing the renal cortical adenoma is its size under 5 mm. That is why any adenoma, which could be diagnosed by means of graphical examination and therefore clinically significant does not exist. Most of tumors are malign epithelial tumors--renal carcinomas (RC). The are classified according Heidelberg classification into 5 elementary types: clear cell, papillary, chromophobe, originating form collecting ducts and not classifiable. Clear cell (conventional) renal carcinoma (CRC) comes most often (70 to 80%), its malign potential rise with increased size of tumor and with the gradient. Five-year survival is achieved in 30-50%. Granular form of CRC carcinoma (7% of all CRC) is the equivalent of poorly differentiated PRC and it has an adverse prognosis. In contrary, the cystic form of CRC (about 6%) in benign. Papillary form of RC has the five-year survival in 84%, malignant are only tumors poorly differentiated. These are tumors with extensive necroses, which brings a fragile consistency and they can be distinguished by graphical examination. Chromophobe type of RC (5%) has the five-year survival in 90%. Poor prognosis has its sarcomatoid form, which can originate from any RC, but most frequently it is derived from the chromophobe type. The form originating from collecting ducts is highly infrequent and very malignant with the five-year survival in 20% only. The unclassified form of RC (3-5%) includes tumors not suiting to the criteria of the previous RC. Other primary renal malignant tumors (sarcomas, Wilms' tumor of adults, medullar carcinoma, carcinoid) are very rare. Comparatively frequent are metastases of other tumors (namely that of lung carcinoma) and renal impairment in leukemia, which are complication not often met by urologist.
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PMID:[Histologic classification of kidney tumors for clinical practice in adults]. 1150 85

There has been a multitude of case reports, case series, hospital-based, and population-based studies that link CD to various types of cancers. When each of these studies is scrutinized, however, there is only enough evidence to support a link between colorectal adenocarcinoma, SBA, and squamous and adenocarcinomas that are associated with perianal fistulizing disease. All of the studies of large bowel adenocarcinoma or SBA follow patients in an era during which there were far fewer effective medicines to treat CD and surgery was more commonplace. The only surveillance study of patients who had extensive, long-duration Crohn's colitis showed a 22% risk for developing neoplasia (low-grade, high-grade, or cancer) after four surveillance examinations. Overall results from this study and the multitude of the other studies show that the risk for cancer in Crohn's colitis is equal to that in UC given equal extent and duration of disease. Patients who have Crohn's colitis that affects at least one third of the colon and with at least 8 years of disease should undergo screening and surveillance, just as in UC. Although the absolute risk for SBA in CD is low (2.2% at 25 years in one study), we should not rule out screening and surveying for this complication that is associated with significant morbidity and mortality in patients who have long-standing, extensive, small bowel disease. The risk for lymphoma and leukemia in CD is low, but immunomodulators and biologics may increase this risk. The evidence that links carcinoid tumors to CD is weak, and population-based studies need to be done. The study of cancers that are associated with CD is an evolving field that surely will change given that immunomodulators and biologics are being used with greater frequency.
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PMID:Cancer in Crohn's disease. 1695 44

Almost one-third of gastrointestinal stromal tumors (GISTs) are discovered incidentally during investigative or therapeutic procedures for unrelated diseases. In this regard, GISTs may coexist with different types of cancer, either synchronously or metachronously. The frequency of this association and the spectrum of neoplasms involved have not been sufficiently analyzed. We conducted a review of the literature and our own records for cases with sporadic GISTs and other malignancies, with emphasis on solid tumors. Neurofibromatosis 1 and Carney triad-associated tumors were excluded. Based on these data, there were 518 cancers in 486 GIST patients among 4813 cases with informative data. The overall frequency of second tumors in different series varied from 4.5% to 33% (mean, 13%). A total of 29 patients had multiple malignancies. GISTs of gastric location were most commonly involved with other neoplasms, reflecting their overall high frequency (60%) of all GISTs. The major types of GIST-associated cancers were gastrointestinal carcinomas (n=228; 47%), lymphoma/leukemia, (n=36; 7%), and carcinomas of prostate (n=43; 9%), breast (n=34; 7%), kidney (n=27; 6%), lung (n=26; 5%), female genital tract (n=25; 5%), and carcinoid tumors (n=13; 3%). Other cancers included soft tissue and bone sarcomas (n=15; 3%), malignant melanoma (n=12; 2%), and seminoma (n=6; 1%). Occurrence of collision tumors and metastases of carcinoma or sarcoma into a GIST (the latter noted in 4 cases) can be challenging diagnostic problems. The potential nonrandom association and causal relationship between GIST and other neoplasms remain to be investigated.
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PMID:Occurrence of other malignancies in patients with gastrointestinal stromal tumors. 1719 25

Patients diagnosed with ulcerative colitis (UC) are known to be at an increased risk of colorectal and liver cancers and leukemia. UC is an autoimmune disease, which may present a wider spectrum of cancers. We wanted to examine the risk of cancer in a large population of UC patients in order to reach high statistical power. A UC research database was constructed by identifying UC patients from the Swedish Hospital Discharge Register and cancer patients from the Cancer Registry. Follow-up of 27,606 UC patients hospitalized for the first time during the years 1964-2004 identified 2,058 patients with cancer. Standardized incidence ratios were calculated for cancer in UC patients by comparing to subjects without hospitalization for UC. The novel tumor sites in UC patients included small intestinal (carcinoid), pancreatic, breast and prostate cancers, nonthyroid endocrine gland tumors, non-Hodgkin lymphoma and multiple myeloma. A total of 11 sites showed an increased risk, which remained at 6 sites when tumors diagnosed in the year of UC hospitalization were excluded; even chronic myeloid leukemia was in excess. Cancer risks depended on the age at first hospitalization for UC. The SIRs for colon, rectal, liver and pancreatic cancers declined by age at hospitalization for UC, while for endocrine tumors the older patients were at higher risk. Our large study identified novel subsequent cancers in UC patients. However, some of these, including small intestinal carcinoids, prostate cancers and nonthyroid endocrine tumors, may be in excess because of intensified medical surveillance of the patients.
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PMID:Cancer risks in ulcerative colitis patients. 1856 19

Cholangiocarcinoma is the second most common primary malignant hepatobiliary neoplasm, accounting for approximately 15% of liver cancers. Diagnosis of cholangiocarcinoma is challenging and the prognosis is uniformly poor, with recurrence rates of 60%-90% after surgical resection. A wide spectrum of neoplastic and nonneoplastic conditions of the biliary tract may masquerade as cholangiocarcinoma, adding to the complexity of management in patients suspected to have cholangiocarcinoma. Mimics of cholangiocarcinoma constitute a heterogeneous group of entities that includes primary sclerosing cholangitis, recurrent pyogenic cholangitis, acquired immunodeficiency syndrome cholangiopathy, autoimmune pancreatitis, inflammatory pseudotumor, Mirizzi syndrome, xanthogranulomatous cholangitis, sarcoidosis, chemotherapy-induced sclerosis, hepatocellular carcinoma, metastases, melanoma, lymphoma, leukemia, and carcinoid tumors. These entities demonstrate characteristic histomorphology and variable clinicobiologic behaviors. The imaging findings of these disparate entities are protean and may be indistinguishable from those of cholangiocarcinoma. In most cases, a definitive diagnosis can be established only with histopathologic examination of a biopsy specimen.
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PMID:Mimics of cholangiocarcinoma: spectrum of disease. 1863 32

Mulibrey nanism (MUL) is a monogenic disorder with prenatal-onset growth failure, typical clinical characteristics, cardiopathy and tendency for a metabolic syndrome. It is caused by recessive mutations in the TRIM37 gene encoding for the peroxisomal TRIM37 protein with ubiquitin-ligase activity. In this work, the frequency and pathology of malignant and benign tumours were analysed in a national cohort of 89 Finnish MUL patients aged 0.7-76 years. The subjects had a clinical and radiological evaluation, and histological and immunohistocemical analyses on specimens obtained from biopsy, surgery or autopsy, were performed. The results show that the MUL patients have disturbed architecture with ectopic tissues and a high frequency of both benign and malignant tumours detectable in several internal organs. A total of 210 tumorous lesions were detected in 66/89 patients (74%). Fifteen malignancies occurred in 13 patients (15%), seven of them in the kidney (five Wilms' tumours), three in the thyroid gland, two gynaecological cancers, one gastrointestinal carcinoid tumour, one neuropituitary Langerhans cell histiocytosis and one case of acute lymphoblastic leukaemia (ALL). Tumours detected by radiology in the liver and other organs mainly comprised strongly dilated blood vessels (peliosis), vascularized cysts and nodular lesions. The lesions showed strong expression of the endothelial cell markers CD34 and CD31 as well as the myocyte marker alpha-smooth muscle actin (alpha-SMA). Our findings show that MUL is associated with frequent malignant tumours and benign adenomatous and vascular lesions, as well as disturbed organ development.
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PMID:High frequency of tumours in Mulibrey nanism. 1934

The major problems of traditional chemotherapy are non-selectivity and non-specificity, resulting in severe toxic side effects. Peptides are a new-generation of drug-delivery vector to increase efficacy of this therapy and avoid the resulting damage. The cytotoxic somatostatin (SST) conjugate JF-10-81 was developed by coupling camptothecin (CPT) to the N-terminus of a SST analog (JF-07-69) using an activated carbamate linker. This conjugate selectively targets somatostatin receptor subtype 2 (SSTR2) and also retains high binding affinity and rapid internalization as well as anti-proliferative activity towards various tumor cells. JF-10-81 was tested for its inhibitory activity against the growth of human tumors which included neuroblastoma (IMR32), pancreatic cancer (CFPAC-1), leukemia (MOLT-4), pancreatic carcinoid (BON) and prostate cancer (PC-3). Both SSTR2 mRNAs and proteins were detected in all these tumor cell lines. The conjugate displayed potent in vivo inhibitory activity, although some of the potency measured in in vitro experiments was lost. JF-10-81 was found to significantly inhibit growth of these SSTR-positive tumors, resulting in 87% tumor reduction in neuroblastoma IMR32 and 97% in leukemia MOLT-4 bearing animals, even inducing regression of CFPAC-1 tumors. SSTR-overexpressing BON tumors were unfortunately relatively CPT-insensitive in vitro, however, JF-10-81 again exhibited in vivo potency presumably by specifically increasing CPT concentrations inside the tumor cells so that the inhibition rate for JF-10-81 was 85%. Also, JF-10-81 was used to treat highly invasive PC-3 tumors where s.c. injections inhibited both tumor growth (almost 60% reduction) and tumor metastasis (over 70%). This conjugate demonstrated its broad and excellent anti-tumor activity by targeting SSTR2-specific tumor tissues, supporting that short peptides and their analogs may be applied as ideal drug-delivery carriers to improve the traditional chemotherapy.
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PMID:Targeted chemotherapy using a cytotoxic somatostatin conjugate to inhibit tumor growth and metastasis in nude mice. 2189 24

Somatic gene mutations constitute key events in the malignant transformation of human cells. Somatic mutation can either actively speed up the growth of tumour cells or relax the growth constraints normally imposed upon them, thereby conferring a selective (proliferative) advantage at the cellular level. Neurofibromatosis type-1 (NF1) affects 1/3,000-4,000 individuals worldwide and is caused by the inactivation of the NF1 tumour suppressor gene, which encodes the protein neurofibromin. Consistent with Knudson's two-hit hypothesis, NF1 patients harbouring a heterozygous germline NF1 mutation develop neurofibromas upon somatic mutation of the second, wild-type, NF1 allele. While the identification of somatic mutations in NF1 patients has always been problematic on account of the extensive cellular heterogeneity manifested by neurofibromas, the classification of NF1 somatic mutations is a prerequisite for understanding the complex molecular mechanisms underlying NF1 tumorigenesis. Here, the known somatic mutational spectrum for the NF1 gene in a range of NF1-associated neoplasms - including peripheral nerve sheath tumours (neurofibromas), malignant peripheral nerve sheath tumours, gastrointestinal stromal tumours, gastric carcinoid, juvenile myelomonocytic leukaemia, glomus tumours, astrocytomas and phaeochromocytomas - have been collated and analysed.
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PMID:Neurofibromatosis type 1-associated tumours: their somatic mutational spectrum and pathogenesis. 2215 6

Tumor lysis syndrome is a life-threatening complication comprising hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia attributed to release of intracellular contents. Although traditionally associated with leukemia and lymphoma after chemotherapy, it is known to occur in solid malignancies. We herein report a rare case of this syndrome after resection of bulky carcinoid tumor of the lung.
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PMID:Tumor Lysis Syndrome After Bilobectomy for Typical Carcinoid Tumor of the Lung. 3021 65


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