An alkylating agent of value against both hematologic malignancies and solid tumors.
An antineoplastic agent used primarily in combination with mechlorethamine, vincristine, and prednisone (the MOPP protocol) in the treatment of Hodgkin's disease.
A relatively slow-growing glioma that is derived from oligodendrocytes and tends to occur in the cerebral hemispheres, thalamus, or lateral ventricle. They may present at any age, but are most frequent in the third to fifth decades, with an earlier incidence peak in the first decade. Histologically, these tumors are encapsulated, relatively avascular, and tend to form cysts and microcalcifications. Neoplastic cells tend to have small round nuclei surrounded by unstained nuclei. The tumors may vary from well-differentiated to highly anaplastic forms. (From DeVita et al., Cancer: Principles and Practice of Oncology, 5th ed, p2052; Adams et al., Principles of Neurology, 6th ed, p655)
An antitumor alkaloid isolated from VINCA ROSEA. (Merck, 11th ed.)
An antineoplastic agent. It has significant activity against melanomas. (from Martindale, The Extra Pharmacopoeia, 31st ed, p564)
A class of drugs that differs from other alkylating agents used clinically in that they are monofunctional and thus unable to cross-link cellular macromolecules. Among their common properties are a requirement for metabolic activation to intermediates with antitumor efficacy and the presence in their chemical structures of N-methyl groups, that after metabolism, can covalently modify cellular DNA. The precise mechanisms by which each of these drugs acts to kill tumor cells are not completely understood. (From AMA, Drug Evaluations Annual, 1994, p2026)
A biologic alkylating agent that exerts its cytotoxic effects by forming DNA ADDUCTS and DNA interstrand crosslinks, thereby inhibiting rapidly proliferating cells. The hydrochloride is an antineoplastic agent used to treat HODGKIN DISEASE and LYMPHOMA.
Neoplasms of the intracranial components of the central nervous system, including the cerebral hemispheres, basal ganglia, hypothalamus, thalamus, brain stem, and cerebellum. Brain neoplasms are subdivided into primary (originating from brain tissue) and secondary (i.e., metastatic) forms. Primary neoplasms are subdivided into benign and malignant forms. In general, brain tumors may also be classified by age of onset, histologic type, or presenting location in the brain.
Neoplasms of the brain and spinal cord derived from glial cells which vary from histologically benign forms to highly anaplastic and malignant tumors. Fibrillary astrocytomas are the most common type and may be classified in order of increasing malignancy (grades I through IV). In the first two decades of life, astrocytomas tend to originate in the cerebellar hemispheres; in adults, they most frequently arise in the cerebrum and frequently undergo malignant transformation. (From Devita et al., Cancer: Principles and Practice of Oncology, 5th ed, pp2013-7; Holland et al., Cancer Medicine, 3d ed, p1082)
Vinblastine derivative with antineoplastic activity against CANCER. Major side effects are myelosuppression and neurotoxicity. Vindesine is used extensively in chemotherapy protocols (ANTINEOPLASTIC COMBINED CHEMOTHERAPY PROTOCOLS).
The use of two or more chemicals simultaneously or sequentially in the drug therapy of neoplasms. The drugs need not be in the same dosage form.
A specific pair of GROUP F CHROMOSOMES of the human chromosome classification.
A complex of related glycopeptide antibiotics from Streptomyces verticillus consisting of bleomycin A2 and B2. It inhibits DNA metabolism and is used as an antineoplastic, especially for solid tumors.
A malignant form of astrocytoma histologically characterized by pleomorphism of cells, nuclear atypia, microhemorrhage, and necrosis. They may arise in any region of the central nervous system, with a predilection for the cerebral hemispheres, basal ganglia, and commissural pathways. Clinical presentation most frequently occurs in the fifth or sixth decade of life with focal neurologic signs or seizures.
A specific pair of human chromosomes in group A (CHROMOSOMES, HUMAN, 1-3) of the human chromosome classification.
An orally administered anthracycline antineoplastic. The compound has shown activity against BREAST NEOPLASMS; LYMPHOMA; and LEUKEMIA.
Time schedule for administration of a drug in order to achieve optimum effectiveness and convenience.
The treatment of a disease or condition by several different means simultaneously or sequentially. Chemoimmunotherapy, RADIOIMMUNOTHERAPY, chemoradiotherapy, cryochemotherapy, and SALVAGE THERAPY are seen most frequently, but their combinations with each other and surgery are also used.
Benign and malignant central nervous system neoplasms derived from glial cells (i.e., astrocytes, oligodendrocytes, and ependymocytes). Astrocytes may give rise to astrocytomas (ASTROCYTOMA) or glioblastoma multiforme (see GLIOBLASTOMA). Oligodendrocytes give rise to oligodendrogliomas (OLIGODENDROGLIOMA) and ependymocytes may undergo transformation to become EPENDYMOMA; CHOROID PLEXUS NEOPLASMS; or colloid cysts of the third ventricle. (From Escourolle et al., Manual of Basic Neuropathology, 2nd ed, p21)
A malignant disease characterized by progressive enlargement of the lymph nodes, spleen, and general lymphoid tissue. In the classical variant, giant usually multinucleate Hodgkin's and REED-STERNBERG CELLS are present; in the nodular lymphocyte predominant variant, lymphocytic and histiocytic cells are seen.
A common genetically determined, chronic, inflammatory skin disease characterized by rounded erythematous, dry, scaling patches. The lesions have a predilection for nails, scalp, genitalia, extensor surfaces, and the lumbosacral region. Accelerated epidermopoiesis is considered to be the fundamental pathologic feature in psoriasis.
Economic aspects of the nursing profession.
The processes of milk secretion by the maternal MAMMARY GLANDS after PARTURITION. The proliferation of the mammary glandular tissue, milk synthesis, and milk expulsion or let down are regulated by the interactions of several hormones including ESTRADIOL; PROGESTERONE; PROLACTIN; and OXYTOCIN.
A procedure consisting of a sequence of algebraic formulas and/or logical steps to calculate or determine a given task.
The actual costs of providing services related to the delivery of health care, including the costs of procedures, therapies, and medications. It is differentiated from HEALTH EXPENDITURES, which refers to the amount of money paid for the services, and from fees, which refers to the amount charged, regardless of cost.
Absolute, comparative, or differential costs pertaining to services, institutions, resources, etc., or the analysis and study of these costs.
The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.

The minimum CD34 threshold depends on prior chemotherapy in autologous peripheral blood stem cell recipients. (1/257)

We analysed 57 patients with non-myeloid malignancies who received a non-purged autologous PBSCT. All had similar mobilisation and conditioning regimens. A high prior chemotherapy score and the number of chemotherapy lines used (P = 0.015 and P = 0.01, respectively) were adverse predictors of CD34 cell yields. Lower CD34 values (P = 0.002) were seen in patients treated with potent stem cell toxins (BCNU, melphalan, CCNU and mustine), designated toxicity factor 4 agents (TF4). All patients infused with grafts containing CD34 cell doses between 1.0 and 2.0 x 10(6)/kg (range 1.25-1.90) engrafted by day 51. The only variable associated with slow platelet recovery was exposure to TF4 (P = 0.007). The majority of patients with CD34 >1.0 x 10(6)/kg achieved rapid and sustained engraftment and the only predictive factor of delayed recovery is prior exposure to stem cell toxins. Potential PBSCT candidates should if possible avoid first line and salvage chemotherapy containing TF4 drugs. We therefore advocate a minimum CD34 threshold of >1.0 x 10(6)/kg in patients without extensive prior chemoradiotherapy, and > or = 2.0 x 10(6)/kg in all other patients.  (+info)

L-Asparagine synthetase in serum as a marker for neoplasia. (2/257)

L-Asparagine synthetase appears in serum approximately 7 days after the s.c. implantation of 1 X 10(5) cells of Leukemia 5178Y/AR (resistant to L-asparaginase) and increases in activity as the neoplasm grows and metastasizes. The principal source of the enzyme is the primary tumor. After intravranial inoculation of tumor, the rate of leakage of the enzyme is more pronounced than when the subcutaneous, intramuscular, or intraperitoneal routes are used. 1-(2-Chloroethyl)-3-cyclohexyl-1-nitrosourea (NSC 79037), a nitro-sourea effective in the palliation of L5178Y/AR, temporarily halts the influx of enzyme into the blood stream, as does surgical excision of the s.c. tumor nodules. Treatment of mice with L-asparaginase within 24 hr of inoculation of the tumor markedly augments both tumor growth and the rate of penetration of L-asparagine synthetase into the circulation. Several other L-asparagine synthetase into the circulation. Several other L-asparaginase-resistant tumors also were found to spill L-asparagine synthetase into the serum, but the correlation between this phenomenon and the specific activity of the enzyme in homogenates of the tumor was imperfect.  (+info)

High-dose BEAM chemotherapy with autologous haemopoietic stem cell transplantation for Hodgkin's disease is unlikely to be associated with a major increased risk of secondary MDS/AML. (3/257)

Hodgkin's disease is curable in the majority of patients, although a proportion of patients are resistant to or relapse after initial therapy. High-dose therapy with autologous stem cell support has become the standard salvage therapy for patients failing chemotherapy, but there have been reports of a high incidence of myelodysplasia/acute myeloid leukaemia (MDS/AML) following such treatment. Patients who receive such therapy form a selected group, however, who have already been subjected to other leukaemogenic factors, such as treatment with alkylating agents. In order to ascertain the true risk of MDS/AML, comparison must be made with other patients subjected to the same risks but not undergoing transplantation. We report a retrospective comparative study of 4576 patients with Hodgkin's disease from the BNLI and UCLH Hodgkin's databases, which includes 595 patients who have received a transplant. Statistical analysis including Cox's proportional hazards multivariate regression model with time-dependent covariates was employed. This analysis reveals that the risk of developing MDS/AML was dominated by three factors, namely quantity of prior therapy (relative risk [RR] 2.01, 95% confidence intervals [CI] 1.49-2.71, for each treatment block, P < 0.0001) and whether the patient had been exposed to MOPP (RR 3.61, 95% CI 1.64-7.95, P = 0.0009) or lomustine chemotherapy (RR 4.53, 95% CI 1.96-10.44, P = 0.001). Following adjustment for these factors in the multivariate model the relative risk associated with transplantation was 1.83 (95% CI 0.66-5.11, P = 0.25). This study provides no evidence of a significantly increased risk of MDS/AML associated with BEAM therapy and autologous transplantation in Hodgkin's disease. Concern over MDS/AML should not mitigate against the timely use of this treatment modality.  (+info)

Procarbazine, lomustine, and vincristine (PCV) chemotherapy for anaplastic astrocytoma: A retrospective review of radiation therapy oncology group protocols comparing survival with carmustine or PCV adjuvant chemotherapy. (4/257)

PURPOSE: To determine any differences in outcome for patients with anaplastic astrocytoma (AA) treated with adjuvant carmustine (BCNU) versus procarbazine, lomustine, and vincristine (PCV) chemotherapy. MATERIALS AND METHODS: The Radiation Therapy Oncology Group (RTOG) database was reviewed for patients with newly diagnosed AA treated according to protocols that included either BCNU or PCV adjuvant chemotherapy. All patients were treated with radiation therapy. The outcome analysis included overall survival, taking into account patient age, extent of resection, Karnofsky performance status (KPS), and treatment group (BCNU v PCV). Stratified and nonstratified Cox proportional hazards models were used, as well as an analysis using matched cases between the groups. RESULTS: A total of 257 patients were treated with BCNU according to RTOG protocols 70-18, 83-02, and 90-06; 175 patients were treated with PCV according to RTOG protocol 94-04. All pretreatment characteristics except KPS were well balanced by treatment group; 61% of the BCNU group had a KPS of 90 to 100 compared with 73% of the PCV group (P =.0075). No statistically significant difference in survival was observed in any age group or by KPS or extent of surgery. The stratified analysis also showed no trends for improved survival by treatment group (P =. 40). The Cox model identified only age, KPS, and extent of surgery as important variables influencing survival, not treatment group. Matching cases between groups using age, KPS, and surgery resulted in 133 matched pairs. No difference in survival was observed (P =. 41). In a Cox model in which each matched pair is a strata, there was no difference between groups (P =.20). CONCLUSION: Using this retrospective analysis, there does not seem to be any survival benefit to PCV chemotherapy. Future phase III studies for patients with AA may need to consider whether BCNU or PCV is used in the control arm.  (+info)

Treatment of children with medulloblastomas with reduced-dose craniospinal radiation therapy and adjuvant chemotherapy: A Children's Cancer Group Study. (5/257)

PURPOSE: Medulloblastoma is the most common malignant brain tumor of childhood. After treatment with surgery and radiation therapy, approximately 60% of children with medulloblastoma are alive and free of progressive disease 5 years after diagnosis, but many have significant neurocognitive sequelae. This study was undertaken to determine the feasibility and efficacy of treating children with nondisseminated medulloblastoma with reduced-dose craniospinal radiotherapy plus adjuvant chemotherapy. PATIENTS AND METHODS: Over a 3-year period, 65 children between 3 and 10 years of age with nondisseminated medulloblastoma were treated with postoperative, reduced-dose craniospinal radiation therapy (23.4 Gy) and 55.8 Gy of local radiation therapy. Adjuvant vincristine chemotherapy was administered during radiotherapy, and lomustine, vincristine, and cisplatin chemotherapy was administered during and after radiation. RESULTS: Progression-free survival was 86% +/- 4% at 3 years and 79% +/- 7% at 5 years. Sites of relapse for the 14 patients who developed progressive disease included the local tumor site alone in two patients, local tumor site and disseminated disease in nine, and nonprimary sites in three. Brainstem involvement did not adversely affect outcome. Therapy was relatively well tolerated; however, the dose of cisplatin had to be modified in more than 50% of patients before the completion of treatment. One child died of pneumonitis and sepsis during treatment. CONCLUSION: These overall survival rates compare favorably to those obtained in studies using full-dose radiation therapy alone or radiation therapy plus chemotherapy. The results suggest that reduced-dose craniospinal radiation therapy and adjuvant chemotherapy during and after radiation is a feasible approach for children with nondisseminated medulloblastoma.  (+info)

Mismatch repair, G(2)/M cell cycle arrest and lethality after DNA damage. (6/257)

The role of the mismatch repair pathway in DNA replication is well defined but its involvement in processing DNA damage induced by chemical or physical agents is less clear. DNA repair and cell cycle control are tightly linked and it has been suggested that mismatch repair is necessary to activate the G(2)/M checkpoint in the presence of certain types of DNA damage. We investigated the proposed role for mismatch repair (MMR) in activation of the G(2)/M checkpoint following exposure to DNA-damaging agents. We compared the response of MMR-proficient HeLa and Raji cells with isogenic variants defective in either the hMutLalpha or hMutSalpha complex. Different agents were used: the cross-linker N-(2-chloroethyl)-N'-cyclohexyl-N-nitrosourea (CCNU), gamma-radiation and the monofunctional methylating agent N-methyl-N-nitrosourea (MNU). MMR-defective cells are relatively sensitive to CCNU, while no differences in survival between repair-proficient and -deficient cells were observed after exposure to gamma-radiation. Analysis of cell cycle distribution indicates that G(2) arrest is induced at least as efficiently in MMR-defective cells after exposure to either CCNU or ionizing radiation. As expected, MNU does not induce G(2) accumulation in MMR-defective cells, which are known to be highly tolerant to killing by methylating agents, indicating that MNU-induced cell cycle alterations are strictly dependent on the cytotoxic processing of methylation damage by MMR. Conversely, activation of the G(2)/M checkpoint after DNA damage induced by CCNU and gamma-radiation does not depend on functional MMR. In addition, the absence of a simple correlation between the extent of G(2) arrest and cell killing by these agents suggests that G(2) arrest reflects the processing by MMR of both lethal and non-lethal DNA damage.  (+info)

Relapses of childhood anaplastic large-cell lymphoma: treatment results in a series of 41 children--a report from the French Society of Pediatric Oncology. (7/257)

PURPOSE: To study response to chemotherapy and the outcome of children treated for a relapsed anaplastic large-cell lymphoma (ALCL) and to evaluate the role of bone marrow transplantation (BMT) in these patients. PATIENTS AND METHODS: Clinical data concerning the 41 relapses that occurred in 119 patients with ALCL enrolled in 3 consecutive studies since 1975 were analysed. First-line treatment consisted of intensive chemotherapy according to the COPAD protocol for the first series of 12 patients treated between 1975 and 1989 and to the SFOP (French Society of Pediatric Oncology) HM protocols for the 30 patients treated between 1989 and 1997. Twenty-eight patients were treated with CV(B)A (CCNU, vinblastine, ara-C with or without bleomycin), and the others with miscellaneous protocols for recurrent disease. Fifteen patients underwent autologous BMT and 1 allogeneic BMT while in CR2. RESULTS: Thirty-six of forty-one (88%) patients achieved CR2. With a median follow-up of 5 years, 12 patients died, 9 of their disease and 29 patients are alive in CR2 (20 patients), CR3 (5 patients), CR4 (2 patients), CR5 (1 patient) or CR6 (1 patient). Overall and disease-free survival are respectively 69% (53%-82%) and 44% (29%-61%) at three years. In univariate analysis, patients treated with ABMT while in CR2 did not appear to have a better outcome than the other. Remarkably, a long-lasting remission was obtained in 8 of 13 patients treated with weekly vinblastine for a relapse including 6 relapses occurring after ABMT. CONCLUSIONS: Relapsed ALCL are highly chemosensitive but over 40% of the patients experience several relapses. Prolonged conventional chemotherapy based on vinblastine might, in some cases, be as efficient as short intensive treatment with ABMT.  (+info)

Mismatch repair and p53 independently affect sensitivity to N-(2-chloroethyl)-N'-cyclohexyl-N-nitrosourea. (8/257)

The contributions of defective mismatch repair (MMR) and the p53-response to cell killing by N-(2-chloroethyl)-N'-cyclohexyl-N-nitrosourea (CCNU) were evaluated. MMR defects were previously shown to be associated with CCNU sensitivity (G. Aquilina et al., Cancer Res., 58: 135-141, 1998). Unexpectedly, eight MMR-deficient variants of the A2780 human ovarian carcinoma cell line were 3-fold more resistant to CCNU than the MMR-proficient parental cells. The variants were members of a preexisting subpopulation of drug-resistant A2780 cells. In addition to deficient expression of the MMR protein hMLH1, an essential component of the hMutL alpha repair complex, the variants exhibited alterations in the expression of other genes that influence drug sensitivity. Although A2780 cells possess a wild-type p53 gene, all of the clones contained a heterozygous G to T tranversion at codon 172. This change resulted in a Val to Phe substitution and was associated with a constitutive production of high levels of p53, which was inactive as a transcriptional activator of bax and p21. The hMLH1/p53 defective variants displayed a less prominent cell cycle arrest and reduced apoptosis after CCNU treatment. In contrast, MMR-defective A2780 variants, which had a similar hMutL alpha defect but retained a wild-type p53, did exhibit the expected CCNU sensitivity. Expression of a dominant-negative p53val135 increased CCNU resistance of both MMR-proficient and MMR-deficient A2780 cells. Thus, defective MMR and p53 influence CCNU sensitivity in opposite directions. Their effects are independent, and sensitization by defective MMR does not require a functional p53 response.  (+info)

The symptoms of oligodendroglioma can vary depending on the location and size of the tumor, but may include headaches, seizures, weakness or numbness in the arms or legs, and changes in personality or behavior.

Oligodendrogliomas are diagnosed through a combination of imaging tests such as MRI or CT scans, and tissue biopsy. Treatment options for oligodendroglioma can include surgery to remove the tumor, radiation therapy, and chemotherapy with drugs such as temozolomide.

Prognosis for oligodendroglioma depends on the location, size, and aggressiveness of the tumor, as well as the age and overall health of the patient. In general, benign oligodendrogliomas have a good prognosis, while malignant ones are more difficult to treat and can be associated with a poorer outcome.

There is ongoing research into new treatments for oligodendroglioma, including clinical trials of innovative drugs and therapies.

Brain neoplasms can arise from various types of cells in the brain, including glial cells (such as astrocytes and oligodendrocytes), neurons, and vascular tissues. The symptoms of brain neoplasms vary depending on their size, location, and type, but may include headaches, seizures, weakness or numbness in the limbs, and changes in personality or cognitive function.

There are several different types of brain neoplasms, including:

1. Meningiomas: These are benign tumors that arise from the meninges, the thin layers of tissue that cover the brain and spinal cord.
2. Gliomas: These are malignant tumors that arise from glial cells in the brain. The most common type of glioma is a glioblastoma, which is aggressive and hard to treat.
3. Pineal parenchymal tumors: These are rare tumors that arise in the pineal gland, a small endocrine gland in the brain.
4. Craniopharyngiomas: These are benign tumors that arise from the epithelial cells of the pituitary gland and the hypothalamus.
5. Medulloblastomas: These are malignant tumors that arise in the cerebellum, specifically in the medulla oblongata. They are most common in children.
6. Acoustic neurinomas: These are benign tumors that arise on the nerve that connects the inner ear to the brain.
7. Oligodendrogliomas: These are malignant tumors that arise from oligodendrocytes, the cells that produce the fatty substance called myelin that insulates nerve fibers.
8. Lymphomas: These are cancers of the immune system that can arise in the brain and spinal cord. The most common type of lymphoma in the CNS is primary central nervous system (CNS) lymphoma, which is usually a type of B-cell non-Hodgkin lymphoma.
9. Metastatic tumors: These are tumors that have spread to the brain from another part of the body. The most common types of metastatic tumors in the CNS are breast cancer, lung cancer, and melanoma.

These are just a few examples of the many types of brain and spinal cord tumors that can occur. Each type of tumor has its own unique characteristics, such as its location, size, growth rate, and biological behavior. These factors can help doctors determine the best course of treatment for each patient.

There are several subtypes of astrocytoma, including:

1. Low-grade astrocytoma: These tumors grow slowly and are less aggressive. They can be treated with surgery, radiation therapy, or chemotherapy.
2. High-grade astrocytoma: These tumors grow more quickly and are more aggressive. They are often resistant to treatment and may recur after initial treatment.
3. Anaplastic astrocytoma: These are the most aggressive type of astrocytoma, growing rapidly and spreading to other parts of the brain.
4. Glioblastoma (GBM): This is the most common and deadliest type of primary brain cancer, accounting for 55% of all astrocytomas. It is highly aggressive and resistant to treatment, often recurring after initial surgery, radiation, and chemotherapy.

The symptoms of astrocytoma depend on the location and size of the tumor. Common symptoms include headaches, seizures, weakness or numbness in the arms or legs, and changes in personality or behavior.

Astrocytomas are diagnosed through a combination of imaging tests such as MRI or CT scans, and tissue biopsy. Treatment options vary depending on the type and location of the tumor, but may include surgery, radiation therapy, chemotherapy, or a combination of these.

The prognosis for astrocytoma varies based on the subtype and location of the tumor, as well as the patient's age and overall health. In general, low-grade astrocytomas have a better prognosis than high-grade tumors. However, even with treatment, the survival rate for astrocytoma is generally lower compared to other types of cancer.

Glioblastomas are highly malignant tumors that can grow rapidly and infiltrate surrounding brain tissue, making them difficult to remove surgically. They often recur after treatment and are usually fatal within a few years of diagnosis.

The symptoms of glioblastoma can vary depending on the location and size of the tumor but may include headaches, seizures, weakness or numbness in the arms or legs, and changes in personality, memory or cognitive function.

Glioblastomas are diagnosed through a combination of imaging tests such as CT or MRI scans, and a biopsy to confirm the presence of cancerous cells. Treatment typically involves surgery to remove as much of the tumor as possible, followed by radiation therapy and chemotherapy to slow the growth of any remaining cancerous cells.

Prognosis for glioblastoma is generally poor, with a five-year survival rate of around 5% for newly diagnosed patients. However, the prognosis can vary depending on factors such as the location and size of the tumor, the patient's age and overall health, and the effectiveness of treatment.

There are several types of gliomas, including:

1. Astrocytoma: This is the most common type of glioma, accounting for about 50% of all cases. It arises from the star-shaped cells called astrocytes that provide support and nutrients to the brain's nerve cells.
2. Oligodendroglioma: This type of glioma originates from the oligodendrocytes, which are responsible for producing the fatty substance called myelin that insulates the nerve fibers.
3. Glioblastoma (GBM): This is the most aggressive and malignant type of glioma, accounting for about 70% of all cases. It is fast-growing and often spreads to other parts of the brain.
4. Brain stem glioma: This type of glioma arises in the brain stem, which is responsible for controlling many of the body's vital functions such as breathing, heart rate, and blood pressure.

The symptoms of glioma depend on the location and size of the tumor. Common symptoms include headaches, seizures, weakness or numbness in the arms or legs, and changes in personality, memory, or speech.

Gliomas are diagnosed through a combination of imaging tests such as CT or MRI scans, and tissue biopsy to confirm the presence of cancer cells. Treatment options for glioma depend on the type and location of the tumor, as well as the patient's overall health. Surgery is often the first line of treatment to remove as much of the tumor as possible, followed by radiation therapy and/or chemotherapy to kill any remaining cancer cells.

The prognosis for glioma patients varies depending on the type and location of the tumor, as well as the patient's overall health. In general, the prognosis is better for patients with slow-growing, low-grade tumors, while those with fast-growing, high-grade tumors have a poorer prognosis. Overall, the 5-year survival rate for glioma patients is around 30-40%.

Hodgkin Disease can spread to other parts of the body through the lymphatic system, and it can affect people of all ages, although it is most common in young adults and teenagers. The symptoms of Hodgkin Disease can vary depending on the stage of the disease, but they may include swollen lymph nodes, fever, night sweats, fatigue, weight loss, and itching.

There are several types of Hodgkin Disease, including:

* Classical Hodgkin Disease: This is the most common type of Hodgkin Disease and is characterized by the presence of Reed-Sternberg cells.
* Nodular Lymphocytic predominant Hodgkin Disease: This type of Hodgkin Disease is characterized by the presence of nodules in the lymph nodes.
* Mixed Cellularity Hodgkin Disease: This type of Hodgkin Disease is characterized by a mixture of Reed-Sternberg cells and other immune cells.

Hodgkin Disease is usually diagnosed with a biopsy, which involves removing a sample of tissue from the affected lymph node or other area and examining it under a microscope for cancer cells. Treatment for Hodgkin Disease typically involves chemotherapy, radiation therapy, or a combination of both. In some cases, bone marrow or stem cell transplantation may be necessary.

The prognosis for Hodgkin Disease is generally good, especially if the disease is detected and treated early. According to the American Cancer Society, the 5-year survival rate for people with Hodgkin Disease is about 85%. However, the disease can sometimes recur after treatment, and the long-term effects of radiation therapy and chemotherapy can include infertility, heart problems, and an increased risk of secondary cancers.

Hodgkin Disease is a rare form of cancer that affects the immune system. It is most commonly diagnosed in young adults and is usually treatable with chemotherapy or radiation therapy. However, the disease can sometimes recur after treatment, and the long-term effects of treatment can include infertility, heart problems, and an increased risk of secondary cancers.

Psoriasis can affect any part of the body, including the scalp, elbows, knees, and lower back. The symptoms of psoriasis can vary in severity, and the condition can have a significant impact on quality of life. In addition to physical discomfort, psoriasis can also cause emotional distress and stigma.

There is no cure for psoriasis, but there are several treatment options available, including topical creams and ointments, light therapy, and systemic medications such as biologic drugs. With proper treatment, many people with psoriasis are able to manage their symptoms and improve their quality of life.

Psoriasis is relatively common, affecting approximately 2-3% of the global population, with a higher prevalence in Caucasians than in other races. It can occur at any age, but typically starts in the late teenage years or early adulthood. Psoriasis is often associated with other health conditions, such as diabetes, heart disease, and depression.

Overall, psoriasis is a complex and multifactorial condition that requires a comprehensive approach to management, including both physical and emotional support. With appropriate treatment and self-care, people with psoriasis can lead full and active lives.

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Parasramka S, Talari G, Rosenfeld M, Guo J, Villano JL (July 2017). "Procarbazine, lomustine and vincristine for recurrent high ... lomustine and vincristine). A mutational analysis of 23 initial low-grade gliomas and recurrent tumors from the same patients ...
5-Year relative survival rate: Age 20-44, 76%. Age 45-54, 67%. Age 55-64, 45%. Procarbazine, lomustine and vincristine have ...
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Vinblastine and lomustine are common chemotherapy agents used to treat mast cell tumors. Toceranib and masitinib, examples of ...
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Bendamustine Lomustine Semustine CID 2578 from PubChem "Carmustine 100mg Powder and solvent for Solution for Infusion - Summary ...
... lomustine). Taselisib (codenamed GDC-0032, RG7604; PIK3CA inhibitor): Development was discontinued due to strong side effects ...
... and in combination with lomustine, versus lomustine alone in patients with recurrent glioblastoma". Journal of Clinical ... In 2016, AstraZeneca completed a phase III trial comparing the efficacy of cediranib alone and cediranib with lomustine to the ... efficacy of lomustine alone in patients with recurrent glioblastoma. The trial failed to meet its primary endpoint and survival ...
... it is often dosed as PCV when combined with lomustine (often called CCNU) and vincristine. Dose should be adjusted for kidney ... and prednisone while for brain cancers such as glioblastoma multiforme it is used with lomustine and vincristine. It is ...
Uramustine or uracil mustard Melphalan Chlorambucil Ifosfamide Bendamustine Nitrosoureas Carmustine Lomustine Streptozocin ...
Other chemotherapy drugs such as chlorambucil, lomustine (CCNU), cytosine arabinoside, and mitoxantrone are sometimes used in ...
Treosulfan L01AB03 Mannosulfan L01AC01 Thiotepa L01AC02 Triaziquone L01AC03 Carboquone L01AD01 Carmustine L01AD02 Lomustine ...
... lomustine MeSH D02.654.692.440.700 - semustine MeSH D02.654.692.480 - methylnitrosourea MeSH D02.654.692.550 - nimustine MeSH ... lomustine MeSH D02.948.594.440.700 - semustine MeSH D02.948.594.490 - methylnitrosourea MeSH D02.948.594.550 - nimustine MeSH ...
Lomustine) (1976) BCNU (Carmustine) (1977) Cis-diamminedichloroplatinum (Cisplatin) (1978) Mitoxantrone (Novantrone) (1988) ...
... lomustine (INN) lonafarnib (USAN) lonapalene (INN) lonaprisan (USAN) lonaprofen (INN) lonazolac (INN) lonidamine (INN) Loniten ...
... lomustine - lonafarnib - loop electrosurgical excision procedure - loop excision - loperamide hydrochloride - losoxantrone - ...
... lomustine, megestrol, mitomycin, mitoxantrone, paclitaxel, procarbazine, tamoxifen, topotecan Some antidepressants like ...
... lomustine, dacarbazine developed by Y Fulmer Shealy, fludarabine, amifostine, clofarabine and the latest pralatrexate (approved ...
Lomustine, chlorambucil), neurotransmitters (dopamine, GABA), nerve growth factor (NGF) inducers, anticonvulsants (Phenytoin, ...
... can refer to: Cyclin U, a human gene that now has an official symbol of CCNO Lomustine, a chemotherapeutic agent Central ...
... lomustine) Droxia/Hydrea (hydroxycarbamide) Empliciti (Elotuzumab) Erbitux (cetuximab) Etopophos (etoposide) Ixempra ( ...
lomustine). Capsules. WARNINGS. CeeNU (lomustine) should be administered under the supervision of a qualified physician ... CeeNU® (lomustine) (CCNU) is one of the nitrosoureas used in the treatment of certain neoplastic diseases. It is 1-(2-chloro- ... Lomustine and its metabolites are known to be substantially excreted by the kidney, and the risk of toxic reactions to this ... CeeNU® (lomustine) Capsules Rx only. 100 mg per capsule. Caution: DO NOT DISPENSE ENTIRE CONTAINER.. Dispense only enough ...
Lomustine: learn about side effects, dosage, special precautions, and more on MedlinePlus ... Before taking lomustine,. *tell your doctor and pharmacist if you are allergic to lomustine, any other medications, or any of ... Taking too much lomustine or taking it too often can cause serious, life-threatening problems. Take only one dose of lomustine ... Lomustine may increase the risk that you will develop other cancers. Talk to your doctor about the risks of taking lomustine. ...
Learn about drug interactions between roflumilast oral and lomustine oral and use the RxList drug interaction checker to check ... roflumilast oral and lomustine oral. roflumilast oral will increase the level or effect of lomustine oral by immune system ... roflumilast oral and lomustine oral. roflumilast oral will increase the level or effect of lomustine oral by immunosuppressive ... Drug interactions with roflumilast oral and lomustine oral. home drug interactions checker , roflumilast oral and lomustine ...
Lomustine Lomustine is used to treat certain types of brain tumors. Lomustine is also used with other medications to treat ... ...
Lomustine therapy is associated with minor transient serum enzyme elevations and has bee … ... Lomustine is an orally administered alkylating agent used alone and in combination with other antineoplastic agents in the ... Lomustine No authors listed In: LiverTox: Clinical and Research Information on Drug-Induced Liver Injury [Internet]. Bethesda ( ... Lomustine and prednisone as a first-line treatment for dogs with multicentric lymphoma: 17 cases (2004-2005). Sauerbrey ML, ...
Lomustine therapy is associated with minor transient serum enzyme elevations and has bee … ... Lomustine is an orally administered alkylating agent used alone and in combination with other antineoplastic agents in the ... Lomustine No authors listed In: LiverTox: Clinical and Research Information on Drug-Induced Liver Injury [Internet]. Bethesda ( ... Lomustine and prednisone as a first-line treatment for dogs with multicentric lymphoma: 17 cases (2004-2005). Sauerbrey ML, ...
LOMUSTINE (UNII: 7BRF0Z81KG) (LOMUSTINE - UNII:7BRF0Z81KG) LOMUSTINE. 9.9 g in 10 g. ... AX PHARMACEUTICAL CORP- lomustine powder. To receive this label RSS feed. Copy the URL below and paste it into your RSS Reader ... AX PHARMACEUTICAL CORP- lomustine powder. Out of scope - Out of scope for RxNorm and will not receive RxNorm normal forms. Out ... AX PHARMACEUTICAL CORP- lomustine powder. If this SPL contains inactivated NDCs listed by the FDA initiated compliance action, ...
Interventions: Eflornithine (CPP-1X; Difluoromethylornithine; DFMO; Vaniqa; eflornithine hydrochloride monohydrate) , lomustine ...
lomustine. Monitor Closely (1)lomustine decreases effects of influenza virus vaccine quadrivalent by pharmacodynamic antagonism ... lomustine. lomustine decreases effects of influenza virus vaccine quadrivalent by pharmacodynamic antagonism. Modify Therapy/ ...
Availability of Lomustine for Glioblastoma Multiforme. Dr. Jeff Ratliff talks with Drs. Howard Colman and Kelly Fritz about the ... availability of lomustine for the treatment of glioblastoma multiforme (GBM) in light of the drugs recent withdrawal from ...
Antineoplastic chemotherapy drugs are a specific type of drug that doctors use to treat certain forms of cancer. Learn more about their uses and effects here.
The conclusions, findings, and opinions expressed by authors contributing to this journal do not necessarily reflect the official position of the U.S. Department of Health and Human Services, the Public Health Service, the Centers for Disease Control and Prevention, or the authors affiliated institutions. Use of trade names is for identification only and does not imply endorsement by any of the groups named above. ...
Lomustine. N-(2-Chloroethyl)-N-cyclohexyl-N-nitrosourea (9CI) 13010-47-4. IP/IJ. R8 M4. RESULTS REPORTED IN JOURNAL ARTICLE. A ...
I am looking forlomustine. I am looking forchemotherapy drugs. added new label for I am looking for ...
FDA approves lomustine, discovered at Southern Research, as cancer treatment.. Lomustine is primarily used in the treatment of ... Lomustine is a chemotherapy drug classified as an alkylating agent. Alkylation damages the DNA of cells, preventing them from ...
Patients receiving chemotherapy got three drugs: procarbazine (P); CCNU (C), which generically is known as lomustine; and ...
Nitrosureas: Carmustine, Lomustine and Streptozocin. Nitrosureas are unique because, unlike most chemotherapy, they can cross ...
Lomustine Ceenu, Gleostine. 10 mg. Chemotherapy Alkylating Agent. Nitrosourea. Yes 1976. Jan. 1, 2002 In Use. ...
Lomustine. A6,AlkAg. FDA approved. FDA approved. 79269. Vistonuridine. TUBB,FU-Antidote. FDA approved. FDA approved. ...
lomustine. cetylpyrd. cetylpyridinium. chew. chewable. chl. chloride. chlordiazepoxid. chlordiazepoxide. chlophed. ...
NextSource acquired the drug lomustine in 2013 and raised its price. Lomustine was first approved by the Federal Drug ... The senators are asking for NextSource documents on the sale of lomustine, company profits from sales of the drug, and any ... But an undated statement about media coverage of the cost increase of lomustine was posted on the Tri-Source Pharmas website. ... "better understand the factors contributing to the rising cost of lomustine, which has increased nearly 1,400 percent since 2013 ...
Lomustine/toxicity*; Lymphocytes/drug effects; Mutagenicity Tests; Sister Chromatid Exchange/drug effects* ...
6. MACC (methotrexate, doxorubicin, cyclophosphamide and lomustine) versus cis-platinum and etoposide in the treatment of ... Methotrexate, doxorubicin, cyclophosphamide, and lomustine.. Chahinian PA; Arnold DJ; Cohen JM; Purpora DP; Jaffrey IS; ...
Common CNS chemotherapies include temozolomide, carmustine (also called BCNU), lomustine (also called CCNU), and bevacizumab. ...
lomustine. Monitor Closely (1)lomustine decreases effects of haemophilus influenzae type b vaccine by pharmacodynamic ... lomustine. lomustine decreases effects of haemophilus influenzae type b vaccine by pharmacodynamic antagonism. Modify Therapy/ ...
lomustine. ofatumumab SC, lomustine. Either increases effects of the other by immunosuppressive effects; risk of infection. Use ... lomustine. Monitor Closely (1)ofatumumab SC, lomustine. Either increases effects of the other by immunosuppressive effects; ...
lomustine. Monitor Closely (1)lomustine and guselkumab both increase immunosuppressive effects; risk of infection. Use Caution/ ... lomustine. lomustine and guselkumab both increase immunosuppressive effects; risk of infection. Use Caution/Monitor. Caution ...
Dacarbazine (DTIC) and the nitrosoureas, carmustine (BCNU) and lomustine (CCNU), produced a 20% objective response rate. ...
  • CeeNU ® (lomustine) (CCNU) is one of the nitrosoureas used in the treatment of certain neoplastic diseases. (nih.gov)
  • Early results of this trial showed that treatment with procarbazine, lomustine (also called CCNU), and vincristine after radiation therapy at the time of initial diagnosis resulted in longer progression-free survival, but not overall survival, than radiation therapy alone. (elsevier.com)
  • 24. Procarbazine, lomustine and vincristine for recurrent high-grade glioma. (nih.gov)
  • Completed: 9-ING-41 combined with standard anticancer agents: The 3+3 dose escalation study design will be used for 8 chemotherapy combination regimens (9-ING-41 plus gemcitabine, doxorubicin, lomustine, carboplatin, irinotecan, nab-paclitaxel plus gemcitabine, paclitaxel plus carboplatin, pemetrexed plus carboplatin) to identify the MTD/RP2D of each regimen. (outcomes4me.com)
  • CeeNU (lomustine) should be administered under the supervision of a qualified physician experienced in the use of cancer chemotherapeutic agents. (nih.gov)
  • 6. MACC (methotrexate, doxorubicin, cyclophosphamide and lomustine) versus cis-platinum and etoposide in the treatment of advanced non-small cell lung cancer. (nih.gov)
  • Your doctor will order laboratory tests before, during, and after your treatment to check your body's response to lomustine to see if your blood cells, liver, kidneys, and lungs are affected by this medication. (medlineplus.gov)
  • Lomustine is also used with other medications to treat Hodgkin's lymphoma (Hodgkin's disease) that has not improved or that has worsened after treatment with other medications. (medlineplus.gov)
  • If you are female, you should use birth control to prevent pregnancy during your treatment with lomustine and for at least 2 weeks after your final dose. (medlineplus.gov)
  • If you are male, you and your female partner should use birth control during your treatment with lomustine and continue for 4 months after your final dose. (medlineplus.gov)
  • Lomustine is an orally administered alkylating agent used alone and in combination with other antineoplastic agents in the treatment of several malignancies including Hodgkin disease, lymphoma, and brain cancer. (nih.gov)
  • Dr. Jeff Ratliff talks with Drs. Howard Colman and Kelly Fritz about the availability of lomustine for the treatment of glioblastoma multiforme (GBM) in light of the drug's recent withdrawal from Medicare Part D coverage. (neurology.org)
  • NextSource acquired the drug lomustine in 2013 and raised its price. (reviewjournal.com)
  • Lomustine was first approved by the Federal Drug Administration in 1976 to treat brain tumors and Hodgkin lymphoma. (reviewjournal.com)
  • The senators are asking for NextSource documents on the sale of lomustine, company profits from sales of the drug, and any communications referring to cost estimates, profit projections and market share analysis. (reviewjournal.com)
  • Lomustine is used to treat certain types of brain tumors. (medlineplus.gov)
  • In a March 22 letter to Tri-Source Pharma CEO and President Robert DiCrisci, the senators asked for documents to "better understand the factors contributing to the rising cost of lomustine, which has increased nearly 1,400 percent since 2013 for the highest dose. (reviewjournal.com)
  • The toxicity of lomustine is similar to other alkylating agents. (nih.gov)
  • 5. Toxicity and efficacy of lomustine and bevacizumab in recurrent glioblastoma patients. (nih.gov)
  • tell your doctor and pharmacist if you are allergic to lomustine, any other medications, or any of the ingredients in lomustine capsules. (medlineplus.gov)
  • However, in instances in which full surgical resection of symptomatic ependymomas is not possible, chemotherapy with lomustine, vincristine, and prednisone, or carboplatin and vincristine, following radiation therapy, may serve a palliative function. (medscape.com)
  • Like cyclophosphamide, lomustine requires activation in the liver to form its active intermediaries which act by modifying and cross linking purine bases in DNA, thus inhibiting DNA, RNA and protein synthesis and leading to programmed cell death (apoptosis) in rapidly dividing cells. (nih.gov)
  • Although its mechanism of action is not completely understood, lomustine causes inhibition of DNA & RNA synthesis resulting from carbamylation of DNA polymerase, alkylation of DNA, and alteration of RNA proteins. (medscape.com)
  • Lomustine inhibits RNA and DNA synthesis through alkylation of DNA and carbamylation of DNA polymerase, and alteration of RNA, enzymes, and proteins. (medscape.com)
  • Your doctor will order laboratory tests before, during, and after your treatment to check your body's response to lomustine to see if your blood cells, liver, kidneys, and lungs are affected by this medication. (medlineplus.gov)
  • Lomustine therapy is associated with minor transient serum enzyme elevations and has been linked to rare cases of clinically apparent acute liver injury. (nih.gov)
  • Clinically apparent liver injury from lomustine has been described, but is uncommon. (nih.gov)
  • Lomustine is often given in combination with other antineoplastic agents, many of which are also hepatotoxic, so the effect of lomustine in causing liver injury is often difficult to assess. (nih.gov)
  • It is not known whether patients with acute liver injury due to lomustine have cross sensitivity to hepatic injury with other alkylating agents. (nih.gov)
  • Take only one dose of lomustine every six weeks. (medlineplus.gov)
  • If you are female, you should use birth control to prevent pregnancy during your treatment with lomustine and for at least 2 weeks after your final dose. (medlineplus.gov)
  • If you are male, you and your female partner should use birth control during your treatment with lomustine and continue for 4 months after your final dose. (medlineplus.gov)
  • You should not breast-feed while taking lomustine and for 2 weeks after your final dose. (medlineplus.gov)
  • Lomustine is usually given in combination with other antineoplastic agents in a single oral dose of 100-130 mg/m 2 in cycles every 6 to 8 weeks. (nih.gov)
  • Lomustine is an orally administered alkylating agent used alone and in combination with other antineoplastic agents in the treatment of several malignancies including Hodgkin disease, lymphoma, and brain cancer. (nih.gov)
  • Lomustine is in a class of medications called alkylating agents. (medlineplus.gov)
  • Mild and transient elevations in serum aminotransferase or alkaline phosphatase levels are found in a high proportion of patients treated antineoplastic regimens that include lomustine. (nih.gov)
  • 1. Increased infiltration of CD8 T cells in recurrent glioblastoma patients is a useful biomarker for assessing the response to combined bevacizumab and lomustine therapy. (nih.gov)
  • 2. Prognostic value and kinetics of circulating endothelial cells in patients with recurrent glioblastoma randomised to bevacizumab plus lomustine, bevacizumab single agent or lomustine single agent. (nih.gov)
  • 3. Retrospective study of carmustine or lomustine with bevacizumab in recurrent glioblastoma patients who have failed prior bevacizumab. (nih.gov)
  • 6. Progression-free and overall survival in patients with recurrent Glioblastoma multiforme treated with last-line bevacizumab versus bevacizumab/lomustine. (nih.gov)
  • 7. Single-agent bevacizumab or lomustine versus a combination of bevacizumab plus lomustine in patients with recurrent glioblastoma (BELOB trial): a randomised controlled phase 2 trial. (nih.gov)