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Expression of the c-Myc proto-oncogene in multiple myeloma and chronic lymphocytic leukemia: an in situ analysis. Expression of the Bcl-2 gene in human multiple myeloma cell lines and normal plasma cells. Differential expression of Bcl-2 in human plasma cell disorders according to proliferation status and malignancy. Response to interferon therapy in patients with multiple myeloma correlates with expression of the Bcl-2 oncoprotein. Blockade of mitogen-activated protein kinase cascade signaling in interleukin 6-independent multiple myeloma cells. Constitutive activation of Stat3 signaling confers resistance to apoptosis in human U266 myeloma cells. Discordant somatic mutation of immunoglobulin variable region genes and bcl-6 genes in chronic lymphocytic leukemia. Paracrine rather than autocrine regulation of myeloma-cell growth and differentiation by interleukin-6. Interleukin-6 gene expression in multiple myeloma: a characteristic of immature myeloma cells. The bone marrow stromal environment is a major factor in myeloma cell resistance to dexamethasone. Biologic effects of anti-interleukin-6 murine monoclonal antibody in advanced multiple myeloma. Production of lymphotoxin, a bone resorbing cytokine, by cultured human myeloma cells. Oncostatin M, leukemia inhibitory factor, and interleukin 6 induce the proliferation of human plasmacytoma cells via the common signal transducer, gp130. Tumor necrosis factor is a survival and proliferation factor for human myeloma cells. Insulin-like growth factor I is a growth and survival factor in human multiple myeloma cell lines. Bone marrow neovascularization, plasma cell angiogenic potential, and matrix metalloproteinase-2 secretion parallel progression of human multiple myeloma. Expression of vascular endothelial growth factor and its receptors in hematopoietic malignancies. Expression of syndecan regulates human myeloma plasma cell adhesion to type I collagen. Interaction of tumor and host cells with adhesion and extracellular matrix molecules in the development of multiple myeloma. Syndecan-1 is a multifunctional regulator of myeloma pathobiology: control of tumor cell survival, growth, and bone cell differentiation. Sequential maturation stages of monoclonal B lineage cells from blood, spleen, lymph node, and bone marrow from a terminal myeloma patient. Identification of immature and mature myeloma cells in the bone marrow of human myelomas. Phenotypic heterogeneity in aneuploid multiple myeloma indicates pre-B cell involvement. Humoral immune deficiency in multiple myeloma patients due to compromised B-cell function. Lymphocyte subsets in the peripheral blood of patients with multiple myeloma and benign monoclonal gammopathy. Natural killer cell activity in monoclonal gammopathies: relation to disease activity. Idiotype-specific T cells in multiple myeloma: targets for an immunotherapeutic intervention? Role of light chain variable region in myeloma with light chain deposition disease: evidence from an experimental model. Renal failure and multiple myeloma: pathogenesis and treatment of renal failure and management of underlying myeloma. Localization of a single binding site for immunoglobulin light chains on human Tamm-Horsfall glycoprotein. Biochemical interaction between Tamm-Horsfall glycoprotein and Ig light chains in the pathogenesis of cast nephropathy. Bence Jones proteins bind to a common peptide segment of Tamm-Horsfall glycoprotein to promote heterotypic aggregation.

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If pulmonary metastases cannot be completely removed, the postthoracotomy survival is shortened for patients with most tumors in comparison to those individuals completely resected. Separate prognostic variables may be combined to enhance the predictive value for survival. Other targets of gene therapy may include those chemotherapy-resistant tumors or those tumors with greater propensity for metastatic spread. These authors recommended that ErbB-2 might be considered as a prognostic factor for patients with osteosarcoma. It has been strongly correlated with early pulmonary metastasis and poor survival. Other preclinical treatment methods may include nebulized interleukin-2 liposomes. In many patients, surgery has been used as salvage treatment after maximal chemotherapy response has been achieved. Systemic toxicity may limit the amount of chemotherapy given to an individual patient. This isolated lung perfusion technique may be done unilaterally, with the contralateral lung serving as an "oxygenator" while the ipsilateral lung is perfused. Bilateral pulmonary perfusion may be performed, although extracorporeal circulatory support (cardiopulmonary bypass) is required. Preclinical studies in rodents with experimental pulmonary metastases from a methylcholanthrene-induced syngeneic sarcoma 169,170 and 171 have shown that chemotherapy may be delivered to pulmonary tissue in significantly higher concentrations than with systemic delivery. In this model, isolated single-lung perfusion with Adriamycin (doxorubicin) was safe and effective. After left thoracotomy, the pulmonary artery and pulmonary vein were isolated and clamped. Then the drug was flushed out before removing the cannulas and restoring circulation. Johnston and colleagues 173 described a continuous perfusion of the lungs with Adriamycin (single lung, continuous perfusion) as a safe technique and subsequently applied their technique clinically. Drug concentrations in normal lung and tumor generally increased with higher drug dosages. Although continuous perfusion with a pump circuit offers some theoretical advantages, the technique is cumbersome, equipment-intensive, and time-consuming, and it has the inherent problem of the incompatibility of Adriamycin and heparin. No hospital deaths occurred, and a short-term (less than 6 months) decrease in nodule size was noted in 3 of 15 patients. A paucity of effective treatment and the potential for high drug concentrations for pulmonary metastases by regional lung perfusion warrants further clinical study. Removal of metastatic carcinoma of the lung and mediastinum: suggestions as to technic. Adenocarcinoma of the kidney with metastasis to the lung cured by nephrectomy and lobectomy. Survival following aggressive resection of pulmonary metastases from osteogenic sarcoma: analysis of prognostic factors. Analysis of prognostic factors in patients undergoing resection of pulmonary metastases from soft tissue sarcomas. Evaluation of computed tomography in the detection of pulmonary metastases: a prospective study. Comparison of computed and conventional whole lung tomography in detecting pulmonary nodules: a prospective radiologic-pathologic study. Comparison of median sternotomy and thoracotomy for resection of pulmonary metastases in patients with adult soft-tissue sarcomas. Multimodality treatment of extra-visceral soft tissue sarcomas M0: state of the art and trends. Evaluation of fluorodeoxyglucose positron emission tomography in the management of soft-tissue sarcomas.


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In all instances, it is recommended that the tumor be resected en bloc with the involved chest wall, with a minimum of 2 cm of normal chest wall removed in all directions beyond the tumor. When necessary, plastic reconstruction can be used to reconstitute the chest wall. Prognosis is related to the completeness of resection and depth of chest wall invasion, with no patients surviving 5 years after incomplete resection. Whether simple removal of the parietal pleura in tumors only invading this structure is adequate remains a contentious issue. A recent report suggested that with sufficient care and experience, pleurectomy is adequate in selected T3 tumors. Since that initial report, most surgeons continue to treat a documented superior sulcus tumor with preoperative radiotherapy of 3000 to 4500 cGy, followed by en bloc resection of the involved lung, chest wall and, frequently, the T1 nerve root. On occasion, palliative resection of such lesions may be required for pain relief. More recently, aggressive curative approaches to remove and replace these adjacent structures have been reported, with some long-term survivors. Invasion of the mediastinal pleura, pericardium, or mediastinal fat also constitutes T3 disease. In many instances, en bloc resection of the involved mediastinal tissue can accomplish a complete resection. In such patients, whenever possible, technical resectability should be determined preoperatively. Tumors invading the diaphragm frequently spread along the diaphragmatic pleura, and most patients present with a malignant pleural effusion (T4) that usually is unresectable. In the occasional patient, focal diaphragmatic invasion can be completely resected by lobectomy and en bloc resection of the diaphragm, replacing this structure with a synthetic mesh or fabric. The existence of N2 disease remains the most controversial area for primary surgical management of lung cancer. Although potentially resectable, once ipsilateral mediastinal or subcarinal lymph nodes (or both) are involved by tumor, the ultimate prognosis is much worse. Selectivity is important before considering surgery for patients with preoperatively identified N2 disease. Adverse prognostic factors include multiple levels of N2 disease, multiple lymph nodes at one level involved with tumor, adenocarcinoma, and extranodal spread of disease. Single-station lymph node involvement with microscopic foci of disease not clinically apparent on clinical staging constitutes most of the subset of patients with minimal N2 disease. This early-stage disease is usually discovered at the time of thoracotomy or at pretreatment mediastinoscopy. Incomplete (R1, R2) resection results in a noncurative treatment, with few if any patients surviving beyond 3 years. Patients found to have multiple lymph node stations involved at final pathologic staging also fare poorly. At the time of surgery, a complete mediastinal lymph node dissection is warranted whenever N2 disease is suspected or known. This more advanced, bulky, or multistation N2 disease usually can be identified preoperatively and is termed clinical N2 disease. It is considered by most surgeons to be inoperable by primary surgery, with few 5-year survivors identified after surgical resection. For most of these patients, primary radiotherapy is still considered the standard treatment for local control. Recognition of prognostic and surgical factors that predict for specific anatomic failure patterns can allow selection of patients for local, systemic, or combined therapy. Isolated local failure rates are particularly high if the procedure is performed to conserve parenchyma in patients with compromised pulmonary function. This trial randomly assigned 210 patients to receive 50 Gy in 25 fractions after surgery versus observation alone. The Council reported higher local recurrences in 276 patients in the surgery-only arms of the trials. It has been shown to improve local control in patients with mediastinal nodal disease but has no proven survival benefit. Positive Margins (R1, R2 Resections) the presence of microscopic disease after curative surgery for early-stage disease at the bronchial resection margin, chest wall, or vascular margin may adversely affect the prognosis of patients. Yet, despite data that suggest that adjuvant radiotherapy reduces local recurrence, the retrospective literature regarding the efficacy of radiotherapy to improve local control is conflicting.

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An erythematous pruritic maculopapular rash that affects the forearms, hands, or feet is typical. Other cutaneous effects include desquamation of the hands and feet, palmar-plantar erythrodysesthesia that may respond to pyridoxine or cooling, 269,270 and onychodystrophy characterized by brown discoloration, ridging, onycholysis, soreness, and brittleness and loss of the nail plate. Both neurosensory and neuromuscular effects are generally less frequent and less severe with docetaxel as compared to paclitaxel. Patients typically complain of paresthesia and numbness, but peripheral motor effects may also occur. Transient arthralgia and myalgia are occasionally noted within days after treatment. Malaise or asthenia have been prominent complaints in patients who have been treated with large cumulative doses, particularly when docetaxel is administered on a continuous weekly schedule. Mild to moderate conjunctivitis, which is responsive to topical corticosteroids, may also occur, particularly with weekly administration. Nausea, vomiting, and diarrhea have also been observed, but severe gastrointestinal toxicity is rare. In patients with advanced breast and ovarian cancers, the cumulative body of randomized study results indicate that both schedules are equivalent, particularly with regard to event-free survival and overall survival, although response rates have occasionally been superior with the 24-hour infusion. There has also been considerable interest in intermittent schedules, particularly those in which paclitaxel is administered as a 1-hour infusion weekly, which results in substantially less myelosuppression than conventional 3- and 24-hour every 3-week schedules. Nevertheless, the weekly schedule may be advantageous for patients who are at high risk of developing severe myelosuppression. A single dose of a corticosteroid (dexamethasone, 20 mg intravenously) administered 30 minutes before treatment has been reported to confer very effective prophylaxis of major hypersensitivity reactions. Paclitaxel solutions should be diluted and stored in glass or polypropylene bottles or suitable plastic bags (polypropylene or polyolefin) and administered through polyethylene-lined administration sets that include an in-line filter with a microporous membrane not greater than 0. The extensive involvement of hepatic metabolism and biliary excretion in the disposition of paclitaxel-similar to that of other anticancer drugs, such as the vinca alkaloids-in which dose modifications are required indicates that doses should be modified in patients with hepatic dysfunction. Official recommendations have not been formulated, but prospective evaluations indicate that patients with moderate to severe elevations in serum concentrations of hepatocellular enzymes or bilirubin (or both) are more likely to develop severe toxicity than patients without hepatic dysfunction. Also similar to the case with paclitaxel, glass bottles or polypropylene or polyolefin plastic products should be used for preparation and storage, and docetaxel should be administered through polyethylene-lined administration sets. The preponderance of data indicates that cell death is principally mediated through a direct effect on microtubules. Estramustine is known to inhibit mitotic microtubule networks and to depolymerize interphase microtubules. Like the taxanes, estramustine can also exert an antiproliferative effect via stabilization of spindle microtubules. The targets of estramustine-b-tubulins-are composed of multiple isotypes encoded by separate cellular genes. Because the binding of different b-tubulin subtypes to a-tubulin alters the dynamic properties of microtubule growth and stability, a change in the relative b-tubulin isotypes may counter the inhibitory and destabilizing effects of estramustine on microtubule assembly. Exposure to estramustine induces both quantitative and qualitative changes in tau, leading to a sevenfold increase in estramustine resistance in some cell lines. Current recommendations include fasting before the oral administration of estramustine phosphate and avoidance of calcium-rich foods and calcium antacids. At conventional dosing schedules, nausea and vomiting can be prevented by antiemetic therapy. Myelosuppression is not associated with estramustine phosphate when administered as a single agent. Commonly observed estrogenic side effects of estramustine therapy include gynecomastia, nipple tenderness, and fluid retention. Caution should be exercised in prescribing estramustine phosphate to patients with congestive heart failure because of the risk for fluid retention and edema. These include venous thrombosis, pulmonary emboli, and cerebrovascular and coronary thrombotic events. Transient elevations in hepatic transaminases occur in approximately one-third of patients receiving estramustine phosphate therapy.

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In the 1990s, reproducible single-agent activity was demonstrated for several new agents. Paclitaxel, docetaxel, vinorelbine, gemcitabine, and irinotecan have been extensively investigated (Table 31. Their definitive evaluation has frequently included a comparison of the new drug with cisplatin versus cisplatin alone (Table 31. Patients treated with cisplatin and vinorelbine had a significantly longer median survival time of 40 weeks. An economic evaluation of this study concluded that this chemotherapy had acceptable efficacy and cost-effectiveness as compared with other common medical interventions. Again, the combination of cisplatin and vinorelbine proved superior to the single agent. An intriguing European study compared vinorelbine with best supportive care in the elderly (70 years). The paclitaxel-plus-cisplatin arms were superior to the etoposide-plus-cisplatin regimen, with no evidence of an increased response rate with a higher paclitaxel dose. A European trial showed cisplatin and paclitaxel to result in median survival (10 months) similar to that of cisplatin and teniposide while being better tolerated. Other randomized trials confirm the activity of cisplatin or carboplatin-paclitaxel regimens and the favorable toxicity profile of the latter combination (Table 31. Comparison of Various Combination Chemotherapy Regimens Encouraging data also exist for docetaxel, 542,543,544 and 545 gemcitabine, 546,547,548,549,550 and 551 and irinotecan. The combination of gemcitabine and cisplatin showed a significant improvement in median survival (7. Identical median survival times of 8 months suggested equivalence of antitumor activity, while the toxicity spectrum of the regimens predictably differed (more nausea and vomiting and myelosuppression with cisplatin, more neurotoxicity with carboplatin). This is an important study, since it will establish the relative activity and toxicity of several novel cisplatin-based regimens versus the combination of paclitaxel and carboplatin. Based on recent evidence, current standard regimens are the doublets of cisplatin in combination with either vinorelbine, paclitaxel, or gemcitabine or the combination of paclitaxel and carboplatin. In selected cases, administration of second-line chemotherapy should be considered. Based on available data from randomized trials, treatment should consist of the combination of cisplatin and vinorelbine, cisplatin and gemcitabine or, alternatively, cisplatin or carboplatin and paclitaxel. Available evidence suggests that patients with a performance status of 2 will have, at best, a minor prolongation of survival time by chemotherapy but may experience significant relief of disease-related symptoms. In patients with stable or responding disease, the treatment duration has traditionally been six cycles of chemotherapy. Historically, this is largely based on the cumulative toxicity observed with cisplatin, which frequently limits to six or less the total number of cycles. The optimal duration of chemotherapy is undergoing evaluation in randomized trials. It is possible that newer regimens, particularly those not containing cisplatin, might be tolerated (and active) for more than six cycles. In patients with stable or responding disease, it might, therefore, make sense to continue therapy beyond six cycles. Patients who progress on or after first-line chemotherapy but continue to have a good performance status may be offered second-line chemotherapy. Such an approach holds promise for the intermediate and long-term identification of more active therapies. The empiric use of sequential chemotherapy regimens as second-, third-, or fourth-line therapy cannot be supported using current data. To differentiate between a second primary lung cancer and a metastasis in synchronous lung lesions or among local recurrence, a new primary lung cancer, and a pulmonary metastasis from a previous resected lung cancer in metachronous lung lesions can be difficult. A second or recurrent lung lesion is considered a metastasis if the histology is identified to the primary tumor and occurs in the opposite lung or a noncontiguous area of the ipsilateral lung.

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Pyridoxine therapy for palmar-plantar erythrodysesthesia associated with Taxotere. Randomized trial of 3-hour versus 24-hour infusion of high-dose paclitaxel in patients with metastatic or locally advanced breast cancer: National Surgical Adjuvant Breast and Bowel Project Protocol B-26. Ninety-six-hour infusional paclitaxel as salvage therapy of ovarian cancer patients previously failing treatment with 3-hour or 24-hour paclitaxel infusion. Dose-dense therapy with weekly 1-hour paclitaxel infusions in the treatment of metastatic breast cancer. Phase I feasibility and pharmacologic study of intraperitoneal paclitaxel: a Gynecologic Oncology Group study. Short-course intravenous prophylaxis for paclitaxel-related hypersensitivity reactions. A randomized multicenter study of single agent paclitaxel (Taxol) given weekly versus every three weeks to patients with ovarian cancer previously treated with platinum therapy. Phase I and pharmacokinetic trial of paclitaxel in patients with hepatic dysfunction. A phase I and pharmacokinetic study of docetaxel in cancer patients with liver dysfunction due to malignancies. Effects of hormone-cytostatic complexes on the rat ventral prostate in vivo and in vitro. Purification and distribution of a major protein in rat prostate that binds estramustine, a nitrogen mustard derivative of estradiol-17 beta. Effect of estramustine phosphate on the assembly of isolated bovine brain microtubules and fast axonal transport in the frog sciatic nerve. Stabilization of microtubule dynamics by estramustine by binding to a novel site in tubulin: a possible mechanistic basis for its antitumor action. Differential uptake of estramustine phosphate metabolites and its correlation with the levels of estramustine binding protein in prostate tumor tissue. Selective antimitotic effects of estramustine correlate with its antimicrotubule properties on glioblastoma and astrocytes. Apoptotic tumor cell death induced by estramustine in patients with malignant glioma. Inhibition of prostate cancer growth by estramustine and etoposide: evidence for interaction at the nuclear matrix. Dansylated estramustine, a fluorescent probe for studies of estramustine uptake and identification of intracellular targets. Identification of potassium flux pathways and their role in the cytotoxicity of estramustine in human malignant glioma, prostatic carcinoma and pulmonary carcinoma cell lines. Estramustine resistance correlates with tau over-expression in human prostatic carcinoma cells. Resistance to the antimitotic drug estramustine is distinct from the multidrug resistant phenotype. P-glycoprotein binding and modulation of the multidrug-resistant phenotype by estramustine. Pharmacokinetics of estramustine phosphate (Estracyt) in prostatic cancer patients. Estramustine phosphate: plasma concentrations of its metabolites following oral administration to man, rat and dog. Impairment of estramustine phosphate absorption by concurrent intake of milk and food. Phase I trial of docetaxel with estramustine in androgen-independent prostate cancer. Rhazinilam mimics the cellular effects of Taxol by different mechanisms of action. The microtubule-stabilizing agent discodermolide competitively inhibits the binding of paclitaxel (Taxol) to tubulin polymers, enhances tubulin nucleation reactions more potently than paclitaxel, and inhibits the growth of paclitaxel-resistant cells. Activities of the microtubule-stabilizing agents epothilones A and B with purified tubulin and in cells resistant to paclitaxel (Taxol). Desoxyepothilone B is curative against human tumor xenografts that are refractory to paclitaxel. The coral-derived natural products eleutherobin and sarcodictyins A and B: effects on the assembly of purified tubulin with and without microtubule-associated proteins and binding at the polymer taxoid site.

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In this group of patients as well, combined-modality therapy (including surgery) is being investigated 410,411 (discussed in Induction Chemoradiotherapy). T4 tumors include those invading mediastinal structures (the carina and trachea, the heart and great vessels, the esophagus or vertebral body) as well as the presence of a malignant pleural effusion. In most series reported, patients were highly selected, with most long-term survivors having T4N0 tumors. Only highly selected patients without N2 disease should be offered such a resection. For this reason, prior to resection of such a tumor, mediastinoscopy should be considered mandatory. In some patients, "extended" sleeve lobectomies (resecting the carina) can be used to preserve pulmonary function. Invasion of Superior Vena Cava Involvement of the superior vena cava has been treated occasionally by en bloc resection and graft replacement. Reported series include only few cases, and the significance of this finding cannot be assessed. It appears likely, however, that only T4 and not N2 lesions can occasionally be cured with such a radical resection. Invasion of Myocardium, Aorta, Esophagus, and Vertebral Body Surgical resection resulting in complete excision of a primary tumor with other mediastinal organ invasion is usually not possible. Palliative incomplete resections have not demonstrated survival or palliation benefit. En bloc resection of the lung with part of the involved aorta, esophagus, or vertebral body, not uncommon in the treatment of superior sulcus tumors, may result in long-term survival for selected patients. An analysis from Japanese investigators suggested that long-term survival is limited to patients with minimal atrial or aortic adventitial involvement in tumors invading great vessels. Despite being nonmalignant, an effusion evident on prior chest radiography has a poor prognosis, with a 5-year survival. However, they concluded that in patients with cytologically negative pleural effusions, unresectability must be documented surgically. Even with malignant pleural effusions, occasional 5-year survivals have been documented when all disease has been eradicated. However, one should never consider a pleural effusion malignant without cytologic or histologic proof. A "bloody" pleural effusion may be due to a traumatic thoracentesis or concomitant pulmonary infarction and not indicate T4 disease. The exact role of postoperative therapies combined with this has not been discussed. It does not appear, however, that these survivals are improved by the addition of surgery. Adjuvant and Neoadjuvant Therapies After complete resection in patients proven to have T4 or N3 disease, radiotherapy has been usually recommended as adjuvant treatment because of the high incidence of locoregional failure after aggressive surgery for this advanced tumor. Because of the paucity of patients reported to have undergone this treatment, the exact role of adjuvant radiotherapy cannot be assessed. It does appear that clinically staged T4 tumors (especially T4N0 disease) do reasonably well after this combined-modality approach. Sixty-three percent of patients underwent a complete resection, and overall survival at 4 years was 19. Despite these encouraging results, in most instances T4 and N3 tumors cannot be resected completely and are usually considered for combined-modality therapy, using radiotherapy as the primary control mechanism. Higgins and Shields 423 reported the results of a randomized trial by the Veterans Administration in which male patients with a variety of histologic subtypes of lung cancer, including small cell lung cancer, were prospectively randomly assigned to receive supportive care only or external-beam radiotherapy. Two hundred forty-six patients were treated with placebo, and 308 male patients were treated to doses of 40 to 50 Gy. In addition, the radiotherapy was inadequate by modern standards, both in terms of the dose delivered (40 to 50 Gy) and the equipment used (orthovoltage). A retrospective study from British Columbia that controlled for tumor stage and other prognostic factors reported improved survival of 79 days in patients receiving high-dose palliative radiotherapy and survival of more than a year in patients receiving radical radiotherapy.

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Laparoscopy may also be of utility in patients with carcinomatosis who should be followed up for response to therapy to determine whether to change therapies or continue the current treatment strategy. The adhesions after multiple tumor debulkings and laparoscopies may ultimately limit the sensitivity of detection and increase the risk of laparoscopy. Open abdominal exploration and palpation of the peritoneal surfaces is extremely sensitive for even small 1- to 2-mm peritoneal surface nodules. Palpation of the areas at high risk should be performed during any cancer surgery for intraperitoneal malignancies. This includes the greater omentum, the deepest recess of the pelvic peritoneum, the base of the small bowel mesentery and transverse mesocolon, the falciform ligament, and the diaphragm. The term was first coined in 1884 by Werth 29 as a description of the gelatinous material filling the peritoneal cavity of a patient with a ruptured cystadenoma of the ovary. In 1901, Fraenkel 30 first associated P peritonei with a ruptured mucocele of the appendix. Because of the relative rarity of this clinical entity, it is generally poorly understood by oncologists. The spectrum of conditions that are considered to fall under the general diagnosis of P peritonei is quite large. The condition of diffuse mucinous ascites can be caused by any tumor that has spread into the peritoneal cavity and produces significant amounts of mucin. These cells can then continue to proliferate and produce copious amounts of mucin despite a completely benign histology, with the inability to invade into tissues and metastasize hematogenously or via lymphatics. The most important prognosticator for patients with mucinous ascites is, therefore, whether the primary tumor is benign or malignant. Clinical evidence of malignancy includes the presence of lymph node metastases and gross evidence of an invasive phenotype. Histologically, malignant tumors will have moderate to abundant cellularity, show evidence of invasion, and demonstrate cellular atypia and nuclear pleomorphism consistent with malignancy. Benign tumors have scant cellularity with no evidence of invasion into tissues and no cellular atypia. In difficult cases, it is helpful to examine the primary tumor carefully to determine whether the primary tumor represents invasion of tumor cells through the wall of the organ or a benign process that has ruptured the wall without invasion. The site of origin of cells producing mucinous ascites often is difficult to define. This is especially the case when, in women, both the appendix and the ovaries are obliterated by tumor. Although the ovary can be a site for mucinous borderline tumors of low malignant potential or mucinous carcinomas, these are almost never associated with diffuse copious mucinous ascites. These tumors often involve the ovaries at early stages but should not be confused with a primary ovarian cancer. Ruptured ovarian follicles may allow for a rich soil and sticky surface on which benign tumor cells can stick and proliferate. In surgical debulking procedures, appendectomy and bilateral oophorectomy should be performed. They have shown distinct difference in survival and prognosis in patients with disseminated peritoneal adenomucinosis as compared to those with carcinomatosis or discordant features (. This work verifies the importance of differentiating a malignant from a benign diagnosis. In their study, the median survival for patients with disseminated peritoneal adenomucinosis had not been reached with a median follow-up of approximately 6 years, whereas the median survival for patients with a malignant tumor producing mucinous ascites was approximately 16 months. It would be best not to use the term P peritonei without further classification into mucinous adenocarcinoma or benign mucinous tumors. The treatment approach should be different for patients with benign mucin-producing tumors as compared to those with mucinous carcinomatosis. Patients with benign tumors should be treated with aggressive surgical debulking to limit the symptoms of compression and abdominal distention caused by extensive mucinous ascites within the abdominal cavity. It has been reported that long-term disease-free survival can be accomplished with repeated tumor debulking. It may be that aggressive regional chemotherapy approaches should not be offered until their efficacy has been better defined in carcinomas. In the case of low-grade mucinous carcinomatosis, the uniformly poor prognosis encourages innovative and aggressive approaches. This includes intensive regional chemotherapy in combination with cytoreduction (as discussed in the Intraperitoneal Chemotherapy section).

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Studies of the effect of methyl-bis(beta-chloroethyl)amine hydrochloride on neoplastic diseases and allied disorders of the hematopoietic system. Increased intensification and total dose of cyclophosphamide in a doxorubicin-cyclophosphamide regimen for the treatment of primary breast cancer: findings from National Surgical Adjuvant Breast and Bowel Project B-22. Long-term survival of patients treated with combination chemotherapy for metastatic breast cancer. Successful treatment of childhood pilocytic astrocytomas metastatic to the leptomeninges with high-dose cyclophosphamide. Pretransplant conditioning with busulfan (Myleran) and cyclophosphamide for nonmalignant diseases. Assessment of engraftment following histocompatible allogeneic bone marrow transplantation. High-dose cyclophosphamide, thiotepa, and carboplatin with autologous marrow support in women with measurable advanced breast cancer responding to 215,219,220 this complication and its irreversibility 20. Complete remission of refractory anemia following a single high dose of cyclophosphamide. Immunoablative high-dose cyclophosphamide without stem-cell rescue for refractory, severe autoimmune disease. Deoxyribonucleic acid cross-linking by 4-hydroperoxycyclophosphamide in cyclophosphamide-sensitive and -resistant L1210 cells. The partitioning of phosphoramide mustard and its aziridinium ions among alkylation and P-N bond hydrolysis reactions. Characterization of cytosolic aldehyde dehydrogenase from cyclophosphamide resistant L1210 cells. Direct demonstration of elevated aldehyde dehydrogenase in human hematopoietic progenitor cells. The role of aldehyde dehydrogenase isozymes in cellular resistance to the alkylating agent cyclophosphamide. A comparison between the hematological side effects of cyclophosphamide and nitrogen mustard. Noninvasive detection of elevated glutathione levels in Mcf-7 cells resistant to 4-hydroperoxycyclophosphamide. Efficacy of ex vivo purging for autologous bone marrow transplantation in the treatment of acute nonlymphoblastic leukemia. Quantitation by gas chromatographychemical ionization mass spectrometry of cyclophosphamide, phosphoramide mustard, and nornitrogen mustard in the plasma and urine of patients receiving cyclophosphamide therapy. Pharmacokinetics of cyclophosphamide and its metabolites in bone marrow transplantation patients. Cytological study of the effect of cyclophosphamide on the epithelium of the urinary bladder in man. Intrasubject variation in children of ifosfamide pharmacokinetics and metabolism during repeated administration. Pharmacokinetics, metabolism and clinical effect of ifosfamide in breast cancer patients. The use of low-dose prednisone and melphalan in the treatment of poor-risk patients with multiple myeloma. Evidence for carrier-mediated transport of melphalan by L5178Y lymphoblasts in vitro. Evidence for active transport of melphalan by two amino acid carriers in L5178Y lymphoblasts in vitro. The effect of an amino acidlowering diet on the rate of melphalan entry into brain and xenotransplanted glioma. Quantitation by gas chromatographychemical ionizationmass spectrometry of phenylalanine mustard in plasma of patients. Pharmacokinetics of high-dose intravenous melphalan in patients undergoing peripheral blood hematopoietic progenitor-cell transplantation. Oral cyclophosphamide versus chlorambucil in the treatment of patients with membranous nephropathy and renal insufficiency. Thiotepa, busulfan and cyclophosphamide as a preparative regimen for allogeneic transplantation for advanced chronic myelogenous leukemia. Modulation of thiotepa antitumor activity in vivo by alteration of liver cytochrome P450-catalyzed drug metabolism.

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Recognition of tyrosinase by tumor infiltrating lymphocytes from a patient responding to immunotherapy. A mutated B-catenin gene encodes a melanoma-specific antigen recognized by tumor infiltrating lymphocytes. A mutated intron sequence codes for an antigenic peptide recognized by cytolytic T lymphocytes on a human melanoma. A gene encoding antigenic peptides of human squamous cell carcinoma recognized by cytotoxic T lymphocytes. The class Irestricted cytotoxic T lymphocyte response to predetermined epitopes in the hepatitis B and C viruses. Utilization of an alternative open reading frame of a normal gene in generating a novel human cancer antigen. A breast and melanoma-shared tumor antigen: T cell responses to antigenic peptides translated from different open reading frames. The intronic region of an incompletely spliced gp100 transcript encodes an epitope recognized by melanoma-reactive tumor infiltrating lymphocytes. Recognition of multiple epitopes in the human melanoma antigen gp100 associated with in vivo tumor regression. Interleukin-2: clinical applications: principles of administration and management of side effects. Trends in the safety high-dose bolus interleukin-2 administration in patients with metastatic cancer. Immunologic and therapeutic evaluation of a synthetic vaccine for the treatment of patients with metastatic melanoma. Observations of the systemic administration of autologous lymphokine-activated killer cells and recombinant interleukin-2 to patients with metastatic cancer. A progress report on the treatment of 157 patients with advanced cancer using lymphokine activated killer cells and interleukin-2 or high-dose interleukin-2 alone. Separation, phenotyping, and limiting dilution analysis of T-lymphocytes infiltrating human solid tumors. Clonal analysis and in situ characterization of lymphocytes infiltrating human breast carcinomas. Immunohistochemical analysis of infiltrating lymphocytes in central nervous system tumors. Interleukin-2 activation of cytotoxic T-lymphocyte infiltrating into human metastatic melanomas. Functional characterization of T lymphocytes propagated from human lung carcinoma. Identification of specific cytolytic immune responses against autologous tumor in humans bearing malignant melanoma. Long-term interleukin-2-dependent growth and cytotoxic activity of tumor-infiltrating lymphocytes from human squamous cell carcinomas of the head and neck. Autologous tumor-specific cytotoxic T lymphocytes in the infiltrate of human metastatic melanomas: activation by interleukin-2 and autologous tumor cells and involvement of the T cell receptor. Immunohistological and functional analyses of lymphoid infiltrates in human glioblastomas. Immunohistochemical analysis of tumor-infiltrating lymphocytes and major histocompatibility antigens in human gliomas and metastatic brain tumors. Interleukin-2 expanded tumor-infiltrating lymphocytes in human renal cell cancer: isolation, characterization, and anti-tumor activity. Lysis by interleukin-2 stimulated tumor-infiltrating lymphocytes of autologous and allogeneic tumor target cells. Functional and phenotypic analysis of tumor-infiltrating lymphocytes isolated from human primary and metastatic liver tumors and cultured in recombinant interleukin-2. Phenotypic and functional analysis of lymphocytes infiltrating pediatric tumors, with a characterization of the tumor phenotype. The role of class 1 antigens in recognition of melanoma cells by tumor-specific cytotoxic T lymphocytes: evidence for shared tumor antigens.


  • https://smhs.gwu.edu/urology/sites/urology/files/Handbook_2017-2018.pdf
  • https://academic.oup.com/jnen/article-pdf/62/3/217/9553163/62-3-217.pdf
  • https://www.tcichemicals.com/assets/cms-pdfs/ReagentGuide_8th_SynthesticOrganicChemistry_MaterialsChemistry.pdf
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