phosphorus-radioisotopes and Lymphoma

An analysis of the risk of progression towards leukemia, carcinoma and myelofibrosis was performed in 93 patients treated by 32P alone (PVSG protocols) since 1970-1979, 395 patients over the age of 65 years treated by 32P with or without maintenance therapy using hydroxyurea (French protocol) since 1980-1994, and 202 patients under the age of 65 treated by either hydroxyurea or pipobroman since 1980. The risk of leukemia, or myelodysplasia, or lymphoma in the 32P-treated patients was 10% at the 10th year, but increase after that time to reach a value of about 30% at the 20th year, in the surviving case. This risk was not dose-related. Despite a marked reduction of the cumulative 32P dose in the patients maintained by hydroxyurea, the actuarial risk was 19% at the 10th year. In the patients treated exclusively by non radio-mimetic agents (hydroxyurea or pipobroman) a risk of 10% at the 10th year was observed. The risk of carcinoma (excluding skin cancers) was about 15% at the 10th year in the 32P-treated cases, a value similar to that generally reported by the French statistics. There was no prevalence of digestive carcinomas. In contrast, the patients receiving 32P and hydroxyurea as maintenance had an excess risk: 29% at the 10th year. In the relatively young cases treated by non radio-mimetic agents, the risk was similar in both arms: 9% at the 10th year, similar to the expected incidence at this age. The risk of myelofibrosis with myeloid metaplasia was still relatively low at the 10th year, about 15% in all arms, but increased towards a value higher than 30% in the patients surviving at the 20th year. At the present time, but in only a few cases with long-term following, no myelo-fibrosis with splenic metaplasia has been observed in the pipobroman-treated cases. The present results, which need to be confirmed (the present analysis has been done in spring 95) suggest that:-the use of non radio-mimetic agents does not protect against leukemic transformation, which may be a consequence of the disease; rather than of the treatment,-maintenance therapy after initial use of 32P increases the risk of both leukemia and carcinoma,-and hydroxyurea does not delay the risk of developing myelo-fibrosis, in comparison with 32P alone.

Topics: Actuarial Analysis; Acute Disease; Carcinoma; Cause of Death; Disease Progression; Follow-Up Studies; Humans; Hydroxyurea; Incidence; Leukemia, Myeloid; Leukemia, Radiation-Induced; Lymphoma; Neoplasms, Radiation-Induced; Phlebotomy; Phosphorus Radioisotopes; Pipobroman; Polycythemia Vera; Prevalence; Primary Myelofibrosis; Risk; Splenomegaly

Malignant pericardial effusion is usually treated only when signs of cardiac tamponade develop. Several methods of treatment have been reported with an overall response rate of approximately 75%. Since our initial study using intrapericardial 32P-colloid instillation as a treatment modality for pericardial effusion demonstrated a significant higher response rate, this study was conducted to further evaluate the efficacy of intrapericardial 32P-colloid in terms of response rates and duration of remissions. Intrapericardial instillation of 185-370 MBq (5-10 mCi) 32P-colloid in 36 patients with malignant pericardial effusion resulted in a complete remission rate of 94.5% (34 patients) whereas two patients did not respond to treatment due to a foudroyant formation of pericardial fluid. The median duration time was 8 months. No side-effects were observed. These results suggest that intrapericardial instillation of 32P-colloid is a simple, reliable and safe treatment strategy for patients with malignant pericardial effusions. Therefore, since further evidence is provided that 32P-colloid is significantly more effective than external radiation or non-radioactive sclerosing agents, this treatment modality should be considered for the management of malignant pericardial effusion.

Topics: Breast Neoplasms; Cardiac Tamponade; Chromium Compounds; Female; Gastrointestinal Neoplasms; Humans; Instillation, Drug; Lung Neoplasms; Lymphoma; Neoplasms; Pericardial Effusion; Phosphorus Radioisotopes; Radiopharmaceuticals

An analysis of the risk of progression towards leukemia, carcinoma and myelofibrosis was performed in 93 patients treated by 32P alone (PVSG protocols) since 1970-1979, 395 patients over the age of 65 years treated by 32P with or without maintenance therapy using hydroxyurea (French protocol) since 1980-1994, and 202 patients under the age of 65 treated by either hydroxyurea or pipobroman since 1980. The risk of leukemia, or myelodysplasia, or lymphoma in the 32P-treated patients was 10% at the 10th year, but increase after that time to reach a value of about 30% at the 20th year, in the surviving case. This risk was not dose-related. Despite a marked reduction of the cumulative 32P dose in the patients maintained by hydroxyurea, the actuarial risk was 19% at the 10th year. In the patients treated exclusively by non radio-mimetic agents (hydroxyurea or pipobroman) a risk of 10% at the 10th year was observed. The risk of carcinoma (excluding skin cancers) was about 15% at the 10th year in the 32P-treated cases, a value similar to that generally reported by the French statistics. There was no prevalence of digestive carcinomas. In contrast, the patients receiving 32P and hydroxyurea as maintenance had an excess risk: 29% at the 10th year. In the relatively young cases treated by non radio-mimetic agents, the risk was similar in both arms: 9% at the 10th year, similar to the expected incidence at this age. The risk of myelofibrosis with myeloid metaplasia was still relatively low at the 10th year, about 15% in all arms, but increased towards a value higher than 30% in the patients surviving at the 20th year. At the present time, but in only a few cases with long-term following, no myelo-fibrosis with splenic metaplasia has been observed in the pipobroman-treated cases. The present results, which need to be confirmed (the present analysis has been done in spring 95) suggest that:-the use of non radio-mimetic agents does not protect against leukemic transformation, which may be a consequence of the disease; rather than of the treatment,-maintenance therapy after initial use of 32P increases the risk of both leukemia and carcinoma,-and hydroxyurea does not delay the risk of developing myelo-fibrosis, in comparison with 32P alone.

Topics: Actuarial Analysis; Acute Disease; Carcinoma; Cause of Death; Disease Progression; Follow-Up Studies; Humans; Hydroxyurea; Incidence; Leukemia, Myeloid; Leukemia, Radiation-Induced; Lymphoma; Neoplasms, Radiation-Induced; Phlebotomy; Phosphorus Radioisotopes; Pipobroman; Polycythemia Vera; Prevalence; Primary Myelofibrosis; Risk; Splenomegaly

The PVSG study is unique in that it is prospective and composed of 432 patients randomized to three treatment arms. This study also provides the opportunity for serial studies of numerous sequential biopsies. Large numbers of cases with sequential biopsies covering the entire long course are essential to appreciate the full spectrum of tissue changes in this disease. The PVSG was initiated in 1967 and in mid-1985 approximately one third of the patients are alive and on protocol. For these reasons, the results must still be considered preliminary. Pretreatment biopsies from patients randomized in the PVSG have been analyzed for total cellularity, megakaryocyte concentration, and reticulin content. Considerable variation in these elements was found in these biopsies. Sequential posttreatment biopsies from these patients have also been studied and correlated with the clinical course of the disease. None of the morphologic parameters analyzed was shown to be of prognostic significance. Early in the course of PV the marrow reticulin content is almost always normal. The length of the developmental stage is unknown and the precise timing of the clinical onset may be difficult. Therefore, the 11% of patients that showed a significant increase in reticulin on initial evaluation may have had PV longer than was indicated clinically. If large numbers of sequential biopsies are studied, an increase in reticulin content can frequently be demonstrated during the active phase of the disease and before the onset of the spent phase. Currently 39 patients (9%) have developed the spent phase, or PPMM. PPMM occurred in about the same incidence in the patients treated with myelosuppressive therapy as by phlebotomy alone, the spent phase occurring in 16 patients treated by phlebotomy alone, 11 with chlorambucil, and 12 with 32P. The course of the reticulin fibrosis is slowly progressive. There is some evidence for regression in a few patients in the erythrocytotic phase, but sampling variation cannot be completely ruled out. At this time in the study, AL has developed in 37 patients (8.6%). The incidence of AL is quite low in the phlebotomy group (three cases). Presumably this represents the natural incidence in PV unmodified by therapeutic agents. The frequency is approximately equal and quite high in the chlorambucil and 32P groups. There are 19 cases in the chlorambucil-treated group and 15 in the 32P-treated group. The leukemias that developed in the PV patients occurred ei

Topics: Acute Disease; Aged; Bloodletting; Bone Marrow; Bone Marrow Cells; Chlorambucil; Combined Modality Therapy; Female; Follow-Up Studies; Humans; Leukemia; Lymphoma; Megakaryocytes; Phosphorus Radioisotopes; Polycythemia Vera; Primary Myelofibrosis; Reticulin; Retrospective Studies

The extracellular accumulation of ATP after activation of T-lymphocytes, as well as the presence of ecto-protein kinases in these cells, led us to propose that T cell surface receptors could be regulated through the reversible phosphorylation of their extracellular domains (ectodomains). Here, in a model system, we used T cell transfectants which express T cell antigen receptor chains lacking intracellular and transmembrane protein domains and 32Pi metabolic labeling of cells to definitively demonstrate phosphorylation of ectodomains of T cell surface proteins. We show that alphabetaTCR ectodomains were phosphorylated intracellularly and constitutively on serine and threonine residues and were then expressed on the T cell surface in phosphorylated form. TCR ectodomains also could be phosphorylated at the cell surface when extracellular [gamma-32P]ATP or [gamma-32P]GTP were used as phosphate donors with the same cells. Consensus phosphorylation sites for serine and threonine protein kinases were found to be strongly evolutionary conserved in both alpha and beta TCR chains constant regions. These results are consistent with the hypothesis, where T cell surface proteins which are phosphorylated intracellularly on their ectodomains, could subsequently be expressed at the cell surface and then be reversibly modified by ectoprotein phosphatase(s) and by ectokinase(s). Such modifications may change T cells cognate interactions by, e.g. affecting TCR-multimolecular complex formation and antigen binding affinity. It is suggested that alphabetaTCR ectodomain phosphorylation could serve as a potential mechanism for regulation of alphabetaTCR-mediated T-lymphocytes response.

Topics: Adenosine Triphosphate; Amino Acid Sequence; Antibodies, Monoclonal; Biological Evolution; Cell Line; Conserved Sequence; Guanosine Triphosphate; Humans; Lymphoma; Membrane Proteins; Phosphates; Phosphoprotein Phosphatases; Phosphorus Radioisotopes; Phosphorylation; Phosphoserine; Phosphothreonine; Receptors, Antigen, T-Cell, alpha-beta; T-Lymphocytes; Tumor Cells, Cultured; Type C Phospholipases

Two proteins with M(r) values of 170 kDa and 200 kDa, respectively, were identified in HOB1 lymphoma cells resistant to 1.0 microM vincristine (designated HOB1/VCR1.0) by Western blot. Using anti-P-glycoprotein monoclonal antibody to immunoprecipitate the protein from the 32P-labeled extract of HOB1/VCR1.0 cells, the major form of the protein was in the area of 200 kDa. When the cells were cultured in 0.5 microM vincristine for 72 h, the major form shifted to the area of 170 kDa. Northern blot analysis of the mdr transcription showed the gene had been overexpressed to a maximum in the cells resistant to 0.5 microM vincristine. [3H]Vincristine uptake study showed the cells with hyperphosphorylated P-glycoprotein accumulated only half the amount of the agent after 60 min of incubation as compared with those with hypophosphorylated protein. The current study suggests hyperphosphorylated P-glycoprotein is a form by which the cells can effectively exploit the protein when it can not be induced any more.

Topics: ATP Binding Cassette Transporter, Subfamily B, Member 1; Drug Resistance, Multiple; Gene Expression; Humans; Lymphoma; Phosphorus Radioisotopes; Phosphorylation; Tritium; Tumor Cells, Cultured; Vincristine

Topics: Adenosine Triphosphate; Adenylyl Cyclases; Animals; Cattle; Cell Line; Cell Membrane; GTP-Binding Proteins; Kinetics; Lymphoma; Macromolecular Substances; Mice; Phosphorus Radioisotopes; Radioisotope Dilution Technique

Labeling the EBV membrane with octadecylrhodamine-b-chloride (R18) we were able to monitor spectrofluorometrically the early events of EBV fusion, under conditions in which we could affect PKC activity. Binding of EBV to Raji cells induces PKC translocation from the cytosol to the plasma membrane and 32P incorporation into its cellular receptor CR2. CR2 phosphorylation is completely inhibited when cells are preincubated with the PKC inhibitor calphostin c. This treatment also generates a strong inhibition of EBV fusion. Taken together this result suggests a key role of CR2 phosphorylation in the EBV entry into Raji cells.

Topics: Adenosine Triphosphate; Cell Membrane; Cytosol; Fluorescent Dyes; Herpesvirus 4, Human; Humans; Ionomycin; Kinetics; Lymphoma; Membrane Fusion; Naphthalenes; Phosphates; Phosphorus Radioisotopes; Phosphorylation; Polycyclic Compounds; Protein Kinase C; Receptors, Complement 3d; Receptors, Virus; Rhodamines; Tetradecanoylphorbol Acetate; Tumor Cells, Cultured

Fourty-three primary cerebral lymphomas (PCL) were histologically classified and examined for genome expression of Epstein Barr Virus (EBV) and human herpes virus 6 (HHV6) using dot blotting, polymerase chain reaction, and Southern blotting. Only 20 tumors (16 high grade and 4 low grade lymphomas) could be suitably placed into a category of the Updated Kiel Classification, whereas the non-classified 23 tumors were highly malignant B-lymphomas and referred to as small-cell (SC) or large-cell (LC) blastic PCL. Most of the LC PCL showed a tumor-like infiltration pattern with high cellular density and little remaining parenchyma, whereas the SC PCL more often showed an inflammation-like pattern characterized by loose arrangement of tumor cells and marked astrocytic, microglial and T-lymphocytic reaction. EBV genome was found in 3/3 AIDS cases, but in none of 40 immunocompetent cases, while HHV6 was detected in 2 tumors of immunocompetent patients. We conclude that (1) the Updated Kiel Classification is not applicable to a majority of PCL, and (2) EBV and HHV6 do not appear to play a major role in the pathogenesis of PCL in immunocompetent subjects.

Topics: Autopsy; Autoradiography; Biopsy; Blotting, Southern; Brain Neoplasms; Genome, Viral; Herpesvirus 4, Human; Herpesvirus 6, Human; Humans; Inflammation; Lymphoma; Lymphoma, AIDS-Related; Phosphorus Radioisotopes; Polymerase Chain Reaction

Topics: Animals; Cell Fractionation; Cell Line; Cell-Free System; Cells, Cultured; Endoribonucleases; Humans; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Lymphoma; Mice; Phosphorus Radioisotopes; Poly A; Polyribosomes; Radioisotope Dilution Technique; Ribonuclease H; RNA, Messenger; RNA, Neoplasm

Androgen receptor heterogeneity and phosphorylation were studied in the human LNCaP cell line. Fluorography after photoaffinity labeling as well as immunoblotting with a specific polyclonal antibody revealed that the human androgen receptor migrated as a closely spaced 110 kD doublet on SDS-polyacrylamide gels. A time-dependent change in the ratio between the two isoforms was not observed after R1881 treatment of intact cells. In nuclear extracts of LNCaP cells that were incubated with [32P]orthophosphate in the presence of 10 nM R1881, a 110 kD phosphorylated protein was demonstrated after immunopurification using a monoclonal antibody against the human androgen receptor. Only a very small amount of this phosphoprotein was detected in the nuclear fraction from cells not treated with R1881. These results indicate that the human androgen receptor in LNCaP cells can be phosphorylated.

Topics: Autoradiography; Blotting, Western; Cell Line; Cell Nucleus; Humans; Lymphoma; Male; Molecular Weight; Phosphates; Phosphorus Radioisotopes; Phosphorylation; Prostatic Neoplasms; Receptors, Androgen; Tumor Cells, Cultured

Following dosing with various levels of sodium arsenite (NaAsO2), differential [32P]-incorporation (turnover) of polypeptide fragments, generated by protease V8, from a set of four closely related stress proteins (SPs), termed 'c','b','x' and 'y', (80,000-84,000 Mr) was investigated by polyacrylamide gel (PAG) autoradiography. These SPs were physically sorted sequentially from five partitions of S-phase of a mouse lymphoma cell line (YAC-1). The fragments of each of the four SPs exhibited differential [32P]-incorporation patterns with progression in S-phase following varied dose levels of NaAsO2. The majority of V8 protease-fragments of the four SPs had identical electrophoretic mobilities. A minority of polypeptides showed varied distribution among the four SPs and these fragments revealed increased [32P]-labeling progressively in S-phase. These fragments were the most sensitive to altered dose levels of NaAsO2. It was suggested that these four SPs are discrete but structurally similar proteins. A group of other SPs (S1, S2 and S3) observed predominantly in S-phase, showed reduction in polypeptide labeling during S with varied dosing of NaAsO2. The [32P]-labeling of fragments from the SPs seems generally to follow an ordered scheme of turnover (phosphorylation-dephosphorylation) during S-phase.

Topics: Animals; Arsenic; Arsenites; Autoradiography; Biomarkers; Cell Nucleus; DNA; Electrophoresis, Polyacrylamide Gel; Heat-Shock Proteins; Hydrolysis; Lymphoma; Mice; Molecular Weight; Phosphorus Radioisotopes; Phosphorylation; S Phase; Sodium Compounds; Tumor Cells, Cultured

A portion of our research involves the investigation of biomarkers as preclinical indicators of toxic stress. Stemming from this effort, we report three unique proteins that phosphorylate and synthesize during the S-phase of lymphoma cells following chemical insult. Mouse lymphoma cell nuclei were physically sorted (using a fluorescence activated cell sorter) from partitions of the cell cycle and specific nuclear proteins in each partition were examined by gel microelectrophoresis. The changes in [32P]-incorporation by stress proteins (SPs) were examined in each of seven partitions following administration of sodium arsenite. Four SPs [80,000-84,000 relative molecular mass (Mr)], designated 'c','b','x', and 'y', underwent significant alterations in [32P]-labeling and each exhibited varying degrees of differential [32P]-incorporation in partition 3 of G1 phase, all five partitions of S-phase, and partition 1 of G2 phase of the cell cycle. Three other predominantly S-phase SPs (designated S1, S2 and S3) were phosphorylated after sodium arsenite treatment. Stress protein S1 was labeled exclusively in S-phase, while proteins S2 and S3 were labeled only in partition 3 of G1 and S-phase. Stress protein S1 possessed an identical isoelectric point, molecular mass, distribution of polypeptide fragments and immunochemical determinants as S-phase SPs found previously in mouse spleen (X') and mouse liver (LP-S). The identical biochemical characteristics of these three S-phase (SPs), found in diverse tissue types, suggest they are homologous.

Topics: Animals; Arsenic; Arsenites; Cell Nucleus; Concanavalin A; Electrophoresis, Gel, Two-Dimensional; Heat-Shock Proteins; Isoelectric Point; Isoproterenol; Liver; Lymphoma; Mice; Molecular Weight; Nuclear Proteins; Peptide Mapping; Phenobarbital; Phosphorus Radioisotopes; S Phase; Sodium Compounds; Spleen; Tumor Cells, Cultured

Cultured mouse lymphoma cells incorporated [3H]leucine and [32P]phosphate into nuclear stress proteins within 3 h after exposure to either elevated temperature (45 degrees C) or sodium arsenite. Radiolabeled proteins were detected by autoradiography after two-dimensional polyacrylamide gel electrophoresis. To determine the cell cycle stage specificity of labeling, nuclei were isolated and sorted into two cell cycle phases using a fluorescent activated cell sorter. After either heat shock or sodium arsenite treatment, the majority of [3H]leucine incorporation into stress proteins occurred during the G0 + G1 phase with minimal labeling in the G2 phase. On the other hand, 32P labeling of stress proteins occurred in both the G0 + G1 and G2 phases after exposure to sodium arsenite, while incorporation of 32P was limited after heat stress. Following sodium arsenite treatment, a distinct set of four stress proteins (80-84 kDa) was detected with [3H]leucine only in G0 + G1 phase, but with [32P]phosphate these stress proteins were labeled in both G0 + G1 and G2. There was differential [32P]phosphate labeling between proteins of the 80-84 kDa set during cell cycling. Individual proteins of this set were isolated from gel plugs after sodium arsenite or heat-shock treatment. Coelectrophoresis of proteins from the two treatment groups showed that they had similar electrophoretic mobilities. All four proteins of the 80-84 kDa set (sodium arsenite induced) possessed similar polypeptide maps after digestion with V8 protease. Cytofluorometric analysis demonstrated a reduction in the number of nuclei in both S and G2 phases of the cell cycle two h after heat shock, but not following sodium arsenite treatment. However, there was a significant depression in the number of nuclei in S and G2 4 h after exposure to sodium arsenite and very modest labeling with 32P of stress proteins was observed at this time.

Topics: Animals; Arsenic; Arsenites; Cell Line; Cell Nucleus; Heat-Shock Proteins; Hot Temperature; Leucine; Lymphoma; Mice; Molecular Weight; Phosphates; Phosphorus Radioisotopes; Sodium Compounds; Sulfhydryl Reagents; Tritium

Topics: Adolescent; Choroid Neoplasms; Ciliary Body; Conjunctiva; Diagnosis, Differential; Diagnostic Errors; Evaluation Studies as Topic; Eye Neoplasms; Humans; Iris; Lymphoma; Melanoma; Neoplasm Metastasis; Phosphorus Radioisotopes; Retinoblastoma

Topics: Adenosine Triphosphate; Animals; Carcinoma, Hepatocellular; Cell Line; Cell-Free System; Chromatography, Thin Layer; Cyclic AMP; Cyclic GMP; Hot Temperature; Liver Neoplasms; Lymphoma; Pentosephosphates; Phosphorus Radioisotopes; Phosphotransferases; Protein Kinases; Rats; Ribose; Tritium

Topics: Adenosine Triphosphatases; Animals; Aza Compounds; Fluorenes; Injections, Intraperitoneal; Leukemia L1210; Leukemia, Experimental; Liver; Lymphoma; Mice; Microscopy, Electron; Phosphates; Phospholipids; Phosphorus Radioisotopes; Piperazines; Structure-Activity Relationship; Thymidine; Tritium

Topics: Animals; Cell Line; Centrifugation, Density Gradient; Chemical Precipitation; Cricetinae; Defective Viruses; DNA Nucleotidyltransferases; Electrophoresis, Paper; Gammaretrovirus; Lymphoma; Mice; Neoplasms, Experimental; Phosphorus Radioisotopes; Rats; Retroviridae; RNA, Viral; Sodium Dodecyl Sulfate; Tritium; Uridine

Topics: Aminohydrolases; Animals; Bromine; Cell Line; Cells, Cultured; Chromatography, DEAE-Cellulose; Culture Media; Cytosine Nucleotides; Deoxycytidine; Deoxyribonucleosides; Humans; Iodine; Kinetics; Lymphoid Tissue; Lymphoma; Male; Mice; Mice, Inbred DBA; Neoplasms, Experimental; Oxidative Phosphorylation; Phosphorus Radioisotopes; Phosphotransferases; Structure-Activity Relationship; Thymine Nucleotides; Tritium

Topics: Humans; Leukemia; Lymphoma; Molecular Conformation; Phosphorus Radioisotopes; RNA, Neoplasm

Topics: Hodgkin Disease; Humans; Leukemia; Lymphoma; Multiple Myeloma; Phosphorus; Phosphorus Radioisotopes; Plasma Cells; Polycythemia Vera

Topics: Adrenocorticotropic Hormone; Cortisone; Leukemia; Lymphoma; Mechlorethamine; Nitrogen Mustard Compounds; Phosphorus; Phosphorus Radioisotopes; Radiotherapy; Spleen; Steroids; Urethane; X-Rays

Topics: Lymphoma; Lymphoma, Follicular; Lymphoma, Non-Hodgkin; Phosphorus; Phosphorus Radioisotopes; Phosphorus, Dietary; Radioactivity

Topics: Adrenocorticotropic Hormone; Cortisone; Folic Acid Antagonists; Humans; Leukemia; Lymphoma; Mechlorethamine; Nitrogen Mustard Compounds; Phosphorus; Phosphorus Radioisotopes; Phosphorus, Dietary; Triethylenemelamine; Urethane

Topics: Adrenal Cortex; Adrenal Cortex Hormones; Appendix; Humans; Hydrocortisone; In Vitro Techniques; Lymphatic System; Lymphoma; Lymphoma, Non-Hodgkin; Nucleic Acids; Phosphorus; Phosphorus Radioisotopes; Spleen

Topics: Humans; Lymphoma; Lymphoma, Non-Hodgkin; Phosphorus; Phosphorus Radioisotopes; Phosphorus, Dietary; Radioactivity

Topics: Humans; Lymphoma; Lymphoma, Follicular; Phosphorus; Phosphorus Radioisotopes; Phosphorus, Dietary; Radioactivity; Radioisotopes

Topics: Liver; Lymphoma; Lymphoma, Non-Hodgkin; Nucleic Acids; Phosphorus; Phosphorus Radioisotopes; Spleen

Topics: Leukemia; Lymphoma; Mechlorethamine; Nitrogen Mustard Compounds; Peptide Nucleic Acids; Phosphorus; Phosphorus Radioisotopes; Urethane

Topics: Humans; Lymphoma; Lymphoma, Non-Hodgkin; Mycosis Fungoides; Phosphorus; Phosphorus Radioisotopes

Topics: Hodgkin Disease; Humans; Lymphoma; Phosphorus; Phosphorus Radioisotopes; Phosphorus, Dietary; Radioactivity

Topics: Animals; Lymphoma; Mice; Neoplasms; Phosphorus; Phosphorus Radioisotopes; Phosphorus, Dietary; Radioactivity

Topics: Hematologic Diseases; Humans; Lymphoma; Neoplasms; Phosphorus; Phosphorus Radioisotopes; Radioactivity

Topics: Animals; Lymphoma; Mice; Neoplasms; Neutrons; Phosphorus; Phosphorus Radioisotopes; Radioactivity; Radiotherapy