Warning About Cancer Questions
|
Mahalo Answers is a great place to start your research into Cancer questions, but it's not the final answer. Mahalo Answers is not a substitute for informed professional advice. If you desire or require professional advice, please consult a qualified provider who is licensed in your state or country. You should always seek independent professional advice before acting on any opinion, advice, or information available on Mahalo Answers. |
answered question
3
Votes
Votes
4
Answers
Answers
M$10.00
Need info about the use of chemotherapy for brain metastases.
I'm looking for results of using chemotherapy for cancer metastases. Links to web pages and/or text would be great. The patient (my sister) is in her 30s and her cancer began as pleomorphic adenoma of the parotid (salivary) gland.
What I want is data that indicates whether chemotherapy works against brain metastases. Even if you only can find writeups of individual patient outcomes (instead of full-fledged studies) that's still useful to me.
I know that some of this information is in subscription-only medical journals, but if the summary has some interesting info, I'd like to see those too.
Thank you!
(From what I understand I am allowed to give tips to multiple answerers. I'm going to try to give tips to everyone who comes up with unique information as long as I don't spend over $20 total).
What I want is data that indicates whether chemotherapy works against brain metastases. Even if you only can find writeups of individual patient outcomes (instead of full-fledged studies) that's still useful to me.
I know that some of this information is in subscription-only medical journals, but if the summary has some interesting info, I'd like to see those too.
Thank you!
(From what I understand I am allowed to give tips to multiple answerers. I'm going to try to give tips to everyone who comes up with unique information as long as I don't spend over $20 total).
voted interesting: lwelch, lindseylgreene, kevinbernard31
answers (4)
Not an MD, not medical advice:
I too am sorry to hear about your sister. I hope this research can help your family.
Found on UpToDate (password protected medical database):
Sorry to copy/paste but I don't want to summarize such important information. References will be given following the (very long) quote. If you would like any of the articles (in full) - please let me know. I should be able to access them and email them to you. Ignore the linked numbers within the quote - they won't work. They reference the references below (which i have numbered for you).
Title: Malignant salivary gland tumors: Treatment of metastatic disease
Author: Scott A Laurie, MD, FRCPC
"Choice of therapy and treatment endpoints — Due to the rarity of MSGTs (malignant salivary gland tumors), there are only limited data (mostly retrospective case series, few prospective trials) to guide the choice of systemic therapy. The greatest amount of data exists for adenoid cystic cancers, for which there are phase II trials of agents and regimens specifically tested in this subgroup. Prospective data for the other histologies are scarce, consisting of a few patients in trials that enrolled all histologies of malignant MSGTs. Older reports of chemotherapy for MSGT did not separate salivary duct cancers from other adenocarcinomas, so there are few data on the responsiveness of this subtype to standard cytotoxic agents. There is an urgent need to conduct quality clinical trials in MSGTs, and every patient should be considered for participation in such studies.
The indolent natural history of some MSGTs, particularly adenoid cystic cancers, must be taken into account when evaluating treatment outcomes from published reports. In a preliminary report of a systematic overview of chemotherapy trials in the adenoid cystic carcinoma subtype, objective responses were infrequent, while disease stabilization was observed more frequently 7. However, in the setting of an indolent cancer, apparent disease stabilization may reflect the variable natural history rather than true treatment efficacy. Thus, reports that include stable disease as an indicator of treatment benefit need to be interpreted carefully in light of this limitation. Moreover, for histologies whose clinical behavior may be indolent, such as adenoid cystic cancer, documentation of disease progression and its rate is required before embarking on any form of systemic treatment, particularly if the patient is being treated on a clinical protocol.
Chemotherapy — The limited available data suggest at least some differences in chemotherapy sensitivity among the histologic subtypes of MSGTs. As an example, in one study, single agent paclitaxel (200 mg/m2 over three hours every 21 days) appeared active against adenocarcinomas and mucoepidermoid carcinomas (8 of 31 responding), but not adenoid cystic carcinomas (none of 14 responding) (show table 2) 8. Whether there are differences with other regimens is difficult to ascertain because of the small numbers of patients with each histology included in the individual reports.
As noted above, there are few data on the responsiveness of salivary duct cancers to specific chemotherapy regimens. In suitable patients, it is reasonable to use the same agents or regimens as are used for adenocarcinomas. (See "Choice of therapy and treatment endpoints" above).
In addition to paclitaxel, cisplatin, mitoxantrone, epirubicin, methotrexate, and vinorelbine appear to have modest single agent activity (show table 2) 9-13. In general, combination regimens result in higher response rates, but they are not clearly superior in terms of survival and may lead to additional toxicity.
CAP regimen — The most commonly studied regimen is CAP (cyclophosphamide 500 mg/m2 IV day 1, doxorubicin 50 mg/m2 day 1, and cisplatin 50 mg/m2 day 1, all repeated every 28 days) 14. Reported response rates are as high as 40 to 50 percent, and some are complete (show table 2) 14-20. The duration of response ranges from three to seven months.
Although the CAP regimen has the greatest amount of data, there are no randomized trials comparing CAP with single agent therapy or with any other combination regimen.
Other multiagent regimens — A number of other regimens besides CAP have been evaluated in patients with advanced or recurrent malignant MSGT (show table 2). There is no suggestion that any is superior to CAP, although randomized trials have not been conducted:
* The addition of 5-fluorouracil to CAP resulted in a 50 percent response rate in 16 evaluable patients, but was associated with significant toxicity, including two treatment related deaths (one from neutropenic sepsis, the other from doxorubicin-related cardiotoxicity) 21.
* A regimen of cisplatin, doxorubicin and 5-fluorouracil (PAF) led to a 35 percent objective response rate in one trial of 17 patients with advanced MSGTs 22. Response duration was 6 to 15 months, and toxicity was tolerable.
Others have published similar experience with ECF (epirubicin plus cisplatin and 5-FU) 23-25. A compilation of data from these reports is presented in the table (show table 2).
* In one of the only randomized trials that has been conducted in patients with MSGT (a randomized phase II trial), 36 patients with advanced disease (22 adenoid cystic, 9 adenocarcinoma, 1 mucoepidermoid, 4 other histologies) were randomly assigned to vinorelbine (25 mg/m2 days 1 and 8, every three weeks) plus cisplatin (80 mg/m2 day 1) or vinorelbine alone (30 mg/m2 weekly) 13. Combination therapy was associated with a significantly higher complete (19 versus 0 percent) and overall response rate (44 versus 20 percent), and a greater likelihood of survival beyond one year (38 versus 5 percent).
However, this result may simply reflect the greater activity of cisplatin as compared to vinorelbine as a single agent rather than a synergistic effect of the combination. Toxicity, in particular nausea and vomiting, was greater in the cisplatin-containing arm.
* Other platinum-based regimens, such as cisplatin-mitoxantrone 26, cisplatin-5-FU 1, carboplatin-paclitaxel 27,28, and cisplatin-bleomycin with either methotrexate or doxorubicin 1,15,29,30 have been reported to lead to objective responses in trials of small numbers of patients, as have regimens that are anthracycline-based but non-platinum containing (show table 2) 15,29.
It is not clear that any of these regimens provides an advantage over single agent therapy or CAP.
Molecularly targeted therapy — The increasing understanding of the underlying molecular changes in MSGTs has led to the identification of several potential therapeutic targets. Although early results from phase II studies of such targeted therapies in MSGTs are interesting and encouraging, the data are too preliminary to recommend the routine use of any of these agents at present.
Imatinib — Approximately 80 percent of adenoid cystic carcinomas express the c-kit tyrosine kinase (TK) receptor 31, and there are individual case reports documenting objective responses with imatinib (Gleevec), an orally active potent inhibitor of the c-kit TK 32,33. However, there were no objective responses in three phase II trials in which a total of 32 patients with adenoid cystic carcinoma were treated with imatinib (400 mg twice daily) 34-36, nor in a fourth trial of lower dose therapy (400 mg daily) in an additional 10 patients 37. Further study is needed to clarify the role of imatinib in the treatment of adenoid cystic carcinoma.
Gefitinib — The epidermal growth factor receptor (EGFR) is often overexpressed in adenoid cystic and mucoepidermoid cancers. Unfortunately, no responses were documented among 29 patients with advanced MSGT (19 adenoid cystic cancers, 2 mucoepidermoid cancers) in a preliminary report of a phase II trial of gefitinib, an orally active EGFR TK inhibitor 34. Ten patients had disease stabilization, which was maintained for at least 16 weeks in five.
Cetuximab — Another method for targeting the EGFR is through anti-EGFR monoclonal antibodies such as cetuximab. In a preliminary report, cetuximab was evaluated in 30 patients (23 with adenoid cystic carcinoma). No objective responses were observed, although 20 of the patients with adenoid cystic carcinoma had disease stabilization for at least six months 38.
Trastuzumab — Up to one-third of mucoepidermoid carcinomas and an even higher proportion of salivary duct cancers overexpress HER2 protein, or have gene amplification as detected by fluorescence in situ hybridization 39-43. In contrast, expression of HER2 is unusual in adenoid cystic carcinomas and adenocarcinomas 40,44.
These findings have prompted exploration of therapies targeting HER2 in mucoepidermoid and salivary duct cancers. In a phase II trial of trastuzumab (Herceptin®), an anti-HER2 monoclonal antibody, one of three patients with mucoepidermoid cancer had a partial response lasting longer than two years, while two others with previously progressive salivary duct carcinomas had disease stabilization for 26 and 40 weeks, respectively 40,45. Further experience with this agent is needed.
Lapatinib — Lapatinib, an orally active dual inhibitor of the TKs of both EGFR and HER2, was studied in a phase II trial of 40 patients with progressive metastatic or recurrent EGFR and/or HER2-overexpressing SGT 46. Of the 19 assessable patients with ACC, there were no objective responses but 15 (79 percent) had stable disease, nine for six months or longer. Among the 17 assessable non-ACC patients, there were also no objective responses, but eight (47 percent) had stable disease, four for six months or longer.
Treatment was well tolerated, and the main toxicities were grade 1 to 2 diarrhea, fatigue, and skin rash.
Bortezomib — The proteasome-ubiquitin pathway is an essential intracellular system that degrades many labile proteins that regulate the cell cycle, apoptosis, transcription, cell adhesion, angiogenesis, and antigen presentation. The transcription factor NF-kappaB, which is expressed in some adenoid cystic cancers 47 and may be associated with an adverse prognosis, is activated only after the proteolysis of its inhibitor, IkappaB, in proteasomes. Thus, at least in theory, inhibition of the NF-kappa B pathway by proteasome inhibitors such as bortezomib (Velcade) may serve to inhibit the growth of adenoid cystic cancers.
In a preliminary report of a study of 25 patients with adenoid cystic carcinoma, there were no objective responses from bortezomib monotherapy, but many patients had disease stabilization, and the median progression-free survival was 8.4 months 48. However, as noted previously, it is difficult to know whether this result reflects antitumor activity or indolent natural history. (See "General treatment principles" above)."
Cited References:
7. Laurie, SA, Su, YB, Pfister, DG, et al. Chemotherapy in the management of metastatic adenoid cystic carcinoma: a systematic review (abstract). Proc Am Soc Clin Oncol 2005; 23:520s. (Abstract available online at www.asco.org/ac/1,1003,_12-002643-00_18-0034-00_19-0031092,00.asp, accessed January 24, 2007).
8. Gilbert, J, Li, Y, Pinto, HA, et al. Phase II trial of taxol in salivary gland malignancies (E1394): A trial of the Eastern Cooperative Oncology Group. Head Neck 2006; 28:197.
9. Licitra, L, Marchini, S, Spinazze, S, et al. Cisplatin in advanced salivary gland carcinoma. A phase II study of 25 patients. Cancer 1991; 68:1874.
10. Schramm, VL Jr, Srodes, C, Myers, EN. Cisplatin therapy for adenoid cystic carcinoma. Arch Otolaryngol 1981; 107:739.
11. Verweij, J, de Mulder, PH, de Graeff, A, et al. Phase II study on mitoxantrone in adenoid cystic carcinomas of the head and neck. EORTC Head and Neck Cancer Cooperative Group. Ann Oncol 1996; 7:867.
12. Vermorken, JB, Verweij, J, de Mulder, PH, et al. Epirubicin in patients with advanced or recurrent adenoid cystic carcinoma of the head and neck: a phase II study of the EORTC Head and Neck Cancer Cooperative Group. Ann Oncol 1993; 4:785.
13. Airoldi, M, Pedani, F, Succo, G, et al. Phase II randomized trial comparing vinorelbine versus vinorelbine plus cisplatin in patients with recurrent salivary gland malignancies. Cancer 2001; 91:541.
14. Dreyfuss AI, Clark JR, Fallon BG, Posner MR, Norris CJ, Miller D. Cyclophosphamide, doxorubicin, and cisplatin combination chemotherapy for advanced carcinomas of salivary gland origin. Cancer 1987; 60:2869.
15. Kaplan, MJ, Johns, ME, Cantrell, RW. Chemotherapy for salivary gland cancer. Otolaryngol Head Neck Surg 1986; 95:165.
16. Licitra, L, Cavina, R, Grandi, C et al. Cisplatin, doxorubicin and cyclophosphamide in advanced salivary gland carcinoma. A phase II trial of 22 patients. Ann Oncol 1996; 7:640.
17. Creagan, ET, Woods, JE, Rubin, J, Schaid, DJ. Cisplatin-based chemotherapy for neoplasms arising from salivary glands and contiguous structures in the head and neck. Cancer 1988; 62:2313.
18. Alberts, D, Manning, M, Couthard, S et al. Adriamycin/cisplatin/cyclophosphamide combination chemotherapy for advanced carcinoma of the parotid gland. Cancer 1981; 47:645.
19. Belani, CP, Eisenberger, MA, Gray, WC. Preliminary experience with chemotherapy in advanced salivary gland neoplasms. Med Pediatr Oncol 1988; 16:197.
20. Tsukuda, M, Kokatsu, T, Ito, K, et al. Chemotherapy for recurrent adeno- and adenoid cystic carcinomas in the head and neck. J Cancer Res Clin Oncol 1993; 119:756.
21. Dimery, I, Legha, S, Shirinian, M. Fluorouracil, doxorubicin, cyclophosphamide and cisplatin combination chemotherapy in advanced or recurrent salivary gland carcinoma. J Clin Oncol 1990; 8:1056.
22. Venook, AP, Tseng, A Jr, Meyers, FJ, et al. Cisplatin, doxorubicin, and 5-fluorouracil chemotherapy for salivary gland malignancies: a pilot study of the Northern California Oncology Group. J Clin Oncol 1987; 5:951.
23. Airoldi, M, Pedani, F, Brando, V, et al. Cisplatin, epirubicin and 5-fluorouracil combination chemotherapy for recurrent carcinoma of the salivary gland. Tumori 1989; 75:252.
24. White, JD, Junor, EJ, McGarva, J, et al. Adenocarcinoma of the salivary gland? A chemo-sensitive disease. Clin Oncol (R Coll Radiol) 2004; 16:159.
25. Farhat, F, Kattan, J, Culine, S, et al. of the combination of 5 fluorouracil, adriamycin and cisplatin (FAP protocol) in the treatment of metastatic cylindroma. Apropos of a case with review of the literature. Bull Cancer 1994; 81:47.
26. Gedlicka, C, Schull, B, Formanek, M, et al. Mitoxantrone and cisplatin in recurrent and/or metastatic salivary gland malignancies. Anticancer Drugs 2002; 13:491.
27. Airoldi, M, Fornari, G, Pedani, F, et al. Paclitaxel and carboplatin for recurrent salivary gland malignancies. Anticancer Res 2000; 20:3781.
28. Ruzich, JC, Ciesla, MC, Clark, JI. Response to paclitaxel and carboplatin in metastatic salivary gland cancer: a case report. Head Neck 2002; 24:406.
29. Posner, MR, Ervin, TJ, Weichselbaum, RR, et al. Chemotherapy of advanced salivary gland neoplasms. Cancer 1982; 50:2261.
30. de Haan, LD, De Mulder, PH, Vermorken, JB, et al. Cisplatin-based chemotherapy in advanced adenoid cystic carcinoma of the head and neck. Head Neck 1992; 14:273.
31. Mino, M, Pilch, BZ, Faquin, WC. Expression of KIT (CD117) in neoplasms of the head and neck: an ancillary marker for adenoid cystic carcinoma. Mod Pathol 2003; 16:1224.
32. Alcedo, JC, Fabrega, JM, Arosemena, JR, Urrutia, A. Imatinib mesylate as treatment for adenoid cystic carcinoma of the salivary glands: report of two successfully treated cases. Head Neck 2004; 26:829.
33. Faivre, S, Raymond, E, Casiraghi, O, et al. Imatinib mesylate can induce objective response in progressing, highly expressing KIT adenoid cystic carcinoma of the salivary glands. J Clin Oncol 2005; 23:6271.
34. Laurie, SA, Licitra, L. Systemic therapy in the palliative management of advanced salivary gland cancers. J Clin Oncol 2006; 24:2673.
35. Hotte, SJ, Winquist, EW, Lamont, E, et al. Imatinib Mesylate in Patients With Adenoid Cystic Cancers of the Salivary Glands Expressing c-kit: A Princess Margaret Hospital Phase II Consortium Study. J Clin Oncol 2005; 23:585.
36. Lin, CH, Yen, RF, Jeng, YM, et al. Unexpected rapid progression of metastatic adenoid cystic carcinoma during treatment with imatinib mesylate. Head Neck 2005; 27:1022.
37. Pfeffer, MR, Talmi, Y, Catane, R, et al. A phase II study of Imatinib for advanced adenoid cystic carcinoma of head and neck salivary glands. Oral Oncol 2007; 43:33.
38. Licitra, L, Locati, LD, Potepan, P, et al. Cetuximab (C225) in recurrent and/or metastatic salivary gland carcinomas (RMSGCs): a monoinstitutional phase II study (abstract). J Clin Oncol 2006; 24:291s. (Abstract available online at www.asco.org/ac/1,1003,_12-002643-00_18-0034-00_19-0031092,00.asp, accessed January 24, 2007).
39. Weed, DT, Gomez-Fernandez, C, Pacheco, J, et al. MUC4 and ERBB2 expression in major and minor salivary gland mucoepidermoid carcinoma. Head Neck 2004; 26:353.
40. Glisson, B, Colevas, AD, Haddad, R, et al. HER2 expression in salivary gland carcinomas: dependence on histological subtype. Clin Cancer Res 2004; 10:944.
41. Jaehne, M, Roeser, K, Jaekel, T, et al. Clinical and immunohistologic typing of salivary duct carcinoma: a report of 50 cases. Cancer 2005; 103:2526.
42. Press, MF, Pike, MC, Hung, G, et al. Amplification and overexpression of HER-2/neu in carcinomas of the salivary gland: correlation with poor prognosis. Cancer Res 1994; 54:5675.
43. Nabili, V, Tan, JW, Bhuta, S, et al. Salivary duct carcinoma: A clinical and histologic review with implications for trastuzumab therapy. Head Neck 2007; 29:907.
44. Dori, S, Vered, M, David, R, Buchner, A. HER2/neu expression in adenoid cystic carcinoma of salivary gland origin: an immunohistochemical study. J Oral Pathol Med 2002; 31:463.
45. Haddad, R, Colevas, AD, Krane, JF, et al. Herceptin in patients with advanced or metastatic salivary gland carcinomas. A phase II study. Oral Oncol 2003; 39:724.
46. Agulnik, M, Cohen, EW, Cohen, RB, et al. Phase II study of lapatinib in recurrent or metastatic epidermal growth factor receptor and/or erbB2 expressing adenoid cystic carcinoma and non adenoid cystic carcinoma malignant tumors of the salivary glands. J Clin Oncol 2007; 25:3978.
47. Zhang, J, Peng, B, Chen, X. Expressions of nuclear factor kappaB, inducible nitric oxide synthase, and vascular endothelial growth factor in adenoid cystic carcinoma of salivary glands: correlations with the angiogenesis and clinical outcome. Clin Cancer Res 2005; 11:7334.
I too am sorry to hear about your sister. I hope this research can help your family.
Found on UpToDate (password protected medical database):
Sorry to copy/paste but I don't want to summarize such important information. References will be given following the (very long) quote. If you would like any of the articles (in full) - please let me know. I should be able to access them and email them to you. Ignore the linked numbers within the quote - they won't work. They reference the references below (which i have numbered for you).
Title: Malignant salivary gland tumors: Treatment of metastatic disease
Author: Scott A Laurie, MD, FRCPC
"Choice of therapy and treatment endpoints — Due to the rarity of MSGTs (malignant salivary gland tumors), there are only limited data (mostly retrospective case series, few prospective trials) to guide the choice of systemic therapy. The greatest amount of data exists for adenoid cystic cancers, for which there are phase II trials of agents and regimens specifically tested in this subgroup. Prospective data for the other histologies are scarce, consisting of a few patients in trials that enrolled all histologies of malignant MSGTs. Older reports of chemotherapy for MSGT did not separate salivary duct cancers from other adenocarcinomas, so there are few data on the responsiveness of this subtype to standard cytotoxic agents. There is an urgent need to conduct quality clinical trials in MSGTs, and every patient should be considered for participation in such studies.
The indolent natural history of some MSGTs, particularly adenoid cystic cancers, must be taken into account when evaluating treatment outcomes from published reports. In a preliminary report of a systematic overview of chemotherapy trials in the adenoid cystic carcinoma subtype, objective responses were infrequent, while disease stabilization was observed more frequently 7. However, in the setting of an indolent cancer, apparent disease stabilization may reflect the variable natural history rather than true treatment efficacy. Thus, reports that include stable disease as an indicator of treatment benefit need to be interpreted carefully in light of this limitation. Moreover, for histologies whose clinical behavior may be indolent, such as adenoid cystic cancer, documentation of disease progression and its rate is required before embarking on any form of systemic treatment, particularly if the patient is being treated on a clinical protocol.
Chemotherapy — The limited available data suggest at least some differences in chemotherapy sensitivity among the histologic subtypes of MSGTs. As an example, in one study, single agent paclitaxel (200 mg/m2 over three hours every 21 days) appeared active against adenocarcinomas and mucoepidermoid carcinomas (8 of 31 responding), but not adenoid cystic carcinomas (none of 14 responding) (show table 2) 8. Whether there are differences with other regimens is difficult to ascertain because of the small numbers of patients with each histology included in the individual reports.
As noted above, there are few data on the responsiveness of salivary duct cancers to specific chemotherapy regimens. In suitable patients, it is reasonable to use the same agents or regimens as are used for adenocarcinomas. (See "Choice of therapy and treatment endpoints" above).
In addition to paclitaxel, cisplatin, mitoxantrone, epirubicin, methotrexate, and vinorelbine appear to have modest single agent activity (show table 2) 9-13. In general, combination regimens result in higher response rates, but they are not clearly superior in terms of survival and may lead to additional toxicity.
CAP regimen — The most commonly studied regimen is CAP (cyclophosphamide 500 mg/m2 IV day 1, doxorubicin 50 mg/m2 day 1, and cisplatin 50 mg/m2 day 1, all repeated every 28 days) 14. Reported response rates are as high as 40 to 50 percent, and some are complete (show table 2) 14-20. The duration of response ranges from three to seven months.
Although the CAP regimen has the greatest amount of data, there are no randomized trials comparing CAP with single agent therapy or with any other combination regimen.
Other multiagent regimens — A number of other regimens besides CAP have been evaluated in patients with advanced or recurrent malignant MSGT (show table 2). There is no suggestion that any is superior to CAP, although randomized trials have not been conducted:
* The addition of 5-fluorouracil to CAP resulted in a 50 percent response rate in 16 evaluable patients, but was associated with significant toxicity, including two treatment related deaths (one from neutropenic sepsis, the other from doxorubicin-related cardiotoxicity) 21.
* A regimen of cisplatin, doxorubicin and 5-fluorouracil (PAF) led to a 35 percent objective response rate in one trial of 17 patients with advanced MSGTs 22. Response duration was 6 to 15 months, and toxicity was tolerable.
Others have published similar experience with ECF (epirubicin plus cisplatin and 5-FU) 23-25. A compilation of data from these reports is presented in the table (show table 2).
* In one of the only randomized trials that has been conducted in patients with MSGT (a randomized phase II trial), 36 patients with advanced disease (22 adenoid cystic, 9 adenocarcinoma, 1 mucoepidermoid, 4 other histologies) were randomly assigned to vinorelbine (25 mg/m2 days 1 and 8, every three weeks) plus cisplatin (80 mg/m2 day 1) or vinorelbine alone (30 mg/m2 weekly) 13. Combination therapy was associated with a significantly higher complete (19 versus 0 percent) and overall response rate (44 versus 20 percent), and a greater likelihood of survival beyond one year (38 versus 5 percent).
However, this result may simply reflect the greater activity of cisplatin as compared to vinorelbine as a single agent rather than a synergistic effect of the combination. Toxicity, in particular nausea and vomiting, was greater in the cisplatin-containing arm.
* Other platinum-based regimens, such as cisplatin-mitoxantrone 26, cisplatin-5-FU 1, carboplatin-paclitaxel 27,28, and cisplatin-bleomycin with either methotrexate or doxorubicin 1,15,29,30 have been reported to lead to objective responses in trials of small numbers of patients, as have regimens that are anthracycline-based but non-platinum containing (show table 2) 15,29.
It is not clear that any of these regimens provides an advantage over single agent therapy or CAP.
Molecularly targeted therapy — The increasing understanding of the underlying molecular changes in MSGTs has led to the identification of several potential therapeutic targets. Although early results from phase II studies of such targeted therapies in MSGTs are interesting and encouraging, the data are too preliminary to recommend the routine use of any of these agents at present.
Imatinib — Approximately 80 percent of adenoid cystic carcinomas express the c-kit tyrosine kinase (TK) receptor 31, and there are individual case reports documenting objective responses with imatinib (Gleevec), an orally active potent inhibitor of the c-kit TK 32,33. However, there were no objective responses in three phase II trials in which a total of 32 patients with adenoid cystic carcinoma were treated with imatinib (400 mg twice daily) 34-36, nor in a fourth trial of lower dose therapy (400 mg daily) in an additional 10 patients 37. Further study is needed to clarify the role of imatinib in the treatment of adenoid cystic carcinoma.
Gefitinib — The epidermal growth factor receptor (EGFR) is often overexpressed in adenoid cystic and mucoepidermoid cancers. Unfortunately, no responses were documented among 29 patients with advanced MSGT (19 adenoid cystic cancers, 2 mucoepidermoid cancers) in a preliminary report of a phase II trial of gefitinib, an orally active EGFR TK inhibitor 34. Ten patients had disease stabilization, which was maintained for at least 16 weeks in five.
Cetuximab — Another method for targeting the EGFR is through anti-EGFR monoclonal antibodies such as cetuximab. In a preliminary report, cetuximab was evaluated in 30 patients (23 with adenoid cystic carcinoma). No objective responses were observed, although 20 of the patients with adenoid cystic carcinoma had disease stabilization for at least six months 38.
Trastuzumab — Up to one-third of mucoepidermoid carcinomas and an even higher proportion of salivary duct cancers overexpress HER2 protein, or have gene amplification as detected by fluorescence in situ hybridization 39-43. In contrast, expression of HER2 is unusual in adenoid cystic carcinomas and adenocarcinomas 40,44.
These findings have prompted exploration of therapies targeting HER2 in mucoepidermoid and salivary duct cancers. In a phase II trial of trastuzumab (Herceptin®), an anti-HER2 monoclonal antibody, one of three patients with mucoepidermoid cancer had a partial response lasting longer than two years, while two others with previously progressive salivary duct carcinomas had disease stabilization for 26 and 40 weeks, respectively 40,45. Further experience with this agent is needed.
Lapatinib — Lapatinib, an orally active dual inhibitor of the TKs of both EGFR and HER2, was studied in a phase II trial of 40 patients with progressive metastatic or recurrent EGFR and/or HER2-overexpressing SGT 46. Of the 19 assessable patients with ACC, there were no objective responses but 15 (79 percent) had stable disease, nine for six months or longer. Among the 17 assessable non-ACC patients, there were also no objective responses, but eight (47 percent) had stable disease, four for six months or longer.
Treatment was well tolerated, and the main toxicities were grade 1 to 2 diarrhea, fatigue, and skin rash.
Bortezomib — The proteasome-ubiquitin pathway is an essential intracellular system that degrades many labile proteins that regulate the cell cycle, apoptosis, transcription, cell adhesion, angiogenesis, and antigen presentation. The transcription factor NF-kappaB, which is expressed in some adenoid cystic cancers 47 and may be associated with an adverse prognosis, is activated only after the proteolysis of its inhibitor, IkappaB, in proteasomes. Thus, at least in theory, inhibition of the NF-kappa B pathway by proteasome inhibitors such as bortezomib (Velcade) may serve to inhibit the growth of adenoid cystic cancers.
In a preliminary report of a study of 25 patients with adenoid cystic carcinoma, there were no objective responses from bortezomib monotherapy, but many patients had disease stabilization, and the median progression-free survival was 8.4 months 48. However, as noted previously, it is difficult to know whether this result reflects antitumor activity or indolent natural history. (See "General treatment principles" above)."
Cited References:
7. Laurie, SA, Su, YB, Pfister, DG, et al. Chemotherapy in the management of metastatic adenoid cystic carcinoma: a systematic review (abstract). Proc Am Soc Clin Oncol 2005; 23:520s. (Abstract available online at www.asco.org/ac/1,1003,_12-002643-00_18-0034-00_19-0031092,00.asp, accessed January 24, 2007).
8. Gilbert, J, Li, Y, Pinto, HA, et al. Phase II trial of taxol in salivary gland malignancies (E1394): A trial of the Eastern Cooperative Oncology Group. Head Neck 2006; 28:197.
9. Licitra, L, Marchini, S, Spinazze, S, et al. Cisplatin in advanced salivary gland carcinoma. A phase II study of 25 patients. Cancer 1991; 68:1874.
10. Schramm, VL Jr, Srodes, C, Myers, EN. Cisplatin therapy for adenoid cystic carcinoma. Arch Otolaryngol 1981; 107:739.
11. Verweij, J, de Mulder, PH, de Graeff, A, et al. Phase II study on mitoxantrone in adenoid cystic carcinomas of the head and neck. EORTC Head and Neck Cancer Cooperative Group. Ann Oncol 1996; 7:867.
12. Vermorken, JB, Verweij, J, de Mulder, PH, et al. Epirubicin in patients with advanced or recurrent adenoid cystic carcinoma of the head and neck: a phase II study of the EORTC Head and Neck Cancer Cooperative Group. Ann Oncol 1993; 4:785.
13. Airoldi, M, Pedani, F, Succo, G, et al. Phase II randomized trial comparing vinorelbine versus vinorelbine plus cisplatin in patients with recurrent salivary gland malignancies. Cancer 2001; 91:541.
14. Dreyfuss AI, Clark JR, Fallon BG, Posner MR, Norris CJ, Miller D. Cyclophosphamide, doxorubicin, and cisplatin combination chemotherapy for advanced carcinomas of salivary gland origin. Cancer 1987; 60:2869.
15. Kaplan, MJ, Johns, ME, Cantrell, RW. Chemotherapy for salivary gland cancer. Otolaryngol Head Neck Surg 1986; 95:165.
16. Licitra, L, Cavina, R, Grandi, C et al. Cisplatin, doxorubicin and cyclophosphamide in advanced salivary gland carcinoma. A phase II trial of 22 patients. Ann Oncol 1996; 7:640.
17. Creagan, ET, Woods, JE, Rubin, J, Schaid, DJ. Cisplatin-based chemotherapy for neoplasms arising from salivary glands and contiguous structures in the head and neck. Cancer 1988; 62:2313.
18. Alberts, D, Manning, M, Couthard, S et al. Adriamycin/cisplatin/cyclophosphamide combination chemotherapy for advanced carcinoma of the parotid gland. Cancer 1981; 47:645.
19. Belani, CP, Eisenberger, MA, Gray, WC. Preliminary experience with chemotherapy in advanced salivary gland neoplasms. Med Pediatr Oncol 1988; 16:197.
20. Tsukuda, M, Kokatsu, T, Ito, K, et al. Chemotherapy for recurrent adeno- and adenoid cystic carcinomas in the head and neck. J Cancer Res Clin Oncol 1993; 119:756.
21. Dimery, I, Legha, S, Shirinian, M. Fluorouracil, doxorubicin, cyclophosphamide and cisplatin combination chemotherapy in advanced or recurrent salivary gland carcinoma. J Clin Oncol 1990; 8:1056.
22. Venook, AP, Tseng, A Jr, Meyers, FJ, et al. Cisplatin, doxorubicin, and 5-fluorouracil chemotherapy for salivary gland malignancies: a pilot study of the Northern California Oncology Group. J Clin Oncol 1987; 5:951.
23. Airoldi, M, Pedani, F, Brando, V, et al. Cisplatin, epirubicin and 5-fluorouracil combination chemotherapy for recurrent carcinoma of the salivary gland. Tumori 1989; 75:252.
24. White, JD, Junor, EJ, McGarva, J, et al. Adenocarcinoma of the salivary gland? A chemo-sensitive disease. Clin Oncol (R Coll Radiol) 2004; 16:159.
25. Farhat, F, Kattan, J, Culine, S, et al. of the combination of 5 fluorouracil, adriamycin and cisplatin (FAP protocol) in the treatment of metastatic cylindroma. Apropos of a case with review of the literature. Bull Cancer 1994; 81:47.
26. Gedlicka, C, Schull, B, Formanek, M, et al. Mitoxantrone and cisplatin in recurrent and/or metastatic salivary gland malignancies. Anticancer Drugs 2002; 13:491.
27. Airoldi, M, Fornari, G, Pedani, F, et al. Paclitaxel and carboplatin for recurrent salivary gland malignancies. Anticancer Res 2000; 20:3781.
28. Ruzich, JC, Ciesla, MC, Clark, JI. Response to paclitaxel and carboplatin in metastatic salivary gland cancer: a case report. Head Neck 2002; 24:406.
29. Posner, MR, Ervin, TJ, Weichselbaum, RR, et al. Chemotherapy of advanced salivary gland neoplasms. Cancer 1982; 50:2261.
30. de Haan, LD, De Mulder, PH, Vermorken, JB, et al. Cisplatin-based chemotherapy in advanced adenoid cystic carcinoma of the head and neck. Head Neck 1992; 14:273.
31. Mino, M, Pilch, BZ, Faquin, WC. Expression of KIT (CD117) in neoplasms of the head and neck: an ancillary marker for adenoid cystic carcinoma. Mod Pathol 2003; 16:1224.
32. Alcedo, JC, Fabrega, JM, Arosemena, JR, Urrutia, A. Imatinib mesylate as treatment for adenoid cystic carcinoma of the salivary glands: report of two successfully treated cases. Head Neck 2004; 26:829.
33. Faivre, S, Raymond, E, Casiraghi, O, et al. Imatinib mesylate can induce objective response in progressing, highly expressing KIT adenoid cystic carcinoma of the salivary glands. J Clin Oncol 2005; 23:6271.
34. Laurie, SA, Licitra, L. Systemic therapy in the palliative management of advanced salivary gland cancers. J Clin Oncol 2006; 24:2673.
35. Hotte, SJ, Winquist, EW, Lamont, E, et al. Imatinib Mesylate in Patients With Adenoid Cystic Cancers of the Salivary Glands Expressing c-kit: A Princess Margaret Hospital Phase II Consortium Study. J Clin Oncol 2005; 23:585.
36. Lin, CH, Yen, RF, Jeng, YM, et al. Unexpected rapid progression of metastatic adenoid cystic carcinoma during treatment with imatinib mesylate. Head Neck 2005; 27:1022.
37. Pfeffer, MR, Talmi, Y, Catane, R, et al. A phase II study of Imatinib for advanced adenoid cystic carcinoma of head and neck salivary glands. Oral Oncol 2007; 43:33.
38. Licitra, L, Locati, LD, Potepan, P, et al. Cetuximab (C225) in recurrent and/or metastatic salivary gland carcinomas (RMSGCs): a monoinstitutional phase II study (abstract). J Clin Oncol 2006; 24:291s. (Abstract available online at www.asco.org/ac/1,1003,_12-002643-00_18-0034-00_19-0031092,00.asp, accessed January 24, 2007).
39. Weed, DT, Gomez-Fernandez, C, Pacheco, J, et al. MUC4 and ERBB2 expression in major and minor salivary gland mucoepidermoid carcinoma. Head Neck 2004; 26:353.
40. Glisson, B, Colevas, AD, Haddad, R, et al. HER2 expression in salivary gland carcinomas: dependence on histological subtype. Clin Cancer Res 2004; 10:944.
41. Jaehne, M, Roeser, K, Jaekel, T, et al. Clinical and immunohistologic typing of salivary duct carcinoma: a report of 50 cases. Cancer 2005; 103:2526.
42. Press, MF, Pike, MC, Hung, G, et al. Amplification and overexpression of HER-2/neu in carcinomas of the salivary gland: correlation with poor prognosis. Cancer Res 1994; 54:5675.
43. Nabili, V, Tan, JW, Bhuta, S, et al. Salivary duct carcinoma: A clinical and histologic review with implications for trastuzumab therapy. Head Neck 2007; 29:907.
44. Dori, S, Vered, M, David, R, Buchner, A. HER2/neu expression in adenoid cystic carcinoma of salivary gland origin: an immunohistochemical study. J Oral Pathol Med 2002; 31:463.
45. Haddad, R, Colevas, AD, Krane, JF, et al. Herceptin in patients with advanced or metastatic salivary gland carcinomas. A phase II study. Oral Oncol 2003; 39:724.
46. Agulnik, M, Cohen, EW, Cohen, RB, et al. Phase II study of lapatinib in recurrent or metastatic epidermal growth factor receptor and/or erbB2 expressing adenoid cystic carcinoma and non adenoid cystic carcinoma malignant tumors of the salivary glands. J Clin Oncol 2007; 25:3978.
47. Zhang, J, Peng, B, Chen, X. Expressions of nuclear factor kappaB, inducible nitric oxide synthase, and vascular endothelial growth factor in adenoid cystic carcinoma of salivary glands: correlations with the angiogenesis and clinical outcome. Clin Cancer Res 2005; 11:7334.
source(s):
Laurie, Scott. Malignant salivary gland tumors: Treatment of metastatic disease. In: UpToDate, Basow, DS (Ed), UpToDate, Waltham, MA, 2008
MDConsult - http://www.utdol.com/online/content/topic.do?topicKey=head_can/16990 (here's the link - I'm pretty sure you won't be able to access it without a password - but go ahead and try it)
All references from the summary above are listed with the summary.
Laurie, Scott. Malignant salivary gland tumors: Treatment of metastatic disease. In: UpToDate, Basow, DS (Ed), UpToDate, Waltham, MA, 2008
MDConsult - http://www.utdol.com/online/content/topic.do?topicKey=head_can/16990 (here's the link - I'm pretty sure you won't be able to access it without a password - but go ahead and try it)
All references from the summary above are listed with the summary.
| Asker's rating: |
Thank you!
Table 2 that is referenced often - could not be copy/pasted into Mahalo Answers. If you would like me to email it to you, I will. You can click on my name and then "ask a question" to me "privately" giving me your email address.
Tip lindseylgreene for this comment
|
Report
Note: I have no professional medical training or experience. The information given here is abstracted from the sources mentioned with it.
Its very sad to know about your sister may God bless her and give you power to fight it.
Case Studies (Individuals):
1. We report on a 45-year-old patient with stage IIIc ovarian cancer, multiple brain metastases, and meningitis carcinomatosa. After three courses of initial chemotherapy, consisting of docetaxel and carboplatin, the patient underwent interval cytoreductive surgery, consisting of hyster-ectomy, bilateral salpingo-oophorectomy, omentectomy, appendectomy, and retroperitoneal lymphadenectomy. Then five courses of the same chemotherapy were given as adjuvant treatment. At the completion of the primary therapy, she achieved a complete remission. Ten months after the completion of the initial treatment, multiple brain metastases with meningitis carcinomatosa were detected. After four courses of the same chemotherapy, she again had a complete response, confirmed by cranial enhanced magnetic resonance imaging (MRI), and she felt well, with relief from the debilitating neurologic symptoms for 4 months. After this 4 months, her disease recurred, with meningitis carcinomatosa, and she requested supportive care only. She died 4 months after this recurrence. Chemotherapy can help to prolong life for some patients with multiple brain metastases and meningitis carcinomatosa from ovarian cancer.
http://www.springerlink.com/content/cx7w0vg64jry5165/
2. Cetuximab in the treatment of metastatic mucoepidermoid carcinoma of the salivary glands: A case report and review of literature. http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2570365
3. Response to paclitaxel in adenoid cystic carcinoma of the salivary glands. http://www3.interscience.wiley.com/journal/116837949/abstract
4. The UK incidence of malignant disease of the minor salivary glands is only 0.6 per million per year. The tumours have a varied histology, can present in any age group and are frequently advanced if located in the sinonasal cavities. In a 20-year review of 21 patients treated for minor salivary gland malignancy in a single institution, it was found that mucoepidermoid tumours were more common in the oral cavity and adenoid cystic carcinomas in the sinonasal tract (p=0.002). Outcome was variable with sinonasal and adenoid cystic carcinoma having a poorer outcome. Kaplan–Meier curves showed that oral tumours had a higher probability of long term survival. Radical surgery with reconstruction and post-operative adjuvant radiotherapy was effective in achieving loco-regional control. There were no local recurrences within 5 years and three after 5 years. Five patients developed metastatic disease within 10 years and a further two after 10 years. Late recurrences occurred and survival was mainly determined by the presence of systemic disease.
http://linkinghub.elsevier.com/retrieve/pii/S0007122604001195
Its very sad to know about your sister may God bless her and give you power to fight it.
Case Studies (Individuals):
1. We report on a 45-year-old patient with stage IIIc ovarian cancer, multiple brain metastases, and meningitis carcinomatosa. After three courses of initial chemotherapy, consisting of docetaxel and carboplatin, the patient underwent interval cytoreductive surgery, consisting of hyster-ectomy, bilateral salpingo-oophorectomy, omentectomy, appendectomy, and retroperitoneal lymphadenectomy. Then five courses of the same chemotherapy were given as adjuvant treatment. At the completion of the primary therapy, she achieved a complete remission. Ten months after the completion of the initial treatment, multiple brain metastases with meningitis carcinomatosa were detected. After four courses of the same chemotherapy, she again had a complete response, confirmed by cranial enhanced magnetic resonance imaging (MRI), and she felt well, with relief from the debilitating neurologic symptoms for 4 months. After this 4 months, her disease recurred, with meningitis carcinomatosa, and she requested supportive care only. She died 4 months after this recurrence. Chemotherapy can help to prolong life for some patients with multiple brain metastases and meningitis carcinomatosa from ovarian cancer.
http://www.springerlink.com/content/cx7w0vg64jry5165/
2. Cetuximab in the treatment of metastatic mucoepidermoid carcinoma of the salivary glands: A case report and review of literature. http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2570365
3. Response to paclitaxel in adenoid cystic carcinoma of the salivary glands. http://www3.interscience.wiley.com/journal/116837949/abstract
4. The UK incidence of malignant disease of the minor salivary glands is only 0.6 per million per year. The tumours have a varied histology, can present in any age group and are frequently advanced if located in the sinonasal cavities. In a 20-year review of 21 patients treated for minor salivary gland malignancy in a single institution, it was found that mucoepidermoid tumours were more common in the oral cavity and adenoid cystic carcinomas in the sinonasal tract (p=0.002). Outcome was variable with sinonasal and adenoid cystic carcinoma having a poorer outcome. Kaplan–Meier curves showed that oral tumours had a higher probability of long term survival. Radical surgery with reconstruction and post-operative adjuvant radiotherapy was effective in achieving loco-regional control. There were no local recurrences within 5 years and three after 5 years. Five patients developed metastatic disease within 10 years and a further two after 10 years. Late recurrences occurred and survival was mainly determined by the presence of systemic disease.
http://linkinghub.elsevier.com/retrieve/pii/S0007122604001195
voted helpful: lwelch, lindseylgreene
I am Not an MD, This is not medical advice, for information only.
Sorry to hear about your sister's illness, sending positive energy your way, good luck to both of you.
There are 4 types of brain tumors, treatment and outcome depend upon type and stage:
This information below is quoted from the M. D. Anderson Cancer Center in Houston, Texas web site. MD Anderson was recently rated as the number one hospital of choice for cancer treatment by physicians.
"Types of Brain Tumors
There are many different types of brain tumors, based on what cells are affected and how they appear under a microscope. Tumors can be classified into four general categories:
Gliomas (7 types of gliomas)
These tumors occur in the glial cells, which help support and protect critical areas of the brain. Gliomas are the most common type of brain tumor in adults, responsible for about 42% of all adult brain tumors. Gliomas are further characterized by the types of cells they affect:
Astrocytoma
Astrocytes are star-shaped cells that protect neurons. Tumors of these cells can spread from the primary site to other areas of the brain, but rarely spread outside the central nervous system. Astrocytomas are graded from I to IV depending on the speed of progression:
Grade I (pilocytic astrocytoma): slow growing, with little tendency to infiltrate surrounding brain tissue. Most common in children and adolescents.
Grade II (diffuse astrocytoma): fairly slow-growing, with some tendency to infiltrate surrounding brain tissue. Mostly seen in young adults.
Grade III (anaplastic/malignant astrocytoma): these tumors grow rather quickly and infiltrate surrounding brain tissue.
Grade IV (glioblastoma multiforme, GBM): an extremely aggressive and lethal form of brain cancer. Unfortunately, it is the most common form of brain tumor in adults, accounting for 67% of all astrocytomas.
Oligodendroglioma
Oligodendrocytes are cells that make myelin, a fatty substance that forms a protective sheath around nerve cells. Oligodendrogliomas, which make up 4% of brain tumors, mostly affect people over 45 years of age. Some subtypes of this tumor are particularly sensitive to treatment with radiation therapy and chemotherapy. Half of patients with oligodendrogliomas are still alive after five years.
Ependymoma
These tumors affect ependymal cells, which line the pathways that carry cerebrospinal fluid throughout the brain and spinal cord. Ependymomas are rare; about 2% of all brain tumors, but are the most common brain tumor in children. They generally don’t affect healthy brain tissue and don’t spread beyond the ependyma. Although these tumors respond well to surgery, particularly those on the spine, ependymomas cannot always be completely removed. The five-year survival rate for patients over age 45 approaches 70%.
2. Meningiomas
These tumors affect the meninges, the tissue that forms the protective outer covering of the brain and spine. One-quarter of all brain and spinal tumors are meningiomas, and up to 85% of them are benign. Meningiomas can occur at any age, but the incidence increases significantly in people over age 65. Women are twice as likely as men to have meningiomas. They generally grow very slowly and often don’t produce any symptoms. In fact, many meningiomas are discovered by accident. Meningiomas can be successfully treated with surgery, but some patients, particularly the elderly, may be candidates for watchful waiting to monitor the disease.
3. Acoustic Neuroma / Schwannomas
Schwann’s cells are found in the sheath that covers nerve cells. Vestibular schwannomas, also known as acoustic neuromas, arise from the 8th cranial nerve, which is responsible for hearing. Specific symptoms of vestibular schwannoma include buzzing or ringing in the ears, one-sided hearing loss and/or balance problems. Schwannomas are typically benign and respond well to surgery.
4. Medulloblastoma
Medulloblastoma is a common brain tumor in children, usually diagnosed before the age of 10. These tumors occur in the cerebellum, which has a crucial role in coordinating muscular movements. Some experts believe that medulloblastomas arise from fetal cells that remain in the cerebellum after birth. Tumors grow quickly and can invade neighboring portions of the brain, as well as spreading outside the central nervous system. Medulloblastoma is slightly more common in boys. Read more about pediatric medulloblastoma."
Additional information:
In a very recent article Acta Oncologica; Jan2009, Vol. 48 Issue 1, p132-136, 5p, 2 charts
Title:Carcinoma ex pleomorphic adenoma of the parotid gland. Study and implications for diagnostics and therapy.
Authors:
Lüers, Jan-Christoffer1 jan-christoffer.lueers@uk-koeln.de
Wittekindt, Claus2
Streppel, M.1
Guntinas-Lichius, Orlando2
They have investigated various therapies and found patients with Stage I tumors, not surprisingly, did much better long term then those with Stage IV tumors. This article did not specifically address metathesis. From the abstract: "Conclusion. Surgical therapy (total or radical parotidectomy) is the method of choice for CXPA of the parotid gland. Stage I tumors have a very good and stage IV tumors a bad prognosis."
Here is another citation that may be helpful:
Chen AM, Garcia J, Bucci MK, Quivey JM, Eisele DW. Recurrent pleomorphic edenoma of the parotid gland: Long-term outcome of patients treated with radiation therapy. Int J Radiat Oncol Biol Phys 66(4):1031-5, 2006.
Abstract.
Purpose: To evaluate the role of radiation therapy in the management of recurrent pleomorphic adenoma of the
parotid gland.
Methods and Materials: Between 1960 and 2004, 34 patients were treated with postoperative radiation therapy
for recurrent pleomorphic adenoma of the parotid gland to a median dose of 5000 cGy (range, 4,500–6,000 cGy).
Median age was 48 years (range, 24–72 years). Gross total resection at the time of surgery before radiation was
achieved in 30 patients (88%), and histologic analysis demonstrated multifocal disease in 16 patients (47%).
Radiation was delivered for a first, second, third, fourth, fifth, and sixth local recurrence in 24%, 21%, 24%,
24%, 6%, and 3% of patients, respectively.
Results: With a median follow-up of 17.4 years (range, 2.3–28.9 years), 2 patients had local recurrences at a
median of 3.4 years after completion of radiation. The 20-year actuarial local control rate was 94%. One patient
developed a second malignancy at approximately 14 years after completion of therapy.
Conclusion: The use of postoperative radiation therapy leads to excellent long-term local control for the
treatment of recurrent pleomorphic adenoma with acceptable late toxicity. Although the incidence of second
malignancy was low in this population, continued follow-up is warranted. © 2006 Elsevier Inc.
Sorry to hear about your sister's illness, sending positive energy your way, good luck to both of you.
There are 4 types of brain tumors, treatment and outcome depend upon type and stage:
This information below is quoted from the M. D. Anderson Cancer Center in Houston, Texas web site. MD Anderson was recently rated as the number one hospital of choice for cancer treatment by physicians.
"Types of Brain Tumors
There are many different types of brain tumors, based on what cells are affected and how they appear under a microscope. Tumors can be classified into four general categories:
Gliomas (7 types of gliomas)
These tumors occur in the glial cells, which help support and protect critical areas of the brain. Gliomas are the most common type of brain tumor in adults, responsible for about 42% of all adult brain tumors. Gliomas are further characterized by the types of cells they affect:
Astrocytoma
Astrocytes are star-shaped cells that protect neurons. Tumors of these cells can spread from the primary site to other areas of the brain, but rarely spread outside the central nervous system. Astrocytomas are graded from I to IV depending on the speed of progression:
Grade I (pilocytic astrocytoma): slow growing, with little tendency to infiltrate surrounding brain tissue. Most common in children and adolescents.
Grade II (diffuse astrocytoma): fairly slow-growing, with some tendency to infiltrate surrounding brain tissue. Mostly seen in young adults.
Grade III (anaplastic/malignant astrocytoma): these tumors grow rather quickly and infiltrate surrounding brain tissue.
Grade IV (glioblastoma multiforme, GBM): an extremely aggressive and lethal form of brain cancer. Unfortunately, it is the most common form of brain tumor in adults, accounting for 67% of all astrocytomas.
Oligodendroglioma
Oligodendrocytes are cells that make myelin, a fatty substance that forms a protective sheath around nerve cells. Oligodendrogliomas, which make up 4% of brain tumors, mostly affect people over 45 years of age. Some subtypes of this tumor are particularly sensitive to treatment with radiation therapy and chemotherapy. Half of patients with oligodendrogliomas are still alive after five years.
Ependymoma
These tumors affect ependymal cells, which line the pathways that carry cerebrospinal fluid throughout the brain and spinal cord. Ependymomas are rare; about 2% of all brain tumors, but are the most common brain tumor in children. They generally don’t affect healthy brain tissue and don’t spread beyond the ependyma. Although these tumors respond well to surgery, particularly those on the spine, ependymomas cannot always be completely removed. The five-year survival rate for patients over age 45 approaches 70%.
2. Meningiomas
These tumors affect the meninges, the tissue that forms the protective outer covering of the brain and spine. One-quarter of all brain and spinal tumors are meningiomas, and up to 85% of them are benign. Meningiomas can occur at any age, but the incidence increases significantly in people over age 65. Women are twice as likely as men to have meningiomas. They generally grow very slowly and often don’t produce any symptoms. In fact, many meningiomas are discovered by accident. Meningiomas can be successfully treated with surgery, but some patients, particularly the elderly, may be candidates for watchful waiting to monitor the disease.
3. Acoustic Neuroma / Schwannomas
Schwann’s cells are found in the sheath that covers nerve cells. Vestibular schwannomas, also known as acoustic neuromas, arise from the 8th cranial nerve, which is responsible for hearing. Specific symptoms of vestibular schwannoma include buzzing or ringing in the ears, one-sided hearing loss and/or balance problems. Schwannomas are typically benign and respond well to surgery.
4. Medulloblastoma
Medulloblastoma is a common brain tumor in children, usually diagnosed before the age of 10. These tumors occur in the cerebellum, which has a crucial role in coordinating muscular movements. Some experts believe that medulloblastomas arise from fetal cells that remain in the cerebellum after birth. Tumors grow quickly and can invade neighboring portions of the brain, as well as spreading outside the central nervous system. Medulloblastoma is slightly more common in boys. Read more about pediatric medulloblastoma."
Additional information:
In a very recent article Acta Oncologica; Jan2009, Vol. 48 Issue 1, p132-136, 5p, 2 charts
Title:Carcinoma ex pleomorphic adenoma of the parotid gland. Study and implications for diagnostics and therapy.
Authors:
Lüers, Jan-Christoffer1 jan-christoffer.lueers@uk-koeln.de
Wittekindt, Claus2
Streppel, M.1
Guntinas-Lichius, Orlando2
They have investigated various therapies and found patients with Stage I tumors, not surprisingly, did much better long term then those with Stage IV tumors. This article did not specifically address metathesis. From the abstract: "Conclusion. Surgical therapy (total or radical parotidectomy) is the method of choice for CXPA of the parotid gland. Stage I tumors have a very good and stage IV tumors a bad prognosis."
Here is another citation that may be helpful:
Chen AM, Garcia J, Bucci MK, Quivey JM, Eisele DW. Recurrent pleomorphic edenoma of the parotid gland: Long-term outcome of patients treated with radiation therapy. Int J Radiat Oncol Biol Phys 66(4):1031-5, 2006.
Abstract.
Purpose: To evaluate the role of radiation therapy in the management of recurrent pleomorphic adenoma of the
parotid gland.
Methods and Materials: Between 1960 and 2004, 34 patients were treated with postoperative radiation therapy
for recurrent pleomorphic adenoma of the parotid gland to a median dose of 5000 cGy (range, 4,500–6,000 cGy).
Median age was 48 years (range, 24–72 years). Gross total resection at the time of surgery before radiation was
achieved in 30 patients (88%), and histologic analysis demonstrated multifocal disease in 16 patients (47%).
Radiation was delivered for a first, second, third, fourth, fifth, and sixth local recurrence in 24%, 21%, 24%,
24%, 6%, and 3% of patients, respectively.
Results: With a median follow-up of 17.4 years (range, 2.3–28.9 years), 2 patients had local recurrences at a
median of 3.4 years after completion of radiation. The 20-year actuarial local control rate was 94%. One patient
developed a second malignancy at approximately 14 years after completion of therapy.
Conclusion: The use of postoperative radiation therapy leads to excellent long-term local control for the
treatment of recurrent pleomorphic adenoma with acceptable late toxicity. Although the incidence of second
malignancy was low in this population, continued follow-up is warranted. © 2006 Elsevier Inc.
Statistically, chemotherapy does not work. I would only use it as a last resort. If you try alternative therapies first, chemotherapy is always an option later. But if you start with chemotherapy, it will destroy the immune system and make alternative treatments impossible later. Remember that cancer indicates a problem with the immune system and chemotherapy destroys cancer cells, but it also destroys cancer-fighting cells too. I have had three family members go through chemotherapy for cancer and only one is still alive, but that is because surgery removed the tumor, not chemo.
Related questions
140 characters left
ask any question
