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)

29 cases of T-cell derived lymphoblastic lymphoma and T-ALL have been analyzed. There is a striking prevalence of the male sex. In the peripheral blood we often find initially an excessive number of white blood cells combined with normal values for the other constituents in about half of the patients; This may be an expression for the rapid occurrence of leukaemia in T-cell lymphosarcoma. In addition to systemic ALL-therapy we performed X-ray irradiation of the mediastinum in 8 of our patients. This yielded to significantly longer first complete remissions. All patients with T-cell LSA/ALL with or without mediastinal mass should be treated in this manner. Cytochemically a strong focal acid phosphatase reaction was found to be acharacteristic of these cells. It has proved to be a screening method for this disease. The cells are T-cell derived and their pattern of surface markers is similar to that found in fetal thymocytes.
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PMID:[Malignant mediastinal lymphoblastic lymphoma with t-cell ALL (author's transl)]. 30 Jan 29

The utility of the lipid-associated sialic acid (LASA or LSA) test as a serum marker for malignancy is reviewed. The name LASA or LSA test is confusing because it suggests that only or mainly lipid-bound sialic acid is measured. In reality, glycoprotein-bound sialic acid is determined predominantly. The assay appears to have a particularly high positivity rate in leukemia, Hodgkin's disease, melanoma, sarcoma, advanced ovarian carcinoma and oropharyngeal tumors, suggesting that LASA may serve as a valuable marker in these malignancies. As a consequence of the rise of sialic acid-rich acute-phase proteins, such as alpha 1-acid glycoprotein, in inflammatory diseases the specificity of LASA and therefore its diagnostic accuracy is low. LASA can be useful for monitoring cancer patients during treatment, especially in combination with other tumor markers.
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PMID:The utility of lipid-associated sialic acid (LASA or LSA) as a serum marker for malignancy. A review of the literature. 162 78

Between 1988 and 1991, feline immunodeficiency virus (FIV) infection status was evaluated in 1,160 cats examined at an oncology referral and general practice in Los Angeles, California. Twenty-nine (2.5%) cats were FIV positive. Neoplasia was present in 18 of the 29 (62%) cats. Sampling for neoplasia was intentionally biased in the oncology referral group. However, 33% (6/18) of FIV-infected cats with neoplasia originated from the general practice. Three neoplastic processes were observed; myeloproliferative disease (MPD; 5/18), lymphoma (LSA; 5/18), and squamous cell carcinoma (SCC; 7/18). One cat had LSA and SCC. Extranodal sites of LSA were common (66%) in FIV-infected cats. Sites of LSA were submandibular and mesenteric lymph nodes, liver, kidneys, periorbital area, and diffuse (heart, pancreas, bladder). Sites of SCC were sublingual (n = 2), nasal planum (n = 3), nasal planum and eyelids (n = 1), and mandible (n = 2). Feline leukemia virus co-infection was observed in 17% (5/29) of FIV-infected cats. The FIV-infected cats with MPD were young (range, 8 months to 13 years; median, 4 years) and had short survival duration (2, 6, 21, 134, 249 days) even in response to aggressive treatment. The FIV-infected cats with LSA were older (median age, 8 years; range, 4 to 14 years) and survived 60 days if untreated. Cats administered chemotherapy survived 39, 45, 217, and 243 days; the latter 2 cats had partial remission of 2 months' duration. Older FIV-infected cats had SCC (median age, 12 years; remission range, 7 to 16 years) because of more frequent association of both diseases in older cats with outdoor environment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neoplasia associated with feline immunodeficiency virus infection in cats of southern California. 166 82

Fourty successive adult patients with lymphoblastic lymphoma entered a study of sequential chemotherapy consisting of an intensive LSA-L2-type protocol to induce first complete remission. Twenty-one patients in first CR (median age 24 years, range 15-43), after receiving a conditioning regimen consisting of cyclophosphamide and total body irradiation, underwent autologous bone marrow transplantation. At this time fourteen patients are alive and well 5-72 months post-transplant (median follow-up 58 months) with an actuarial disease free survival of 66%. These early results suggest that high-dose chemoradiotherapy followed by autologous bone marrow transplantation may improve long-term disease free survival in advanced stage adult lymphoblastic lymphoma.
Leukemia 1991
PMID:Autologous bone marrow transplantation for adult advanced stage lymphoblastic lymphoma in first CR. A study of the NHLCSG. 189 Aug 65

A cell-line, designated LSA-1, was derived from a thymic lymphosarcoma that occurred in a cat with experimentally induced feline leukemia virus (FeLV) infection. LSA-1 cells possessed surface receptors and antigens of normal T-lymphocytes, but were unresponsive to interleukin-2 stimulation. The LSA cell-line was found to constitutively produce and release an interferon into the culture supernatants. Production of this interferon was enhanced in certain clones of the original LSA-1 cell lines. The interferon produced by LSA-1 cells and some of its clones was compared to the standard alpha, beta, and gamma interferons of cats. Unlike alpha and beta interferons, which were acid, SDS, and heat stable, LSA interferon was acid labile and SDS and heat stable. In comparison, standard feline gamma interferon was acid, SDS, and heat labile. LSA interferon had a molecular weight of 20,000 daltons, compared to 17-19,000 daltons for gamma, 19-25,000 for beta, and 25-45,000 daltons for alpha interferons. Standard feline interferons were active only on cat cell lines, with the exceptions of alpha interferon, which also reacted with MDCK canine cells. LSA interferon resembled the standard feline alpha interferon because it also reacted with feline and canine cells. It was concluded that LSA interferon was an atypical acid labile alpha interferon, resembling in this respect the abnormal alpha interferon seen in humans with AIDS and SLE, and mice with retrovirus infections. LSA-1 cells produced high levels of FeLV structural proteins but very little infectious virus. This effect was due to endogenously produced interferon; LSA cell clones that were selected for low interferon production produced much higher levels of infectious FeLV than parent cells or clones selected for high interferon production. Cat cells pretreated with LSA or with standard feline alpha and beta interferons, and then infected with FeLV, produced high levels of FeLV proteins but very little infectious virus.
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PMID:A feline retrovirus induced T-lymphoblastoid cell-line that produces an atypical alpha type of interferon. 300 26

ICO-G-2 hybridoma clone was obtained after fusion of spleen cells from BALB/c mice immunized with cells from a patient with acute myelomonoblastic leukemia (AMML) and P3 X 63 Ag8.653 cells, using 50% polyethyleneglycol, molecular weight 1500 KD. The antigen with a molecular weight of 100 KD was present only on polymorphonuclear neutrophils and eosinophils of the peripheral blood. The antigen expression was also found on the majority of myeloid precursors and some nuclear erythroid cells. CFU-GM did not express the antigen. Monoclonal antibodies ICO-G-2 reacted with blast cells of some patients with AML, AMML and CML. The antibodies did not react with cells from patients with AMonL, CMonL, ALL, CLL and LSA. Such pattern of reactivity makes these monoclonal antibodies useful for the differential diagnosis of acute nonlymphocytic leukemias and CML in blast crisis.
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PMID:[Monoclonal antibodies to the antigen of myeloid cells]. 362 Jun 54

437 children with acute lymphoblastic leukaemia (ALL) have been treated at 9 different institutions in Austria utilizing common protocols and central registration between 1974 and 1984. 227 patients (132 boys and 95 girls, group I) were treated between 1974 and 1980 using 3 consecutive protocols (KMK, O 76, A 78), which were essentially derived from the Memphis studies VII and VIII. Patients with a high risk of relapse were treated according to the LSA 2-L2 protocol. 210 patients (112 boys and 98 girls, group II) were consecutively treated following the BFM protocols 76/79 and 81/83. In this group, treatment intensity was adjusted to the initially determined individual risk of relapse (BFM risk score or risk factor). To date, the life table analysis demonstrates that the probability of continuous complete remission for patients in group II is 60% after 5 and 3 years (BFM 76/79 and BFM 81/83, respectively), whereas group I reaches a level of 37.3%. The prognostic difference between risk and non-risk patients in both studies of group II was eliminated. Despite a higher morbidity and non-leukaemia-related mortality in group II, the therapeutic success can be attributed to the intensification of induction therapy.
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PMID:[Cooperative studies in the treatment of acute lymphoblastic leukemia in children in Austria--report of 10 years' experience]. 388 79

In the current study, we examined whether ligation of CB2 receptors would lead to induction of apoptosis in tumors of immune origin and whether CB2 agonist could be used to treat such cancers. Exposure of murine tumors EL-4, LSA, and P815 to delta-9-tetrahydrocannabinol (THC) in vitro led to a significant reduction in cell viability and an increase in apoptosis. Exposure of EL-4 tumor cells to the synthetic cannabinoid HU-210 and the endogenous cannabinoid anandamide led to significant induction of apoptosis, whereas exposure to WIN55212 was not effective. Treatment of EL-4 tumor-bearing mice with THC in vivo led to a significant reduction in tumor load, increase in tumor-cell apoptosis, and increase in survival of tumor-bearing mice. Examination of a number of human leukemia and lymphoma cell lines, including Jurkat, Molt-4, and Sup-T1, revealed that they expressed CB2 receptors but not CB1. These human tumor cells were also susceptible to apoptosis induced by THC, HU-210, anandamide, and the CB2-selective agonist JWH-015. This effect was mediated at least in part through the CB2 receptors because pretreatment with the CB2 antagonist SR144528 partially reversed the THC-induced apoptosis. Culture of primary acute lymphoblastic leukemia cells with THC in vitro reduced cell viability and induced apoptosis. Together, the current data demonstrate that CB2 cannabinoid receptors expressed on malignancies of the immune system may serve as potential targets for the induction of apoptosis. Also, because CB2 agonists lack psychotropic effects, they may serve as novel anticancer agents to selectively target and kill tumors of immune origin.
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PMID:Targeting CB2 cannabinoid receptors as a novel therapy to treat malignant lymphoblastic disease. 1209 57

Lichen sclerosus (LS), also known as lichen sclerosus et atrophicus, is a chronic inflammatory mucocutaneous disease affecting the genital and/or extragenital areas. Although LS usually occurs alone, its coexistence in morphea patients has been reported in 5.7% and 38.0% (genital LS) of cases, in two series (1). A 74-year-old woman presented with a 6-month history of multiple asymptomatic, shiny , indurated, brownish large flat plaques located on the abdomen (Figure 1, a-b) and back, intermingled with slightly atrophic, white-colored, guttate, and patchy areas (Figure 1, d-e). Both punch biopsies of the sclerotic plaques on the back and abdomen showed findings consistent with morphea (Figure 1, c, f). Furthermore, the punch biopsy of a well-demarcated white plaque on the back revealed findings compatible with LS (Figure 1, f). Remarkably, there were also multiple white-colored lesions on the sites of pregnancy-induced striae distensae (SD) (Figure 2, a-b) on the lower abdomen and an old appendectomy scar (Figure 2, c). There was no anogenital involvement. A diagnosis of morphea-LS overlap was established and white lesions located on the surgical scar and SD were clinically evaluated as LS. Methotrexate (15 mg/week) achieved a partial regression of morphea plaques in three months. However, white LS lesions remained unchanged. Our patient presented with coexistence of LS and morphea on different sites of the trunk and on the same lesion. Additionally, one of the isolated LS lesions was located on a surgical scar. Occurrence of LS on skin grafts, irradiated areas, injection sites, or burn/surgical scars has been attributed to the Koebner phenomenon, also called isomorphic response, defined as "the formation of the skin lesions in the same morphology of the existing disease on the areas of various cutaneous injuries" (2). LS is classified under the Koebner category-III (occasional lesions) (2). However, in a case of morphea with features of LS that developed in 1 month following a herpes zoster infection has been suggested to represent "Wolf's isotopic response" (3), which was originally defined as "the occurrence of a new skin disease at the site of another, unrelated and already healed skin disorder" with a time interval between the first and second diseases ranging from months to several years (4). Remarkably, typical morphea plaques in our patient did not involve the surgical scar, in contrast to a cohort in which 16% of 329 patients developed initial morphea lesions at sites of prior (surgery) or ongoing/repetitive (chronic friction) skin trauma (5). SD appear on skin as atrophic linear bands mostly due to rapid weight changes, pregnancy, Cushing syndrome, or prolonged use of corticosteroids (6). The mechanism underlying the occurrence of several diseases on striae is still elusive. Blunt trauma occurring during the development of striae has been suggested to cause the Koebner phenomenon in patients with vitiligo, psoriasis, and lichen planus (7), but it has been suggested that the occurrence of leukemia cutis on SD in a patient reflects Wolf's isotopic response (8). Although chronic graft-versus-host disease, urticarial vasculitis, keloid, lupus erythematosus, diffuse normolipemic plane xanthoma, and drug-induced cutaneous eruptions have been reported to occur on striae (6,9), such an association with LS as in our patient has not been previously documented in the literature. Concomitant occurrence of LS patches on different previous lesions such as a surgical scar and SD in our patient raises the possibility of a common underlying mechanism. As mentioned above, the terms "Koebner phenomenon" or "Wolf's isotopic response" have been used to designate the development of some diseases in injured areas. However, Happle and Kluger (10) claimed in a recent statement that "there is no clear-cut criterion to distinguish isotopic response from Koebner phenomenon and all reactions of this kind represent examples of Koebner phenomenon", which seems to be the best way to describe the site-specific occurrence of LS lesions in our patient.
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PMID:Lichen Sclerosus on the Sites of Striae Distensae and a Surgical Scar in a Patient with Coexistent Morphea. 3103 93