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)

Choroid plexus neoplasms are rare epithelial tumors of the central nervous system. A carcinoma of the choroid plexus occurred in a child from a family with the breast cancer-sarcoma syndrome (Li-Fraumeni or SBLA syndrome), an inherited condition characterized by the development of diverse neoplasms (sarcoma, breast cancer, brain tumors, leukemia, adrenal cortical carcinoma, and others). Choroid plexus carcinomas were identified in two kindreds previously reported with the syndrome. The literature contains reports of choroid plexus neoplasms occurring in families and in individuals with multiple primary tumors. Choroid plexus neoplasm may be a manifestation of the inherited proclivity to tumor development in the breast cancer-sarcoma syndrome.
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PMID:Choroid plexus tumors in the breast cancer-sarcoma syndrome. 224 7

Increased energy intake and physical inactivity have been shown to heighten the risk of breast, large bowel, and other cancers. Large body size and fatness, as measured by adult stature, body weight and body mass indices, are positively related to a variety of cancers, including breast, colorectum, prostate, endometrium, kidney, and ovary, as well as to total cancer incidence or mortality in many investigations, although conflicting reports exist. Adult weight gain has also been specifically implicated in a few etiologic studies of breast and large bowel cancer. Furthermore, increased birthweight and childhood stature have been linked to increased risk of leukemia, lymphoma, osteogenic sarcoma, and central nervous system malignancies between infancy and young adulthood. Greater body weight also adversely affects breast cancer survival. These findings are complementary and support a role for positive energy balance in promoting human carcinogenesis. Potential mechanisms are discussed.
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PMID:Energy balance, body size, and cancer. 225 89

The incidence of second primary tumors was studied through record-linkage in 2,968 thyroid cancer patients reported to the Swedish Cancer Registry during the period 1958-1975. The cohort was matched with the Swedish Cancer Registry between 1959 and 1984. A total of 283 second primary tumors were reported more than one year after thyroid cancer diagnosis, and the standardized incidence ratio (SIR) was 1.18 (95% confidence interval = 1.03-1.31). A significant elevated risk of cancer of the kidney, endocrine glands, and nervous system was noted. Men had a higher risk (SIR = 1.37; 95% CI = 1.06-1.70) than women (SIR = 1.11; 95% CI = 0.96-1.28). Patients who were 36-45 years at the time of the thyroid cancer diagnosis were at highest risk of developing a second primary tumor (SIR = 1.35; 95% CI = 0.99-1.81). Significantly elevated risks were seen 5-9 years after the thyroid cancer diagnosis (SIR = 1.44; 95% CI = 1:14-1.69), and the SIR was close to unity after greater than or equal to 15 years of followup. Previously described elevated risks of subsequent leukemia and breast cancer were not confirmed in this study. Close medical surveillance, thyroid cancer treatment, hereditary factors, and a high frequency of autopsy could all contribute to the elevated risk of a second primary tumor in these patients.
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PMID:Second primary tumors following thyroid cancer. A Swedish record-linkage study. 226 Dec

We have identified an identical reciprocal translocation between the long arms of chromosomes 3 and 21 with breakpoints at bands 3q26 and 21q22, [t(3;21)(q26;q22)], in the malignant cells from five adult patients with therapy-related myelodysplastic syndrome (t-MDS) or acute myeloid leukemia (t-AML). Primary diagnoses were Hodgkin's disease in two patients and ovarian carcinoma, breast cancer, and polycythemia vera in one patient each. Patients had been treated with chemotherapy including an alkylating agent for their primary disease 1 to 18 years before the development of t-MDS or t-AML. We have not observed the t(3;21) in over 1,500 patients with a myelodysplastic syndrome or acute myeloid leukemia arising de novo or in over 1,000 patients with lymphoid malignancies. We have previously reported that the t(3;21) occurs in Philadelphia chromosome-positive chronic myelogenous leukemia (CML). Thus, the t(3;21) appears to be limited to t-MDS/t-AML and CML, both of which represent malignant disorders of an early hematopoietic precursor cell. These results provide a new focus for the study of therapy-related leukemia at the molecular level.
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PMID:t(3;21)(q26;q22): a recurring chromosomal abnormality in therapy-related myelodysplastic syndrome and acute myeloid leukemia. 226 51

We studied the creatine kinase (CK) isoenzyme pattern in sera from 332 patients affected by hepatic cirrhosis and several neoplastic diseases (102 cirrhosis, 36 hepatocarcinoma, 16 metastatic liver tumor, 40 breast cancer, 18 other neoplastic diseases and 120 cases of leukemia or lymphoma) to evaluate both its diagnostic utility for cancer diagnosis and its power as a prognostic index. Type-2 macro CK (mitochondrial creatine kinase) was detected, with no statistical difference in cirrhosis (14%), hepatocarcinoma (16%), metastatic liver tumor (31%), breast cancer (5%) and other tumors (6%). It was not detected in any patient with leukemia or lymphoma. The presence of type-2 macro CK was unrelated to the stage of either cirrhosis or hepatocarcinoma, according to Child and Okuda, respectively, nor was it correlated to serum cytolytic enzyme levels or to gamma-globulin levels. In cirrhotics, type-2 macro CK was not linked to serum levels of the following tumor markers: alpha-fetoprotein, pseudouridine and gamma-glutamyltransferase isoenzymes complexed to low-density lipoprotein. In addition, the atypical band persisted in several patients with cirrhosis monitored for six months who did not show any evidence of evolution toward hepatocarcinoma. Thus, type-2 macro CK has poor diagnostic sensitivity for neoplastic diseases, and lacks prognostic value both in cirrhosis and neoplastic diseases.
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PMID:Serum type-2 macro-creatine kinase isoenzyme is not a useful marker of severe liver diseases or neoplasia. 228 11

Plasma lipid-bound sialic acid (LSA) was assayed in normal volunteers, patients with non-malignant diseases, and a variety of cancer patients. Mean plasma LSA in 50 normal volunteers, 16 patients with non-malignant diseases, 54 breast cancer, 17 lung cancer, 15 colon cancer, 7 ovarian cancer, 5 prostate cancer, 4 leukemia, 4 gastrointestinal, 3 thyroid cancer, 3 pancreas cancer and 2 adrenal cancer patients were 17.7, 23.2, 58, 85, 56.7, 46.2, 56.7, 53.3, 31.1, 33.2 and 119.5 mg/dl, respectively. None of the normal volunteers had elevated plasma LSA values. Plasma LSA level was not significantly different in male and female volunteers. Two out of 114 different cancer patients had plasma LSA levels within normal range exhibiting 98.2% sensitivity of the assay. Plasma LSA, which is relatively simple to assay, may be used as a tumor marker in wide variety of neoplastic diseases.
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PMID:Plasma lipid-bound sialic acid alterations in neoplastic diseases. 229 88

We have provided an in-depth, longitudinal, clinical/genetic/pathologic investigation of a family consonant with the sarcoma, breast cancer and brain tumors, lung and laryngeal cancer, leukemia, lymphoma, and adrenalcortical carcinoma syndrome. The pattern of cancer expression involves all three germinal layers with transmission through multiple generations. Segregation of these cancers occur in a manner consonant with an autosomal dominant mode of genetic transmission. It is hoped that recognition of the significance of this tumor pattern within families will provide an impetus for cancer surveillance, control, and laboratory research in the quest for clues to biomarkers which correlate with its cancer-prone genotype.
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PMID:SBLA syndrome revisited. 230 Mar 90

The effective treatment of systemic cancer began in the 1950s on two fronts, i.e., childhood leukemia and choriocarcinoma. These two diseases were successfully treated as a direct result of the use of antifolate methotrexate. The demonstration of complete durable remissions in these diseases quickly led to development of other anticancer drugs, tested using the prospective clinical trials. In the 1960s as the number of active drugs increased, combination chemotherapy was introduced. Other systemic cancers, such as Hodgkin's, large cell lymphoma, and testicular cancer, became curable in the 1970s. For the common low-growth fraction solid tumors, the curability of systemic disease remained elusive until the introduction of adjuvant therapy to treat micrometastases. The past decade of the 1980s has seen improvement in the outcomes for breast cancer, osteosarcoma, and possible colon cancer utilizing adjunctive chemotherapy. The 1980s also saw the introduction of biologic therapies that have further improved the outcomes of several leukemias and produced consistent responses in patients with renal cell and melanoma. The 1990s will undoubtedly see more improvements as the effects of current drugs will be enhanced not only by improved integration of systemic and local therapies but also by utilizing cytokines and biologic response modifiers in concert with cytotoxics. Moreover, as we understand more about the process of cancer induction, promotion, and progression, more specific anti-cancer approaches will be developed to control cancer even before clinical cancer is diagnosed. Underlying and facilitating the improvement in cancer therapy have been not only the experimental results of many laboratory scientists but also the outcomes from many controlled clinical trials, the laboratory of clinical scientists.
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PMID:Progress in the systemic treatment of cancer. Concepts, trials, drugs, and biologics. 230 52

Leukemia following chemotherapy for breast cancer was studied among patients diagnosed during 1973-1985 within the population-based tumor registries in the Surveillance, Epidemiology, and End Results Program. Among 13,734 women given initial chemotherapy, 24 developed acute nonlymphocytic leukemia (ANLL) compared to 2.1 expected based on general population rates (observed/expected = 11.5; 95% confidence interval = 7.4-17.1). Overall, 58 excess ANLL occurred per 100,000 women-years at risk for patients treated with chemotherapy. The cumulative incidence was 0.7% at 10 years. Risk remained high over all periods of observation up to 9 years after treatment. Among 7974 women treated only with surgery during 1973 and 1974, a period before the widespread use of adjuvant chemotherapy for breast cancer, ANLL was not significantly increased (observed = 7, expected = 5.1). A case-control study was then conducted in Connecticut to evaluate in more detail the risk associated with adjuvant chemotherapy in the general population. Among 20 cases (17 incident leukemias and 3 deaths due to preleukemia) and 60 matched controls, alkylating agents were linked to an 11.9-fold risk of ANLL and preleukemia (95% confidence interval = 2.6-55). Chemotherapy regimens including melphalan were related to a higher risk of leukemic conditions than those including cyclophosphamide. These data suggest that women in the general population treated with adjuvant chemotherapy for breast cancer are at an increased risk of leukemia, that the risk remains high among long-term survivors, and that risk differs by type of alkylating agent administered.
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PMID:Leukemia following chemotherapy for breast cancer. 232

The CMF regimen as an adjuvant therapy for breast cancer with axillary node involvement has become "standard therapy" at least for some subsets of patients (according to the Second Consensus Development Conference on Adjuvant Chemotherapy for Breast Cancer). The acute toxicity of such a regimen is usually mild and well tolerated; the late toxicity is mainly represented by amenorrhea. Here a case of acute non-lymphoid-leukemia (ANLL) after six CMF cycles is reported.
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PMID:Acute non lymphoid leukemia following CMF treatment as adjuvant therapy in positive node breast cancer. Case report. 233 Jun 10


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