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PubMed1995

[Hematologic neoplasms and pregnancy].

Hematologic neoplasms diagnosed during pregnancy, present significant difficulties in patient management. Besides the strictly medical facts, moral, ethical and religious issues should be strongly considered. For the optimal management of individual situations an integrated multidisciplinary approach is mandatory. Hodgkin's disease, acute leukemias, non Hodgkin's lymphoma and less frequently chronic myelogenous leukemia have been reported in pregnant women. Curative treatment for most of these diseases include intensive chemotherapy regimens. Potential damage to the fetus is a major concern, due to the teratogenic effects of antimetabolites, alkylating agents and radiation therapy. Effect of pregnancy in each of these neoplasms is discussed. Although some rules of management exist, dangerous generalizations should be avoided. Particular obstetric considerations such as timing of delivery, and therapeutic abortion should be carried out on an individual basis. The emotional impact of the situation must not be underestimated.

Antineoplastic Agents↗
PubMed1994

Cell lineage involvement of recurrent chromosomal abnormalities in hematologic neoplasms.

Analysis of most hematologic neoplasms indicates the involvement of one or more cell lineages in the bone marrow and/or the blood but rules out the involvement of all lineages in any one neoplasm. It is important to detect lineage involvement in order to clarify which stem cells are involved in leukemia, to predict prognosis, and to select appropriate treatment. Our aim was to study the cell lineage involvement of some of the recurrent chromosomal abnormalities seen in hematological neoplasms. The direct morphology-antibody-chromosomes (MAC) method was used. The deletion 20q in myeloproliferative diseases (MPD), the deletion of 5q and t(1;7) in myelodysplastic syndromes (MDS), and t(3;3) in acute myeloid leukemia subtype M7 (AML-M7) were seen in all or at least in two myeloid lineages. These were interpreted as stem cell abnormalities. Deletion 13q in MPD, t(8;21) in AML-M2 and t(15;17) in AML-M3 were seen in granulocytic lineages only; t(14;18) in non-Hodgkin's lymphoma and trisomy 12 as the sole abnormality in chronic lymphocytic leukemia (B-CLL) were seen only in immunoglobulin light chain clonal B cells; inversion 14 in T-CLL was seen only in T cells, whereas t(15;14) in acute lymphocytic leukemia with eosinophilia (ALL-EO) was seen in lymphoid stem cells but not in mature granulocytes or lymphocytes. Additional abnormalities (in addition to the Philadelphia chromosome) in chronic myeloid leukemia (CML) were seen in all myeloid cell lineages and also in mature granulocytes, B cells, and large granular lymphocytes. Abnormalities in Hodgkin's disease were restricted to CD30-positive Reed-Sternberg cells. Trisomy 8 and monosomy 7 are abnormalities that may be present in either stem cells or any of the single cell lineages.

Blast Crisis↗
PubMed2000

[Resistance to cytostatics in hematologic neoplasm cells. Part III].

Resistance to cytotoxic drugs is a serious drawback in the treatment of patient with tumours, both of the haemopoietic and non-haemopoietic origin. The cytotoxic effect of drugs on the malignant cells manifests as the process of apoptosis. In the resistant malignant cells, apoptosis becomes prevented by several mechanisms. The multidrug resistance (MDR) is one of the principal mechanisms when the cancer cells develop resistance to multiple chemically and functionally unrelated cytotoxic compounds. The decrease of the cytotoxic drug concentration at the molecular target site may come from activation of some efflux membrane systems participating in the transport of cytotoxic drugs out of the cell (e.g. Pgp, MDR, and LRP). Another mechanism of resistance is the increased enzymatic detoxification of the drug by glutathion-S-transferase system. Changes in the molecular target of the cytotoxic drug such as topoisomerase molecule can be also responsible for the resistance. At least two additional mechanisms of resistance of tumour cells were identified. Resistance can come from either deregulation of proapoptotic mechanisms in tumour cells or by increased activity of reparation processes which control the damaged molecule of DNA. Several methods that detect the cause of resistance in distinct cell populations have been developed. The great effort is now focused on both the detection of mechanisms of the resistance and on the clinical procedures of overcoming the resistance to cytotoxic drugs.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1983

[Clinical effects of human lymphoblastoid interferon in patients with hematologic neoplasms].

Sixteen patients with hematologic neoplasms were treated with Human Lymphoblastoid Interferon (HL-BI) derived from Namalwa cell line. They were 6 multiple myeloma, 8 acute leukemia and 2 malignant lymphoma patients. All patients were previously treated with anticancer agents except one case with multiple myeloma. HLBI, 3.0 X 10(6) IU/day, was daily administered by intramuscular injection at least for 4 weeks. Three of 6 multiple myeloma responded to HLBI with a decrease of more than 25% in serum myeloma protein level. A case with pleural effusion due to massive infiltration of myeloma cells treated with intrathoratic administration of HLBI, in whom complete disappearance of pleural effusion was recognized. On the other hand, no patients with acute leukemia and malignant lymphoma responded except one case with acute lymphocytic leukemia, in which bone marrow lymphoblasts decreased transiently. Fever episodes, 13 of 16 cases, were more frequently seen but were manageable. Transient leukocytopenia and thrombocytopenia were also observed in 4 and 7 of 8 cases, respectively. No anaphylactoid reaction was seen. Thus, HLBI was expected useful in the clinical management of multiple myeloma.

Adult↗
PubMed1997

Benzene and the dose-related incidence of hematologic neoplasms in China. Chinese Academy of Preventive Medicine--National Cancer Institute Benzene Study Group.

BACKGROUND: Benzene is a widely distributed environmental contaminant known to cause leukemia, particularly acute nonlymphocytic leukemia, and perhaps other hematologic neoplasms and disorders. Few epidemiologic studies, however, have been able to address relationships between the extent of benzene exposure and the level of risk. PURPOSE: A large cohort study was carried out in China to evaluate the risks of developing specific hematologic neoplasms and selected related disorders in relationship to quantitative estimates of occupational benzene exposure. METHODS: A cohort of 74828 benzene-exposed and 35805 unexposed workers employed from 1972 through 1987 in 12 cities in China was identified and followed to determine the incidence of hematologic neoplasms and related disorders. Estimates of benzene exposure were derived from work histories and available historic benzene measurements. Existing pathologic material and supporting medical records were reviewed to establish diagnoses of disease. Relative risks (RRs) (i.e., ratios of incidence rates for specific hematologic neoplasms and related disorders in the benzene-exposed group to incidence rates in the unexposed group) were determined by use of Poisson regression analysis, with stratification by age and sex. RESULTS: For workers historically exposed to benzene at average levels of less than 10 parts per million (ppm), the RR for all hematologic neoplasm combined was 2.2 (95% confidence interval [CI] = 1.1-4.2), and, for the combination of acute nonlymphocytic leukemia and related myelodysplastic syndromes, the RR was 3.2 (95% CI = 1.0-10.1). For individuals who were occupationally exposed to benzene at constant levels of 25 ppm or more, the RR for the combination of acute nonlymphocytic leukemia and related myelodysplastic syndromes was 7.1 (95% CI = 2.1-23.7). Workers with 10 or more years of benzene exposure had an RR of developing non-Hodgkin's lymphoma of 4.2 (95% CI = 1.1-15.9), and the development of this neoplasm was linked most strongly to exposure that had occurred at least 10 years before diagnosis (i.e., distant exposure) (P for trend = .005, two-sided). In contrast, the risk for the combination of acute nonlymphocytic leukemia and related myelodysplastic syndromes was significantly increased among those with more recent benzene exposure (P for trend = .003, two-sided), but it was not linked to distant exposure (P for trend = .51, two-sided). CONCLUSIONS: The results of this study suggest that benzene exposure is associated with a spectrum of hematologic neoplasms and related disorders in humans. Risks for these conditions are elevated at average benzene-exposure levels of less than 10 ppm and show a tendency, although not a strong one, to rise with increasing levels of exposure. The temporal pattern of benzene exposure appears to be important in determining the risk of developing specific diseases.

Age Distribution↗
PubMed1990

[Acute renal failure in patients with hematologic neoplasms].

The retrospective study of acute renal failure (ARF) in patients with hematologic neoplasms was carried out. ARF occurred in 32 (6.1%) of 526 patients with hematologic neoplasms. Twenty-one (66%) patients recovered from ARF, but only 7 (22%) survived and were discharged from the hospital and 25 (78%) died of ARF or other complications. In 17 patients with leukemia or malignant histiocytosis, sepsis and/or disseminated intravascular coagulation were the most common causes of ARF, and all 17 patients died. In 11 patients with multiple myeloma, ARF was always attributable to the underlying disease, and the clinical course improved with the initiation of blood purification therapy (hemodialysis, plasma exchange) and chemotherapy. Five patients in blast crisis of chronic myelogenous leukemia or non-Hodgkin's lymphoma developed ARF as a result of tumor lysis syndrome. In this group, renal function improved with hemodialysis but only 2 patients survived. Patients with oliguria had worse outcomes than those without oliguria. Survival appeared to depend not on renal function but on the underlying disease, the cause of ARF, and other complications. These findings suggest that, in patients with hematologic neoplasms complicated by ARF, early initiation of blood purification therapy will improve the prognosis.

Acute Kidney Injury↗
PubMed1990

[A co-operative study on prophylactic effect of oral administration of high-dose amphotericin B syrup for systemic fungal infection in patients with hematological neoplasms. Chugoku-Shikoku Study Group of Mycosis with Hematologic Disease].

The prophylactic effect of the oral administration of high-dose amphotericin B syrup for the systemic fungal infection was studied in 36 patients with hematological neoplasms. Twenty nine patients received 2,400 mg/day of Amphotericin B syrup for during the remission induction therapy. One patient received 1,200 mg/day, 3 received 800 mg/day and 3 received 400 mg/day of Amphotericin B syrup. The prophylactic effect was recognized in 24 of 36 patients, 66.7%. As adverse effects gastrointestinal symptoms such as nausea and vomiting, hypochloremia and hypopotassemia associated with hypochloremia was observed in one patient, respectively, however, they were all controllable. The blood levels of Amphotericin B in patients received 2,400 mg/day was 0.092 +/- 0.055 micrograms/ml (n = 40) on 7th day and 0.110 +/- 0.046 micrograms/ml (n = 21) on 28th day, respectively. The administration of high-dose of Amphotericin B syrup is expected not only for the prophylaxis but also for the treatment of the systemic fungal infection.

Administration, Oral↗
PubMed1997

Molecular epidemiology of hematological neoplasms--present status and future directions.

The field of molecular epidemiology, using modern epidemiological approaches and taking the advantage of the advances in molecular biology can provide new tools for the exploration of etiological determinants, either environmental or hereditary, in the development of hematological neoplasms. It is now possible to identify some host susceptibility characteristics, to measure the effective dose of exposure, and to identify early, pre-clinical biological effects, using sensitive and specific biomarkers. The significant variation in the incidence of hematological neoplasms in different geographical areas, races, and age groups, the high rates of familial aggregation in certain populations, the involvement of protooncogenes and tumor suppressor genes in the development of hematological neoplasms, as well as of many environmental agents such as chemicals, radiation, and viruses, support the important role of molecular epidemiology in the investigation of the development of hematological neoplasms.

Animals↗
PubMed1993

[Usefulness of polymerase chain reaction (PCR) technique in making early diagnosis and treatment of cytomegalovirus and Pneumocystis carinii-pneumonia in patients with hematological neoplasms].

Recently, the incidence of opportunistic infections in patients with hematological neoplasms has been markedly increasing. However, early and definitive diagnosis and treatment of these infections remain difficult. In this study, we report three patients, a 47-year-old female with ATL, a 54-year-old female with CML and a 65-year-old female with ATL. All these cases were complicated with pneumonia caused by Pneumocystis carinii (Pc) or cytomegalovirus (CMV). They were successfully treated with sulfamethoxazole/trimethoprim or ganciclovir after detection of the respective microorganisms from sputum samples in the early stage of the infections by polymerase chain reaction (PCR) method. The above clinical evidence demonstrated the PCR technique to be a rapid and sensitive diagnostic procedure for the detection of Pc or CMV and to be helpful for the early initiation of appropriate treatment of the infections in patients with hematological neoplasms.

Aged↗
PubMed2004

CD56+ hematological neoplasms presenting in the skin: a retrospective analysis of 23 new cases and 130 cases from the literature.

BACKGROUND: The aim of this study was to define prognostic parameters and guidelines for diagnosis and treatment for CD56+ hematological neoplasms with first presentation in the skin. PATIENTS AND METHODS: The study group included 153 cases (23 new and 130 from the literature). According to the World Health Organization classification, the group included 15 nasal and 38 nasal-type natural killer (NK)/T-cell lymphomas, 63 blastic NK-cell lymphomas, 14 cutaneous CD30+ lymphoproliferations, 10 cases of myeloid leukemia, six cases of subcutaneous panniculitis-like T-cell lymphoma (SCPLTCL) and seven peripheral T-cell lymphomas, unspecified. RESULTS: In general, these CD56+ hematological neoplasms had a poor prognosis, with only 27% of patients alive after a median follow-up of 12 months. The median survival was 13 months. Nasal and nasal-type NK/T-cell lymphomas and CD56+ SCPLTCL had the worst prognosis, with a median survival of 5, 6 and 5 months, respectively. Only nasal-type NK/T-cell lymphomas presenting with only skin lesions had a somewhat better prognosis (median survival 27 months). In blastic NK-cell lymphomas (median survival 14 months), age </=40 years, aggressive treatment with acute leukemia protocols and high TdT expression were associated with a more favorable prognosis. Striking similarities in histology, immunophenotype, clinical presentation and clinical behavior were found between blastic NK-cell lymphomas and CD56+ myeloid leukemias. CONCLUSIONS: CD56+ hematological neoplasms presenting in the skin have a poor prognosis, except for primary cutaneous CD30+ lymphoproliferations. The striking similarities between blastic NK-cell lymphomas and CD56+ myeloid leukemias presenting in the skin provide a rationale to treat these patients with more aggressive regimens, rather than with CHOP(-like) regimens and radiotherapy, which have proven to be inadequate therapies for this neoplasm.

Adolescent↗
PubMed2001

Early diagnosis and treatment of pulmonary opportunistic infection by using polymerase chain reaction and beta-glucan in patients with hematological neoplasms.

The early diagnosis of 58 patients with hematological neoplasms accompanied by severe pulmonary infections of Pneumocystis carini (Pc), or Cytomegalovirus (CMV) pneumonia was made by polymerase chain reaction (PCR) using sputum samples, and of pulmonary mycosis by measuring blood beta-glucan levels by a Limulus test. The effectiveness of early treatment for opportunistic infection based on these early stage diagnosis was evaluated and the results of pathological analyses of the lung at autopsy were analyzed. PCR identified Pc pneumonia in 7 of the total 58 patients (12.1%), and early treatment was effective in all 7 patients (100%). PCR identified CMV pneumonia in 5 patients (8.6%), and early treatment was effective in 2 of the 5 patients. The level of beta-glucan confirmed mycotic pneumonia in 9 of these 58 patients (15.5%), and early treatment was effective in 7 of these (66.7%). These findings indicate that PCR and the beta-glucan method effectively enabled clinicians to diagnose pulmonary opportunistic infection in the early stage in 21 of the 58 patients (36.2%), and that early treatment was effective in 16 of the 21 patients (76.2%). The results of the pathological analyses of the lung at autopsy were: pulmonary tumor cell infiltration in a total of 5 patients (2 with ATL, 2 with NAE and 1 with AML); infection in a total of 6 patients (2 with ML and 4 with ATL); and diffused alveolar damage in a total of 4 patients (2 with ML, 1 with ATL and 1 with AML). CMV infection was confirmed in a total of 5 patients (2 with ML and 3 with ATL), and mucormycosis in a total of 2 patients (1 with ML and 1 with ATL). Despite these findings, Pc and other fungi or bacteria were not detected. Early diagnosis and treatment by the present PCR and beta-glucan method were useful, but the underlying disease and its disease state influenced the clinical outcomes of patients with terminal pulmonary infection caused by CMV or mucor, suggesting that prevention and early diagnostic measures for these infections remain to be established.

Aged↗
PubMedDate not supplied

[Conventional and multicolor FICTION as tools for the interdisciplinar study of hematological neoplasms].

Interdisciplinary technologies allowing a comprehensive characterization of cancer cells are becoming increasingly important in the routine diagnostics and research of hematological neoplasms, and in malignancies in general. One of those methods is the FICTION technique (Fluorescence Immunophenotyping and Interphase Cytogenetics as a Tool for the Investigation of Neoplasms). This technique allows the simultaneous study of the basic morphology as well as immunophenotypic and genetic markers of tumor cells. However, the low number of fluorescent substances utilized in a single assay restricts the number of markers that can be studied by FICTION. Recently, a multicolor variant has been developed and termed M-FICTION which in addition to cellular morphology and immunophenotype allows the investigation of multiple chromosomal aberrations in only one assay. In the present review, we present a detailed overview on the conventional and multicolor FICTION techniques and we discuss their multiple applications in the field of hematological neoplasms.

English Abstract↗
PubMed1999

Familial aggregation of nonhematological malignancies in relatives of patients with hematological neoplasms.

Familial aggregation of nonhematological malignant disorders (NHMD) was compared in 189 families of patients with hematological neoplasms (HN) with a control group of 36 families of patients with benign hematological disorders and a second group of 33 families of patients with diabetes mellitus. A self-administered questionnaire was used requesting from each family a full list of first- and second-degree relatives, their vital status, current age or age at death, and a list of their chronic diseases, including all malignant disorders. There was no evidence of a significantly increased tendency for developing NHMD among relatives of patients with HN as compared to controls (adjusted odds ratio of 0.88; 95% confidence interval 0.61-1.27). Moreover, in the HN group, no significant difference in the frequency of NHMD was found between the families with and without familial aggregation of HN. Based on the present analysis and our previous observations on familial aggregation of HN, we conclude that the increased aggregation of malignant disorders among relatives of patients with HN is unique to the hematopoietic system and might result from a genetic predisposition to HN in these families.

Adolescent↗
PubMed2001

[Feasibility of early tapering and discontinuation of cyclosporine to intensify the graft-versus-leukemia effect in patients with advanced hematologic neoplasms].

Twenty patients with advanced hematological malignancies at high risk of relapse who had each received a bone marrow transplant from a matched sibling were registered between October 1996 and January 2000. Cyclosporine (CSP) was tapered on day 40 and stopped on day 50 in 10 patients without prior grade II-IV acute graft-versus-host disease (GVHD), relapse or active infection. These patients were eligible for early tapering of CSP. Although grade II/III acute GVHD was observed in three patients and chronic GVHD in eight patients after CSP tapering, no patients died of GVHD. Three patients died due to disease relapse and one patient died of idiopathic interstitial pneumonia while in remission. The probability of event-free survival at 2 years was 60%. These result indicate that early tapering and withdrawal of CSP is feasible and may provide a graft-versus-leukemia effect in patients with advanced leukemia.

Adult↗
PubMed1993

2 chlorodeoxyadenosine activity and cross resistance patterns in primary cultures of human hematologic neoplasms.

2-Chlorodeoxyadenosine (2-CDA) is an adenosine deaminase resistant analogue of deoxyadenosine which has shown clinical activity in human hematologic neoplasms. The exact mode of action of this drug remains the subject of investigation. We applied the Differential Staining Cytotoxicity (DiSC) assay to 50 human tumour specimens obtained from patients with a variety of hematologic malignancies to characterise the activity spectrum of 2-CDA. We evaluated the disease-specific activity of this agent in vitro and compared its relative cytotoxicity with that of other antineoplastic agents in current clinical use. Comparisons were conducted against nitrogen mustard, doxorubicin, vincristine and cytosine arabinoside. Our results indicate that 2-CDA has activity in myeloid and many lymphoid neoplasms but that multiple myeloma specimens reveal significant resistance. Cross resistance studies reveal a correlation between 2-CDA and the alkylator nitrogen mustard but no correlation between 2-CDA and doxorubicin, vincristine nor cytosine arabinoside. The results suggest 2-CDA activity in many human hematologic neoplasms with the clear exception of multiple myeloma and further suggest a relationship between this agent and alkylators of the mustard class. The DiSC assay may provide useful insights in the pre-clinical evaluation of new antineoplastic drugs and may help to elucidate drug activities and mechanisms of action.

Cladribine↗
PubMed2006

Heterogeneous CD52 expression among hematologic neoplasms: implications for the use of alemtuzumab (CAMPATH-1H).

PURPOSE: CD52 is a GPI-linked glycoprotein expressed by B cells, T cells, monocytes, and macrophages. The humanized monoclonal antibody alemtuzumab (CAMPATH-1H) is specific for CD52 and is Food and Drug Administration - approved for the treatment of relapsed or refractory chronic lymphocytic leukemia (CLL). The utility of CAMPATH in the treatment of other hematologic neoplasms has been explored; however, a comprehensive survey of CD52 expression among a broad spectrum of WHO-defined tumor types has not been completed. EXPERIMENTAL DESIGN: We evaluated 294 hematologic neoplasms for the presence of CD52 using standard immunohistochemical techniques on paraffin-embedded biopsy specimens fixed with formalin, B-Plus, Zenker's acetic acid, or B5-formalin. RESULTS: The vast majority of low-grade B cell lymphoproliferative disorders (CLL/small lymphocytic leukemia, follicular lymphoma, lymphoplasmacytic lymphoma, hairy cell leukemia, and mucosa-associated lymphoid tissue lymphomas) express CD52. In addition, we found that the majority of precursor B cell acute lymphoblastic leukemia/lymphomas express this antigen. In contrast, there is surprising heterogeneity in CD52 expression among more aggressive B cell lymphomas, with 25% of cases of diffuse large B cell lymphoma and Burkitt lymphoma demonstrating no detectable CD52. In addition, the majority of neoplasms of the T cell lineage are negative for the antigen, including most cases of precursor T cell acute lymphoblastic leukemia/lymphoma, anaplastic large cell lymphoma, and peripheral T cell lymphoma, not otherwise specified. Finally, the vast majority of cases of acute myeloid leukemia, Hodgkin lymphoma, and multiple myeloma are negative for CD52 expression. CONCLUSION: In contrast with CLL, the variable expression of CD52 among other hematologic malignancies suggests that target validation on a case-by-case basis will likely be necessary to guide the rational analysis of CAMPATH therapy.

Acute Disease↗
PubMed1993

Cytogenetic deletion maps of hematologic neoplasms: circumstantial evidence for tumor suppressor loci.

Research in oncogenetics has led to the identification of two major classes of tumor-associated genes, oncogenes and tumor suppressor genes. In a wide variety of solid tumor types, mutations of both groups of genes have been implicated in the tumorigenic process. In hematologic neoplasms, on the other hand, most attention has focused on illegitimate activation of oncogenes, e.g., deregulation leading to disturbed transcriptional activity and structural rearrangements resulting in hybrid genes. Whether loss or mutational inactivation of tumor suppressor genes also plays an essential role in the genesis of tumors of the hematopoietic system has received less attention. Because such inactivation can be the result of karyotypically detectable loss of chromosomal material, cytogenetic studies may prove helpful in pinpointing genomic sites that harbor tumor suppressor genes. The present study is based on a total of 12,473 cytogenetically abnormal hematologic neoplasms reported in the literature to date. Among these, we selected the 6,422 cases with sole clonal chromosomal abnormalities in order to include only aberrations of importance in the genesis, rather than in the progression, of these neoplasms. All tumors with monosomies or structural abnormalities resulting in loss of chromosomal material were compiled, and for every such structural aberration, i.e., deletion, unbalanced translocation, isochromosome, and ring chromosome, the chromosome bands lost were ascertained. This cytogenetic deletion mapping revealed that the most commonly lost chromosomes were Y and 7 in acute myeloid leukemia (AML), myelodysplastic syndromes (MDS), and chronic myeloproliferative disorders (MPD); X, Y, 7, 20, and 21 in acute lymphocytic leukemia (ALL); X, Y, and 17 in chronic lymphoproliferative disorders (LPD); and X and Y in non-Hodgkin's lymphoma (NHL). Chromosome segments/bands lost due to unbalanced structural abnormalities in at least 5% of the cases were 5q13-33, 7q22-36, 9q13-31, 11q23-25, 12p12-13, 17p11-13, and 20q11-13 in AML; 5q13-35 and 20q11-13 in MDS; 5q22-23, 7q22, 13q12-22, 17p11-13, and 20q11-13 in MPD; 6q15-27, 9p11-24, 12p12-13, and 19p13 in ALL; 6q16-27, 11q21-25, 13q13-14, and 14q32 in LPD; and 6q21-27, 11q13-25, and 14q24-32 in NHL. Based on these findings, three conclusions can be drawn. First, there is no good correspondence between total and partial monosomies, the only exception being -7 and 7q-, both of which are common in myeloid neoplasms. This indicates different pathogenetic effects of total and partial losses.(ABSTRACT TRUNCATED AT 400 WORDS)

Chromosome Aberrations↗