Dacarbazine
Melanoma
Bleomycin
Mechlorethamine
Hodgkin Disease
Antineoplastic Agents, Alkylating
Procarbazine
Antineoplastic Combined Chemotherapy Protocols
Doxorubicin
Nimustine
Carmustine
Mesna
Interferon-alpha
Combined Modality Therapy
Prednisone
O(6)-Methylguanine-DNA Methyltransferase
Disease-Free Survival
Treatment Outcome
Cisplatin
Survival Analysis
Tamoxifen
Neoplasm Metastasis
Sarcoma
Cyclophosphamide
Drug Administration Schedule
Neoplasm Staging
Niacinamide
Etoposide
Vindesine
Ifosfamide
DNA Modification Methylases
Organophosphorus Compounds
Survival Rate
Melanoma, Experimental
Kaplan-Meier Estimate
Interleukin-2
Remission Induction
Disease Progression
Pheochromocytoma
Absorption, metabolism, and excretion of 14C-temozolomide following oral administration to patients with advanced cancer. (1/1313)
The purpose of this study is to characterize the absorption, metabolism, and excretion of carbon 14-labeled temozolomide (14C-TMZ) administered p.o. to adult patients with advanced solid malignancies. On day 1 of cycle 1, six patients received a single oral 200-mg dose of 14C-TMZ (70.2 microCi). Whole blood, plasma, urine, and feces were collected from days 1-8 and on day 14 of cycle 1. Total radioactivity was measured in all samples. TMZ, 5-(3-methyltriazen-1-yl)imidazole-4-carboxamide (MTIC), and 4-amino-5-imidazole-carboxamide (AIC) concentrations were determined in plasma, and urine and plasma samples were profiled for metabolite/degradation products. Maximum TMZ plasma concentrations were achieved between 0.33 to 2 h (mean, 1.2 h), and half-life, apparent volume of distribution, and oral clearance values averaged 1.9 h, 17 liters/m2, and 104 ml/min/m2, respectively. A first-order absorption, one-compartment linear model, which included first-order formation of MTIC from TMZ and elimination of MTIC via degradation to AIC, and a peripheral distribution compartment for AIC, adequately described the plasma TMZ, MTIC, and AIC concentrations. MTIC systemic clearance was estimated to be 5384 ml/min/m2, and the half-life was calculated to be 2.5 min. Metabolite profiles of plasma at 1 and 4 h after treatment showed that 14C-derived radioactivity was primarily associated with TMZ, and a smaller amount was attributed to AIC. Profiles of urine samples from 0-24 h revealed that 14C-TMZ-derived urinary radioactivity was primarily associated with unchanged drug (5.6%), AIC (12%), or 3-methyl-2,3-dihydro-4-oxoimidazo[5,1-d]tetrazine-8-carboxyl ic acid (2.3%). The recovered radioactive dose (39%) was principally eliminated in the urine (38%), and a small amount (0.8%) was excreted in the feces. TMZ exhibits rapid oral absorption and high systemic availability. The primary elimination pathway for TMZ is by pH-dependent degradation to MTIC and further degradation to AIC. Incomplete recovery of radioactivity may be explained by the incorporation of AIC into nucleic acids. (+info)Interactive effects of inhibitors of poly(ADP-ribose) polymerase and DNA-dependent protein kinase on cellular responses to DNA damage. (2/1313)
DNA-dependent protein kinase (DNA-PK) and poly(ADP-ribose) polymerase (PARP) are activated by DNA strand breaks and participate in DNA repair. We investigated the interactive effects of inhibitors of these enzymes [wortmannin (WM), which inhibits DNA-PK, and 8-hydroxy-2-methylquinazolin-4-one (NU1025), a PARP inhibitor] on cell survival and DNA double-strand break (DSB) and single-strand break (SSB) rejoining in Chinese hamster ovary-K1 cells following exposure to ionizing radiation (IR) or temozolomide. WM (20 microM) or NU1025 (300 microM) potentiated the cytotoxicity of IR with dose enhancement factors at 10% survival (DEF10) values of 4.5 +/- 0.6 and 1.7 +/- 0.2, respectively. When used in combination, a DEF10 of 7.8 +/- 1.5 was obtained. WM or NU1025 potentiated the cytotoxicity of temozolomide, and an additive effect on the DEF10 value was obtained with the combined inhibitors. Using the same inhibitor concentrations, their single and combined effects on DSB and SSB levels following IR were assessed by neutral and alkaline elution. Cells exposed to IR were post-incubated for 30 min to allow repair to occur. WM or NU1025 increased net DSB levels relative to IR alone (DSB levels of 1.29 +/- 0.04 and 1.20 +/- 0.05, respectively, compared with 1.01 +/- 0.03 for IR alone) and the combination had an additive effect. WM had no effect on SSB levels, either alone or in combination with NU1025. SSB levels were increased to 1.27 +/- 0.05 with NU1025 compared with IR alone, 1.02 +/- 0.04. The dose-dependent effects of the inhibitors on DSB levels showed that they were near maximal by 20 microM WM and 300 microM NU1025. DSB repair kinetics were studied. Both inhibitors increased net DSB levels over a 3 h time period; when they were combined, net DSB levels at 3 h were identical to DSB levels immediately post-IR. The combined use of DNA repair inhibitors may have therapeutic potential. (+info)Prospective randomized trial of the treatment of patients with metastatic melanoma using chemotherapy with cisplatin, dacarbazine, and tamoxifen alone or in combination with interleukin-2 and interferon alfa-2b. (3/1313)
PURPOSE: The combination of chemotherapy with immunotherapeutic agents such as interleukin-2 and interferon alfa-2b has been reported to provide improved treatment results in patients with metastatic melanoma, compared with the use of chemotherapy alone. We have performed a prospective randomized trial in patients with metastatic melanoma, comparing treatment with chemotherapy to treatment with chemoimmunotherapy. PATIENTS AND METHODS: One hundred two patients with metastatic melanoma were prospectively randomized to receive chemotherapy composed of tamoxifen, cisplatin, and dacarbazine or this same chemotherapy followed by interferon alfa-2b and interleukin-2. Objective responses, survival, and toxicity in the two groups were evaluated at a median potential follow-up of 42 months. RESULTS: In 52 patients randomized to receive chemotherapy, there were 14 objective responses (27%), including four complete responses. In 50 patients randomized to receive chemoimmunotherapy, there were 22 objective responses (44%) (P2 = .071), including three complete responses. In both treatment groups, the duration of partial responses was often short, and there was a trend toward a survival advantage for patients receiving chemotherapy alone (P2 = .052; median survival of 15.8 months compared with 10.7 months). Treatment-related toxicities were greater in patients receiving chemoimmunotherapy. CONCLUSION: With the treatment regimens used in this study, the addition of immunotherapy to combination chemotherapy increased toxicity but did not increase survival. The use of combination chemoimmunotherapy regimens is not recommended in the absence of well-designed, prospective, randomized protocols showing the benefit of this treatment strategy. (+info)Combination of chemotherapy with interleukin-2 and interferon alfa for the treatment of metastatic melanoma. (4/1313)
PURPOSE: The primary objective of this clinical study was to assess the feasibility of administering recombinant interleukin-2 and recombinant interferon alfa-2a before and after combination cytotoxic chemotherapy. After encouraging initial responses, the study was expanded to further evaluate the therapeutic potential, clarify the toxicities of this regimen, and explore any associated immunologic changes. PATIENTS AND METHODS: Eighty-four patients with metastatic melanoma, including patients with brain metastases, were treated on this 6-week protocol. Patients received combination cisplatin (25 mg/m2/d) and dacarbazine (220 mg/m2/d) on days 1 through 3 and 22 through 24 plus carmustine (150 mg/m2) on day 1. Interleukin 2 (13.5 million IU/m2/d) and interferon alfa (6 MU/m2/d) were administered on days 4 through 8 and 17 through 21. RESULTS: Among 83 patients assessable for response, 12 complete and 34 partial responses were documented (55% response rate). The median time to disease progression was 7 months, the median survival from study entry was 12.2 months, and the median survival from diagnosis of metastatic disease was 15.5 months. Although patients were hospitalized to receive treatment, intensive care unit support generally was not needed. Dose-limiting toxicities were related to elevations in serum bilirubin and serum creatinine levels. No patient developed a grade 4 clinical toxicity. Treatment produced a skin depigmentation, which was associated with prolonged survival. CONCLUSION: A plateau in both the survival and time to progression curves beyond 2 years (15% of the patients) and a greater than 10% disease-free survival beyond 4 years indicate that there may be a long-term benefit for some patients. The limited toxicity of this regimen should permit its use in most oncology settings. A randomized trial of chemoimmunotherapy versus chemotherapy should be performed to establish the value of chemoimmunotherapy for melanoma. (+info)Msh2 status modulates both apoptosis and mutation frequency in the murine small intestine. (5/1313)
Deficiency in genes involved in DNA mismatch repair increases susceptibility to cancer, particularly of the colorectal epithelium. Using Msh2 null mice, we demonstrate that this genetic defect renders normal intestinal epithelial cells susceptible to mutation in vivo at the Dlb-1 locus. Compared with wild-type mice, Msh2-deficient animals had higher basal levels of mutation and were more sensitive to the mutagenic effects of temozolomide. Experiments using Msh2-deficient cells in vitro suggest that an element of this effect is attributable to increased clonogenicity. Indeed, we show that Msh2 plays a role in the in vivo initiation of apoptosis after treatment with temozolomide, N-methyl-N'-nitro-N-nitrosoguanidine, and cisplatin. This was not influenced by the in vivo depletion of O6-alkylguanine-DNA-alkyltransferase after administration of O6-benzylguanine. By analyzing mice mutant for both Msh2 and p53, we found that the Msh2-dependent apoptotic response was primarily mediated through a p53-dependent pathway. Msh2 also was required to signal delayed p53-independent death. Taken together, these studies characterize an in vivo Msh2-dependent apoptotic response to methylating agents and raise the possibility that Msh2 deficiency may predispose to malignancy not only through failed repair of mismatch DNA lesions but also through the failure to engage apoptosis. (+info)Treatment of neoplastic meningitis with intrathecal temozolomide. (6/1313)
Neoplastic meningitis (NM) results from leptomeningeal dissemination of cancers arising within the central nervous system or metastasizing to the leptomeninges from systemic neoplasms. The inability to produce therapeutic drug levels intrathecally (i.t.) with systemic administration and the minimal efficacy of chemotherapeutic agents currently available for direct i.t. use limit therapy. Temozolomide [8-carbamoyl-3-methylimidazo[5,1-d]-1,2,3,5-tetrazin-4([3H])-one] is a novel methylating agent with proven activity against intraparenchymal malignant gliomas (MGs). Insolubility of the standard formulation prevents its efficacious use as an i.t. agent, however. To overcome this obstacle, we have developed a unique microcrystalline formulation of temozolomide with greatly enhanced solubility. Treatment of athymic rats bearing subarachnoid MER- human MG xenografts with four doses of i.t. microcrystalline temozolomide over a 2-week period produced a 142% increase in median survival at individual doses of 2.2 micromol (P = 0.0073) and a >367% increase in median survival at individual doses of 6.8 micromol (P = 0.0015). At the higher dose tested, three of eight rats treated developed no neurological symptoms and had no evidence of residual tumor on histological examination after treatment. Use of this microcrystalline formulation in athymic rats bearing subarachnoid MER+ human MG xenografts increased median survival >132% (P < 0.0058) at both dose levels tested. Toxicity directly attributable to the i.t. administration of microcrystalline temozolomide was exhibited in the highest dose groups only and was limited to small patchy areas of focal demyelination involving <5% of spinal cord long tracks. (+info)DNA repair methyltransferase (Mgmt) knockout mice are sensitive to the lethal effects of chemotherapeutic alkylating agents. (7/1313)
We have generated mice deficient in O6-methylguanine DNA methyltransferase activity encoded by the murine Mgmt gene using homologous recombination to delete the region encoding the Mgmt active site cysteine. Tissues from Mgmt null mice displayed very low O6-methylguanine DNA methyltransferase activity, suggesting that Mgmt constitutes the major, if not the only, O6-methylguanine DNA methyltransferase. Primary mouse embryo fibroblasts and bone marrow cells from Mgmt -/- mice were significantly more sensitive to the toxic effects of the chemotherapeutic alkylating agents 1,3-bis(2-chloroethyl)-1-nitrosourea, streptozotocin and temozolomide than those from Mgmt wild-type mice. As expected, Mgmt-deficient fibroblasts and bone marrow cells were not sensitive to UV light or to the crosslinking agent mitomycin C. In addition, the 50% lethal doses for Mgmt -/- mice were 2- to 10-fold lower than those for Mgmt +/+ mice for 1,3-bis(2chloroethyl)-1-nitrosourea, N-methyl-N-nitrosourea and streptozotocin; similar 50% lethal doses were observed for mitomycin C. Necropsies of both wild-type and Mgmt -/mice following drug treatment revealed histological evidence of significant ablation of hematopoietic tissues, but such ablation occurred at much lower doses for the Mgmt -/- mice. These results demonstrate the critical importance of O6-methylguanine DNA methyltransferase in protecting cells and animals against the toxic effects of alkylating agents used for cancer chemotherapy. (+info)A Phase I and pharmacokinetic study of temozolomide and cisplatin in patients with advanced solid malignancies. (8/1313)
Temozolomide (TMZ) is an oral imidazotetrazinone that is spontaneously converted to 5-(3-methyltriazen-1-yl)imidazole-4-carboxamide (MTIC) at physiological pH. MTIC methylates DNA at the O6 position of guanine, although this lesion may be repaired by the enzyme O6-alkylguanine-DNA alkyltransferase (AGAT). In this study, TMZ was combined with cisplatin (CDDP), because both agents have single-agent activity against melanoma and other tumor types. Additionally, CDDP has been shown to inactivate AGAT, and subtherapeutic concentrations of CDDP have been shown to increase the sensitivity of leukemic blasts to TMZ. This Phase I study sought to determine the toxicities, recommended dose, and pharmacological profile of the TMZ/CDDP combination. Patients were treated with oral TMZ daily for 5 consecutive days together with CDDP on day 1 (4 h after TMZ) every 4 weeks at the following TMZ (mg/m2/day)/CDDP (mg/m2) dose levels: 100/75, 150/75, 200/75, and 200/100. Plasma samples were obtained on days 1 and 2 to evaluate the pharmacokinetic parameters of TMZ alone and in combination with CDDP. Fifteen patients received a total of 44 courses of TMZ/CDDP. The principal toxicities of the regimen consisted of neutropenia, thrombocytopenia, nausea, and vomiting, which were intolerable in two of six new patients treated at the 200/100 mg/m2 dose level. Of five patients receiving 17 courses at the next lower dose level (200/75 mg/m2), none experienced dose-limiting toxicity. Antitumor activity was observed in patients with non-small cell lung cancer, squamous cell carcinoma of the tongue, and leiomyosarcoma of the uterus. Pharmacokinetic studies of TMZ revealed the following pertinent parameters (mean +/- SD): time to maximum plasma concentration (Tmax) = 1.1+/-0.6 h (day 1) and 1.7+/-0.9 h (day 2); elimination half-life (t1/2) = 1.74+/-0.22 h (day 1) and 2.35+/-0.70 h (day 2); and clearance (Cl(s)/F) = 115+/-27 ml/min/m2 (day 1) and 141+/-109 ml/min/m2 (day 2). TMZ drug exposure, described by the area under the plasma concentration-time curve (AUCinfinity) and the maximum plasma concentration (Cmax), was similar on days 1 and 2. On the basis of these results, the recommended doses for Phase II clinical trials are TMZ 200 mg/m2/day for 5 days with 75 mg/m2 CDDP on day 1, every 4 weeks. The addition of CDDP did not affect the tolerable dose of single-agent TMZ (200 mg/m2/day x 5 days), nor did it substantially alter the pharmacokinetic behavior of TMZ. (+info)There are several types of melanoma, including:
1. Superficial spreading melanoma: This is the most common type of melanoma, accounting for about 70% of cases. It usually appears as a flat or slightly raised discolored patch on the skin.
2. Nodular melanoma: This type of melanoma is more aggressive and accounts for about 15% of cases. It typically appears as a raised bump on the skin, often with a darker color.
3. Acral lentiginous melanoma: This type of melanoma affects the palms of the hands, soles of the feet, or nail beds and accounts for about 5% of cases.
4. Lentigo maligna melanoma: This type of melanoma usually affects the face and is more common in older adults.
The risk factors for developing melanoma include:
1. Ultraviolet (UV) radiation exposure from the sun or tanning beds
2. Fair skin, light hair, and light eyes
3. A history of sunburns
4. Weakened immune system
5. Family history of melanoma
The symptoms of melanoma can vary depending on the type and location of the cancer. Common symptoms include:
1. Changes in the size, shape, or color of a mole
2. A new mole or growth on the skin
3. A spot or sore that bleeds or crusts over
4. Itching or pain on the skin
5. Redness or swelling around a mole
If melanoma is suspected, a biopsy will be performed to confirm the diagnosis. Treatment options for melanoma depend on the stage and location of the cancer and may include surgery, chemotherapy, radiation therapy, or a combination of these. Early detection and treatment are key to successful outcomes in melanoma cases.
In conclusion, melanoma is a type of skin cancer that can be deadly if not detected early. It is important to practice sun safety, perform regular self-exams, and seek medical attention if any suspicious changes are noticed on the skin. By being aware of the risk factors, symptoms, and treatment options for melanoma, individuals can take steps to protect themselves from this potentially deadly disease.
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.
There are several types of skin neoplasms, including:
1. Basal cell carcinoma (BCC): This is the most common type of skin cancer, and it usually appears as a small, fleshy bump or a flat, scaly patch. BCC is highly treatable, but if left untreated, it can grow and invade surrounding tissue.
2. Squamous cell carcinoma (SCC): This type of skin cancer is less common than BCC but more aggressive. It typically appears as a firm, flat, or raised bump on sun-exposed areas. SCC can spread to other parts of the body if left untreated.
3. Melanoma: This is the most serious type of skin cancer, accounting for only 1% of all skin neoplasms but responsible for the majority of skin cancer deaths. Melanoma can appear as a new or changing mole, and it's essential to recognize the ABCDE signs (Asymmetry, Border irregularity, Color variation, Diameter >6mm, Evolving size, shape, or color) to detect it early.
4. Sebaceous gland carcinoma: This rare type of skin cancer originates in the oil-producing glands of the skin and can appear as a firm, painless nodule on the forehead, nose, or other oily areas.
5. Merkel cell carcinoma: This is a rare and aggressive skin cancer that typically appears as a firm, shiny bump on the skin. It's more common in older adults and those with a history of sun exposure.
6. Cutaneous lymphoma: This type of cancer affects the immune system and can appear as a rash, nodules, or tumors on the skin.
7. Kaposi sarcoma: This is a rare type of skin cancer that affects people with weakened immune systems, such as those with HIV/AIDS. It typically appears as a flat, red or purple lesion on the skin.
While skin cancers are generally curable when detected early, it's important to be aware of your skin and notice any changes or unusual spots, especially if you have a history of sun exposure or other risk factors. If you suspect anything suspicious, see a dermatologist for an evaluation and potential biopsy. Remember, prevention is key to avoiding the harmful effects of UV radiation and reducing your risk of developing skin cancer.
1. Sudden, brief episodes of shivering or trembling, often accompanied by feelings of coldness or a raised temperature. Chills can be a symptom of infection, inflammation, or other medical conditions.
2. A feeling of intense coldness or shivering that is not related to an actual drop in body temperature. This type of chill can be caused by emotional factors, such as anxiety or fear, or by certain medications.
3. A sudden, brief episode of trembling or shaking, often accompanied by feelings of nervousness or apprehension. Chills can be a symptom of neurological conditions, such as Parkinson's disease or multiple sclerosis.
4. In medicine, chills can also refer to a type of seizure that is characterized by shivering or trembling movements. These types of seizures are often seen in people with epilepsy.
5. Chills can also be a symptom of withdrawal from certain substances, such as alcohol or drugs.
6. In some cases, chills can be a symptom of a more serious underlying medical condition, such as a severe infection, inflammatory disorder, or blood disorder. It is important to seek medical attention if you experience persistent or severe chills, especially if they are accompanied by other symptoms such as fever, pain, or difficulty breathing.
7. Chills can also be a side effect of certain medications, such as antidepressants or antipsychotics.
8. Some people may experience chills as a result of exposure to cold temperatures or changes in weather. This is usually not a cause for concern and can be treated with warm clothing, blankets, or other forms of heat therapy.
In general, chills are a symptom that can have many different causes, and it is important to seek medical attention if they persist or worsen over time.
Neoplastic metastasis can occur in any type of cancer but are more common in solid tumors such as carcinomas (breast, lung, colon). It is important for cancer diagnosis and prognosis because metastasis indicates that the cancer has spread beyond its original site and may be more difficult to treat.
Metastases can appear at any distant location but commonly found sites include the liver, lungs, bones, brain, and lymph nodes. The presence of metastases indicates a higher stage of cancer which is associated with lower survival rates compared to localized cancer.
Sarcomas can arise in any part of the body, but they are most common in the arms and legs. They can also occur in the abdomen, chest, or head and neck. There are many different types of sarcoma, each with its own unique characteristics and treatment options.
The causes of sarcoma are not fully understood, but genetic mutations, exposure to radiation, and certain chemicals have been linked to an increased risk of developing the disease. Sarcomas can be challenging to diagnose and treat, as they often grow slowly and may not cause symptoms until they are advanced.
Treatment for sarcoma typically involves a combination of surgery, radiation therapy, and chemotherapy. The specific treatment plan will depend on the type of sarcoma, its location, and the stage of the disease. In some cases, amputation may be necessary to remove the tumor.
Prognosis for sarcoma varies depending on the type of cancer, the size and location of the tumor, and the stage of the disease. In general, the prognosis is best for patients with early-stage sarcoma that is confined to a small area and has not spread to other parts of the body.
Overall, sarcoma is a rare and complex form of cancer that requires specialized treatment and care. While the prognosis can vary depending on the specific type of cancer and the stage of the disease, advances in medical technology and treatment options have improved outcomes for many patients with sarcoma.
2. Our research focuses on identifying the genetic mutations that contribute to experimental melanoma and developing targeted therapies.
3. The patient's experimental melanoma had spread to her lungs and liver, so we recommended chemotherapy and immunotherapy treatments.
Disease progression can be classified into several types based on the pattern of worsening:
1. Chronic progressive disease: In this type, the disease worsens steadily over time, with a gradual increase in symptoms and decline in function. Examples include rheumatoid arthritis, osteoarthritis, and Parkinson's disease.
2. Acute progressive disease: This type of disease worsens rapidly over a short period, often followed by periods of stability. Examples include sepsis, acute myocardial infarction (heart attack), and stroke.
3. Cyclical disease: In this type, the disease follows a cycle of worsening and improvement, with periodic exacerbations and remissions. Examples include multiple sclerosis, lupus, and rheumatoid arthritis.
4. Recurrent disease: This type is characterized by episodes of worsening followed by periods of recovery. Examples include migraine headaches, asthma, and appendicitis.
5. Catastrophic disease: In this type, the disease progresses rapidly and unpredictably, with a poor prognosis. Examples include cancer, AIDS, and organ failure.
Disease progression can be influenced by various factors, including:
1. Genetics: Some diseases are inherited and may have a predetermined course of progression.
2. Lifestyle: Factors such as smoking, lack of exercise, and poor diet can contribute to disease progression.
3. Environmental factors: Exposure to toxins, allergens, and other environmental stressors can influence disease progression.
4. Medical treatment: The effectiveness of medical treatment can impact disease progression, either by slowing or halting the disease process or by causing unintended side effects.
5. Co-morbidities: The presence of multiple diseases or conditions can interact and affect each other's progression.
Understanding the type and factors influencing disease progression is essential for developing effective treatment plans and improving patient outcomes.
Symptoms of pheochromocytoma can include:
* Rapid heartbeat
* High blood pressure
* Sweating
* Weight loss
* Fatigue
* Headaches
* Nausea and vomiting
If left untreated, pheochromocytoma can lead to complications such as heart failure, stroke, and even death. Therefore, it is important that individuals who experience any of the above symptoms seek medical attention as soon as possible.
Treatment options for pheochromocytoma may include surgery to remove the tumor, medication to manage symptoms, and in some cases, radiation therapy. In rare cases, the tumor may recur after treatment, so regular monitoring is necessary to ensure that any new symptoms are detected early on.
Overall, while pheochromocytoma is a rare and potentially life-threatening condition, prompt medical attention and appropriate treatment can help manage symptoms and prevent complications.
Dacarbazine
Triazenes
Undifferentiated pleomorphic sarcoma
Chemotherapy
ABVD
Melanoma
Alkylating antineoplastic agent
Pheochromocytoma
John Angus Hickman
Arabinopyranosyl-N-methyl-N-nitrosourea
Budd-Chiari syndrome
Fotemustine
Temozolomide
Adjuvant therapy
Portal hypertension
Genta (company)
Neuroblastoma RAS viral oncogene homolog
Procarbazine
Uveal melanoma
Trabectedin
Vemurafenib
Immune-related response criteria
Ovarian stem cell
Sclerosing epithelioid fibrosarcoma
DNA repair
Neoplasm
Selumetinib
O-6-methylguanine-DNA methyltransferase
Binimetinib
Somatostatinoma
Dacarbazine - St. Jude Children's Research Hospital
Dacarbazine for Injection, USP
Dacarbazine - Health Library | NewYork-Presbyterian
Dacarbazine: MedlinePlus Drug Information
MedlinePlus - Search Results for: DACARBAZINE
Dacarbazine - PubMed
Dacarbazine - PubMed
Dacarbazine - Drugs and Lactation Database (LactMed®) - NCBI Bookshelf
Solitary fibrous tumor: phase II study on TRabectedin versus Adriamycin plus DAcarbazine in advanced patients (STRADA) | ior
DGIdb - DACARBAZINE Drug Record
A randomized phase III study comparing dacarbazine, BCNU, cisplatin and tamoxifen with dacarbazine and interferon in advanced...
Celdaz Dacarbazine 500mg Injection - Omkar Pharma
Artesunate in the treatment of metastatic uveal melanoma--first experiences
Antineoplastic drugs and chemotherapy: Types and side effects
LncRNA POU3F3 Contributes to Dacarbazine Resistance of Human Melanoma Through the MiR-650/MGMT Axis. | Front Oncol;11: 643613,...
A Study of Unesbulin in Participants With Advanced Leiomyosarcoma (LMS) - Full Text View - ClinicalTrials.gov
These highlights do not include all the information needed to use TAFINLAR safely and effectively. See full prescribing...
Experimental mouse tumour models: what can be learnt about human cancer immunology? | Nature Reviews Immunology
View of Brentuximab vedotin in combination with doxorubicin, vinblastine and dacarbazine for first-line treatment of stage IV...
Nail Changes | Types of Nail Changes
Melanoma Research
Teva-Ofloxacin - Uses, Side Effects, Interactions - MedBroadcast.com
Table 2 - Analysis of MarketScan Data for Immunosuppressive Conditions and Hospitalizations for Acute Respiratory Illness,...
Budd-Chiari Syndrome: Practice Essentials, Background, Pathophysiology
Adjuvant Nivolumab versus Ipilimumab in Resected Stage III or IV Melanoma | NEJM
Radiotherapy: Changing the Game in Immunotherapy: Trends in Cancer
Hodgkin Lymphoma Treatment (PDQ®) (Health professionals) | OncoLink
Melanoma12
- Dacarbazine for Injection is indicated in the treatment of metastatic malignant melanoma. (nih.gov)
- Dacarbazine is used to treat melanoma (a type of skin cancer) that has spread to other parts of your body. (medlineplus.gov)
- When dacarbazine is used to treat melanoma, it may be injected once a day for 10 days in a row every 4 weeks or it may be injected once a day for 5 days in a row every 3 weeks. (medlineplus.gov)
- A randomized phase III study comparing dacarbazine, BCNU, cisplatin and tamoxifen with dacarbazine and interferon in advanced melanoma. (ox.ac.uk)
- The purpose of this study was to compare the response rate, overall and 1-year survival in patients with advanced melanoma treated with a standard therapy, dacarbazine and interferon-alpha (DTIC/IFN), or combination chemotherapy, consisting of dacarbazine, BCNU, cisplatin and tamoxifen (DBCT). (ox.ac.uk)
- LncRNA POU3F3 Contributes to Dacarbazine Resistance of Human Melanoma Through the MiR-650/MGMT Axis. (bvsalud.org)
- Alkylating agents are critical therapeutic options for melanoma , while dacarbazine ( DTIC )-based chemotherapy showed poor sensitivity in clinical trials. (bvsalud.org)
- Significantly, Dacarbazine, a currently available chemotherapy drug used to treat melanoma and other types of cancer, was found to be completely inactive in the same tests. (przoom.com)
- 2. Bcl-2 antisense (oblimersen sodium) plus dacarbazine in patients with advanced melanoma: the Oblimersen Melanoma Study Group. (nih.gov)
- 7. Radioimmunotherapy of experimental human metastatic melanoma with melanin-binding antibodies and in combination with dacarbazine. (nih.gov)
- 12. Phase II trial of dacarbazine and thalidomide for the treatment of metastatic melanoma. (nih.gov)
- 16. Re-evaluating the role of dacarbazine in metastatic melanoma: what have we learned in 30 years? (nih.gov)
DTIC-Dome1
- Dacarbazine (also called DTIC or DTIC-Dome®) is an anticancer medicine. (stjude.org)
Chemotherapy3
- Dacarbazine injection must be given in a hospital or medical facility under the supervision of a doctor who is experienced in giving chemotherapy medications for cancer. (medlineplus.gov)
- Liver damage may occur more often in people that are receiving other cancer chemotherapy drugs along with dacarbazine treatment. (medlineplus.gov)
- Dacarbazine remains the standard chemotherapy for this condition. (ox.ac.uk)
Metastatic1
- This study will compare the efficacy and safety of unesbulin plus dacarbazine versus placebo plus dacarbazine in participants with unresectable or metastatic, relapsed or refractory LMS who have received at least 1 prior line of systemic therapy. (clinicaltrials.gov)
Injection18
- Dacarbazine for Injection, USP is a white to pale yellow colored solid which is light sensitive. (nih.gov)
- Dacarbazine for Injection, USP is reconstituted and administered intravenously (pH 3-4). (nih.gov)
- Dacarbazine for Injection, USP is an anticancer agent. (nih.gov)
- After intravenous administration of dacarbazine for injection, the volume of distribution exceeds total body water content suggesting localization in some body tissue, probably the liver. (nih.gov)
- In man, dacarbazine for injection is extensively degraded. (nih.gov)
- In addition, Dacarbazine for Injection is also indicated for Hodgkin's disease as a second-line therapy when used in combination with other effective agents. (nih.gov)
- Dacarbazine for Injection is contraindicated in patients who have demonstrated a hypersensitivity to it in the past. (nih.gov)
- Hemopoietic depression is the most common toxicity with dacarbazine for injection and involves primarily the leukocytes and platelets, although, anemia may sometimes occur. (nih.gov)
- Hemopoietic toxicity may warrant temporary suspension or cessation of therapy with dacarbazine for injection. (nih.gov)
- however, it has also been reported in some patients treated with dacarbazine for injection alone. (nih.gov)
- Anaphylaxis can occur following the administration of dacarbazine for injection. (nih.gov)
- Dacarbazine injection has caused birth defects in animals. (medlineplus.gov)
- This medication has not been studied in pregnant women, but it is possible that it may also cause birth defects in babies whose mothers received dacarbazine injection during pregnancy. (medlineplus.gov)
- You should not use dacarbazine injection while you are pregnant or plan to become pregnant unless your doctor decides that this is the best treatment for your condition. (medlineplus.gov)
- Talk to your doctor about the risks of using dacarbazine injection. (medlineplus.gov)
- Dacarbazine injection comes as a powder to be mixed with liquid to be injected intravenously (into a vein) over 1 minute or infused intravenously over 15 to 30 minutes by a doctor or nurse in a medical facility. (medlineplus.gov)
- tell your doctor and pharmacist if you are allergic to dacarbazine, any other medications, or any of the ingredients in dacarbazine injection. (medlineplus.gov)
- A formulation for preparing Ondansetron HCl-Doxorubicin HCl-Dacarbazine Injection. (ijpc.com)
Deticene1
- 5. [Dacarbazine: deticene]. (nih.gov)
Therapeutic1
- At therapeutic concentrations dacarbazine is not appreciably bound to human plasma protein. (nih.gov)
Antineoplastic1
- Most sources consider breastfeeding to be contraindicated during maternal antineoplastic drug therapy, especially alkylating agents such as dacarbazine. (nih.gov)
Vinblastine1
- The regimen consisted of doxorubicin 40 mg, bleomycin 16 units, vinblastine 9.6 mg and dacarbazine 600 mg, all given over a 2-hour period every 2 weeks. (nih.gov)
Intravenously1
- Participants will receive unesbulin 300 milligrams (mg) tablets administered orally twice weekly in each 3-week treatment cycle in combination with dacarbazine 1000 mg/meter squared (m^2) intravenously (IV) once every 21 days. (clinicaltrials.gov)
Tumor1
- PRZOOM - /newswire/ - Geneva, Switzerland, 2008/03/11 - Anavex 7-1037 reduces rate of cancer tumor growth 69% in pre-clinical studies, compared to currently marketed drug Dacarbazine showing no measurable activity ("ANAVEX") . (przoom.com)
Toxicity1
- DBCT was associated with significantly greater haematological toxicity, and a greater need for time spent in hospital (5.75 days/treatment cycle vs 2.29 with dacarbazine and interferon). (ox.ac.uk)
Experimental1
- Under the experimental conditions tested, the control drug Dacarbazine did not show any measurable activity against this patient-derived xenograft. (przoom.com)
Combination1
- Participants will receive placebo matching to unesbulin tablets administered orally twice weekly in each 3-week treatment cycle in combination with dacarbazine 1000 mg/m^2 IV once every 21 days. (clinicaltrials.gov)
Patients1
- 16 patients) or the chemotherapeutic dacarbazine (seven patients). (aacr.org)
Side effects1
- Dacarbazine may cause side effects. (medlineplus.gov)
Drug1
- Dacarbazine was used as a control drug and was administered for five consecutive days at a dose of 80 mg/kg. (przoom.com)
Agents1
- It is recommended that dacarbazine be administered under the supervision of a qualified physician experienced in the use of cancer chemotherapeutic agents. (nih.gov)
Receive1
- The doctor will prescribe medicine to keep you from feeling sick and throwing up after you receive dacarbazine. (stjude.org)
Administration1
- In mice, administration of dacarbazine resulted in the induction of angiosarcomas of the spleen. (nih.gov)
Addition1
- The second patient first experienced a stabilization of the disease after the addition of ART to Dacarbazine, followed by objective regressions of splenic and lung metastases. (nih.gov)
DESCRIPTION1
- Dacarbazine will be administered as per the dose and schedule specified in the arm description. (clinicaltrials.gov)
Health1
- Dacarbazine can pose a health hazard to caregivers. (stjude.org)
Doctor1
- Your doctor will order certain tests to check your body's response to dacarbazine. (medlineplus.gov)
Malignant melanoma3
- Dacarbazine for Injection is indicated in the treatment of metastatic malignant melanoma. (nih.gov)
- Dacarbazine (also known as DTIC) is an intravenously administered alkylating agent used in the therapy of Hodgkin disease and malignant melanoma. (nih.gov)
- Hypersensitivity to dacarbazine in patients with metastatic malignant melanoma]. (nih.gov)
Sinusoidal obstruct4
- Dacarbazine therapy has been associated with serum enzyme elevations during therapy and occasional cases of severe and distinctive acute hepatic failure, probably caused by acute sinusoidal obstruction syndrome. (nih.gov)
- More importantly, dacarbazine is associated with a severe and distinctive liver injury which typically arises during the second or third cycle of therapy and most likely represents severe acute sinusoidal obstruction syndrome. (nih.gov)
- Unlike with other alkylating agents, sinusoidal obstruction syndrome caused by dacarbazine is associated with the usual chemotherapy doses, not the higher doses used in myeloablation in preparation for bone marrow transplantation. (nih.gov)
- Defibrotide has been approved for treatment of severe sinusoidal obstruction syndrome with solid organ failure in patients undergoing hematopoietic cell transplantation, but has not been specifically approved for the acute liver failure associated with dacarbazine use. (nih.gov)
Cancer chemotherapy1
- Liver damage may occur more often in people that are receiving other cancer chemotherapy drugs along with dacarbazine treatment. (medlineplus.gov)
Temozolomide4
- Temozolomide was "slightly more toxic" than dacarbazine, but it had an acceptable safety profile, Dr. Patel said. (medscape.com)
- There was a higher rate of lymphopenia (reported by 45% of patients on temozolomide and 9% on dacarbazine), although the rates for the other hematologic adverse events (leucopenia, anemia) and nonhematologic events (such as fatigue, nausea, and vomiting) were similar for both drugs. (medscape.com)
- When asked whether temozolomide might be preferred because it is an oral drug and the results suggest it is about the same as dacarbazine, Dr. Patel replied: "This trial was designed to show an improvement in survival, and it would take a larger trial to show that the oral drug is equivalent to the intravenous drug. (medscape.com)
- So temozolomide is no better than dacarbazine, but we don't know that dacarbazine is good," he said. (medscape.com)
Zeen1
- Dacarbazine (da kar' ba zeen) is a triazene analogue of 5-aminoimidazole-4-carboxamide, a precursor in purine biosynthesis. (nih.gov)
DTIC1
- Dacarbazine is popularly known as DTIC and was approved for use in the United States in 1975. (nih.gov)
Hepatic2
- abametapir will increase the level or effect of dacarbazine by affecting hepatic enzyme CYP1A2 metabolism. (medscape.com)
- givosiran will increase the level or effect of dacarbazine by affecting hepatic enzyme CYP1A2 metabolism. (medscape.com)
Intravenous2
- After intravenous administration of dacarbazine for injection, the volume of distribution exceeds total body water content suggesting localization in some body tissue, probably the liver. (nih.gov)
- Dacarbazine is given by intravenous infusion typically for five to ten days in cycles of every 3 to 4 weeks. (nih.gov)
Mechanism of act1
- Procarbazine is an alkylating agent with mechanism of action similar to that of dacarbazine. (medscape.com)
Purine2
- Dacarbazine is in a class of medications known as purine analogs. (medlineplus.gov)
- Dacarbazine may act as a purine analogue and antimetabolite. (nih.gov)
Carboxamide1
- Besides unchanged dacarbazine, 5-aminoimidazole -4 carboxamide (AIC) is a major metabolite of dacarbazine excreted in the urine. (nih.gov)
Protein2
- At therapeutic concentrations dacarbazine is not appreciably bound to human plasma protein. (nih.gov)
- Dacarbazine is an alkylating agent that inhibits DNA, RNA, and protein synthesis. (medscape.com)
Severe1
- Dacarbazine can cause a severe decrease in the number of blood cells in your bone marrow. (medlineplus.gov)
Liver1
- Dacarbazine may cause serious or life-threatening liver damage. (medlineplus.gov)
Dose3
- 1 The average cumulative excretion of unchanged dacarbazine in the urine is 40% of the injected dose in 6 hours. (nih.gov)
- Dacarbazine has been shown to be teratogenic in rats when given in doses 20 times the human daily dose on day 12 of gestation. (nih.gov)
- Dacarbazine when administered in 10 times the human daily dose to male rats (twice weekly for 9 weeks) did not affect the male libido, although female rats mated to male rats had higher incidence of resorptions than controls. (nih.gov)
Therapy1
- Dacarbazine has been the standard therapy for this group of patients for the past 20 years or so," said lead investigator Poulam Patel, MD, from Nottingham University, in the United Kingdom, "and so far nothing has surpassed it. (medscape.com)
Effects3
- Dacarbazine may cause side effects. (medlineplus.gov)
- dacarbazine decreases effects of adenovirus types 4 and 7 live, oral by pharmacodynamic antagonism. (medscape.com)
- dacarbazine decreases effects of influenza virus vaccine quadrivalent, adjuvanted by pharmacodynamic antagonism. (medscape.com)
Results1
- The results of this trial suggest that dacarbazine should remain the standard treatment. (medscape.com)
Treatment2
- Dr. Jost also made the point that dacarbazine, although a standard treatment in this patient population for years, is unproven. (medscape.com)
- The role of glucocorticoids in the treatment of fulminant hepatitis induced by dacarbazine. (nih.gov)
Treat2
- Dacarbazine is used to treat melanoma (a type of skin cancer) that has spread to other parts of your body. (medlineplus.gov)
- When dacarbazine is used to treat melanoma, it may be injected once a day for 10 days in a row every 4 weeks or it may be injected once a day for 5 days in a row every 3 weeks. (medlineplus.gov)