Questions on Erbitux
Questions on Erbitux
Just found out that my colon cancer (stage IV - peritoneal mets) was the "wild" type genetically.... I started Erbitux about a month and a half ago.... I have broken out with the worst acne of my life.... Now I am 43 and I am not complaining, especially since fulfori whipped my butt for almost a year... I am now on folfox, avastin, and erbitux..... My onc says the acne is a good sign - it means the erbitux is helping, but my understanding of this drug is that it keeps the cancer from getting worse and has no killing abilities.... I am on tetracycline and am going to pick up some clindamycin ointment prescribed by the onc now.... My question is what were your side effects (if any) on erbitux, what you did for it, how long it lasted and did it help you in your battle with colon cancer..... Thanks in advance!!!! trudi
Diagnosed April Fool's Day 2008 with Grade 4 mucinous adenocarcinoma of the sigmoid colon with peritoneal mets
4/23/08 colon resection
May 08 - folfiri
Nov 08 - irinotecan and avastin
April 09 - changed to folfox, erbitux, and avastin
CTC currently 0
4/23/08 colon resection
May 08 - folfiri
Nov 08 - irinotecan and avastin
April 09 - changed to folfox, erbitux, and avastin
CTC currently 0
-
Guest
Re: Questions on Erbitux
Hi,
I'm not on erbitux so I can't offer any personal insight but I did find this article that might answer some of your questions:
Erbitux Offers 'cure' Potential To 3 Out Of 4 Advanced Colon Cancer Patients - But Conditions Apply http://www.medicalnewstoday.com/articles/122267.php
Researchers have narrowed down the conditions in metastatic colorectal cancer (mCRC) where treatment with the targeted biologic therapy Erbitux (cetuximab) is most likely to succeed. Results from two studies presented this month at the European Society for Medical Oncology (ESMO) congress in Stockholm, Sweden, showed that patients with a specific but common genetic make-up in their tumours, and whose cancer-spread was confined to the liver, have a greater than 75 per cent chance of going on to potentially curative surgery. If secondary tumours shrink sufficiently with therapy they can be removed surgically; and when a surgeon is able to remove all traces of tumours - by no means an easy feat to accomplish - patients are technically cured and go on to live many years. Oncologists use the term 'cure' reservedly knowing cancers can sometimes recur years later but historically, at least one in five patients who has had all their cancer removed is still alive well after 10 years.
Colorectal cancer tumours that express the KRAS gene in a natural or 'wild-type' state showed a high response to Erbitux and chemotherapy in the two studies at ESMO but a lower response to chemotherapy alone. Patients whose tumours have a mutated version of the KRAS gene derived no additional benefit from adding Erbitux to their chemotherapy regimen.
Within the last few years, scientists have discovered that KRAS genes influence a protein that plays a role in cancer cell growth and proliferation. The wild-type KRAS gene is activated by growth factors that bind to the epidermal growth factor receptor (EGFR) on the surface of tumour cells. When EGFR inhibitors like Erbitux block the receptors, wild-type KRAS gene activity is turned off. But mutant KRAS genes are persistently in an activated form and so cannot be "turned off" by EGFR inhibitors. As a result, they carry on stimulating cancer growth regardless because they do not need the EGFR to dictate their activity. Tumours with mutant KRAS genes may not respond to Erbitux but they are still receptive to chemotherapy and research is in progress to develop drugs which will boost the efficacy of chemotherapy for these tumour types.
CRYSTAL clear findings
New data were presented at ESMO from the large randomised phase III trial CRYSTAL where first-line therapy with Erbitux and FOLFIRI chemotherapy was compared against FOLFIRI alone in 1198 patients with mCRC. The trial originally took no account of whether or not patients' tumours had wild-type or mutant KRAS genes. Now the researchers have gone back to analyse tumour samples and have been able to see that roughly two thirds had wild-type, and one third, mutant KRAS genes. By comparing the treatment outcomes of patients with wild-type KRAS against those with mutant KRAS, they have been able to gauge just how important the KRAS factor is.
Those with the wild-type KRAS gene, who received additional Erbitux with their chemotherapy, were more likely to respond well, were less likely to see their cancer get worse, and were more often able to undergo complete surgical removal of their metastases than people who did not receive the drug. As a group they lived longer than people who did not add Erbitux to chemotherapy. People with the mutant KRAS gene did less well regardless of whether they received Erbitux with their chemotherapy or not.
In the CRYSTAL trial, 540 (45%) of the original 1198 people participating had tumour tissue samples that could be evaluated for KRAS status. Two thirds of these, 346 (65%), had KRAS wild-type genes and one third (35%), mutant KRAS. Of patients with the mutant KRAS gene 40% responded to FOLFIRI chemotherapy treatment, ie, their tumours shrank, but adding Erbitux did not increase the response rate. Of the patients with wild-type KRAS, however, 59% responded to Erbitux and FOLFIRI overall compared to 43% who received FOLFIRI alone. More impressively, of those with wild-type KRAS and tumours confined to the liver, 77% had a response to Erbitux and FOLFIRI, compared to 50% who responded to FOLFIRI alone. Lead investigator Professor Eric Van Cutsem of Gasthuisberg University Hospital, Leuven, Belgium said: "This is a very high response and is potentially important because it means 3 out of 4 people might be able to shrink their tumours sufficiently for them to be resected (surgically removed) and for some this can lead to cure."
At one year 43% of patients with the wild-type KRAS gene had kept their disease in check using the combined treatment compared to 25% with chemotherapy alone. Overall survival data from the CRYSTAL study showed more than half of patients (51%) with wild-type KRAS were still alive after two years if they received Erbitux and chemotherapy compared to 41% of those getting chemotherapy alone. Median overall survival in wild-type KRAS patients was 24.9 months for the Erbitux and chemotherapy group but only 21 months for patients receiving chemotherapy alone. By the time this analysis was done some of the patients in the chemotherapy alone group had been given Erbitux after their disease worsened. This was likely to improve their survival time. The overall median survival of patients with the mutant KRAS gene was below 18 months irrespective of whether they received Erbitux or not.
CELIM focused on liver metastases
The second study at ESMO was CELIM, a phase II study of 111 patients with mCRC who had either large secondary liver tumours or five or more liver tumours that were initially inoperable. In this study all patients received first-line Erbitux but were randomised to receive one of two different chemotherapy regimens in addition - FOLFOX6 or FOLFIRI - both of which proved very effective, according to the investigators. When these patients' tumours were analysed for KRAS gene status, 70% were found to have the wild-type KRAS.
Interim results of CELIM were presented at ESMO by lead investigator Dr Gunnar Folprecht of University Hospital Carl Gustav Carus, Dresden, Germany. Overall, 75% of patients responded to treatment and 42% shrank their tumours sufficiently to undergo surgery, he reported. Of these 35% were left with no residual cancer. In the patients with wild-type KRAS, 79% responded to treatment, 43% were able to undergo surgery and 34% had all traces of cancer removed. "The especially interesting findings of this study were the very high response rates, the good outcome in terms of resectability and the short time it took before patients were able to undergo surgery," he commented. Patients had only 8 cycles of therapy before being evaluated for surgery. If their tumours had not shrunk sufficiently they continued on treatment. But most patients needed only 8 cycles of treatment before they were ready for surgery and the usual time to operation was only five months, he noted.
"I believe these data together with the CRYSTAL data show that Erbitux and one standard chemotherapy provide probably the best option for mCRC where tumours show wild-type KRAS," he concluded.
The growing evidence about the impact of KRAS gene type on the success of Erbitux - shown also in other studies this year such as OPUS and EVEREST - is leading increasingly to a consensus among oncologists that all patients being considered for treatment with EGFR-targeting drugs like Erbitux should first be tested to see whether or not they have the wild-type or mutant KRAS gene. If the mutant KRAS gene is detected, they believe there is no point in these drugs, which are expensive, being prescribed. Although patients tolerate Erbitux well it produces a skin rash and can cause diarrhoea in some. In some European countries, reimbursement for Erbitux treatment is now restricted to use in patients with wild-type KRAS. Diagnostic tests for KRAS are becoming widely available in Europe, according to Professor Van Cutsem, who believes most oncologists should have access to them before the end of the year. "We are truly entering an era of personalised medicine in cancer therapy where treatment is tailored to the individual," he added.
Meanwhile the search goes on for other tumour biomarkers to predict even more accurately what impact a treatment is likely to have. This is happening not just in mCRC but in cancers at other sites, to help identify which treatments work best for particular tumour types. Getting the treatment that is right for them first will give cancer patients the best chance of beating their disease.
hwww.erbitux-international.com
I'm not on erbitux so I can't offer any personal insight but I did find this article that might answer some of your questions:
Erbitux Offers 'cure' Potential To 3 Out Of 4 Advanced Colon Cancer Patients - But Conditions Apply http://www.medicalnewstoday.com/articles/122267.php
Researchers have narrowed down the conditions in metastatic colorectal cancer (mCRC) where treatment with the targeted biologic therapy Erbitux (cetuximab) is most likely to succeed. Results from two studies presented this month at the European Society for Medical Oncology (ESMO) congress in Stockholm, Sweden, showed that patients with a specific but common genetic make-up in their tumours, and whose cancer-spread was confined to the liver, have a greater than 75 per cent chance of going on to potentially curative surgery. If secondary tumours shrink sufficiently with therapy they can be removed surgically; and when a surgeon is able to remove all traces of tumours - by no means an easy feat to accomplish - patients are technically cured and go on to live many years. Oncologists use the term 'cure' reservedly knowing cancers can sometimes recur years later but historically, at least one in five patients who has had all their cancer removed is still alive well after 10 years.
Colorectal cancer tumours that express the KRAS gene in a natural or 'wild-type' state showed a high response to Erbitux and chemotherapy in the two studies at ESMO but a lower response to chemotherapy alone. Patients whose tumours have a mutated version of the KRAS gene derived no additional benefit from adding Erbitux to their chemotherapy regimen.
Within the last few years, scientists have discovered that KRAS genes influence a protein that plays a role in cancer cell growth and proliferation. The wild-type KRAS gene is activated by growth factors that bind to the epidermal growth factor receptor (EGFR) on the surface of tumour cells. When EGFR inhibitors like Erbitux block the receptors, wild-type KRAS gene activity is turned off. But mutant KRAS genes are persistently in an activated form and so cannot be "turned off" by EGFR inhibitors. As a result, they carry on stimulating cancer growth regardless because they do not need the EGFR to dictate their activity. Tumours with mutant KRAS genes may not respond to Erbitux but they are still receptive to chemotherapy and research is in progress to develop drugs which will boost the efficacy of chemotherapy for these tumour types.
CRYSTAL clear findings
New data were presented at ESMO from the large randomised phase III trial CRYSTAL where first-line therapy with Erbitux and FOLFIRI chemotherapy was compared against FOLFIRI alone in 1198 patients with mCRC. The trial originally took no account of whether or not patients' tumours had wild-type or mutant KRAS genes. Now the researchers have gone back to analyse tumour samples and have been able to see that roughly two thirds had wild-type, and one third, mutant KRAS genes. By comparing the treatment outcomes of patients with wild-type KRAS against those with mutant KRAS, they have been able to gauge just how important the KRAS factor is.
Those with the wild-type KRAS gene, who received additional Erbitux with their chemotherapy, were more likely to respond well, were less likely to see their cancer get worse, and were more often able to undergo complete surgical removal of their metastases than people who did not receive the drug. As a group they lived longer than people who did not add Erbitux to chemotherapy. People with the mutant KRAS gene did less well regardless of whether they received Erbitux with their chemotherapy or not.
In the CRYSTAL trial, 540 (45%) of the original 1198 people participating had tumour tissue samples that could be evaluated for KRAS status. Two thirds of these, 346 (65%), had KRAS wild-type genes and one third (35%), mutant KRAS. Of patients with the mutant KRAS gene 40% responded to FOLFIRI chemotherapy treatment, ie, their tumours shrank, but adding Erbitux did not increase the response rate. Of the patients with wild-type KRAS, however, 59% responded to Erbitux and FOLFIRI overall compared to 43% who received FOLFIRI alone. More impressively, of those with wild-type KRAS and tumours confined to the liver, 77% had a response to Erbitux and FOLFIRI, compared to 50% who responded to FOLFIRI alone. Lead investigator Professor Eric Van Cutsem of Gasthuisberg University Hospital, Leuven, Belgium said: "This is a very high response and is potentially important because it means 3 out of 4 people might be able to shrink their tumours sufficiently for them to be resected (surgically removed) and for some this can lead to cure."
At one year 43% of patients with the wild-type KRAS gene had kept their disease in check using the combined treatment compared to 25% with chemotherapy alone. Overall survival data from the CRYSTAL study showed more than half of patients (51%) with wild-type KRAS were still alive after two years if they received Erbitux and chemotherapy compared to 41% of those getting chemotherapy alone. Median overall survival in wild-type KRAS patients was 24.9 months for the Erbitux and chemotherapy group but only 21 months for patients receiving chemotherapy alone. By the time this analysis was done some of the patients in the chemotherapy alone group had been given Erbitux after their disease worsened. This was likely to improve their survival time. The overall median survival of patients with the mutant KRAS gene was below 18 months irrespective of whether they received Erbitux or not.
CELIM focused on liver metastases
The second study at ESMO was CELIM, a phase II study of 111 patients with mCRC who had either large secondary liver tumours or five or more liver tumours that were initially inoperable. In this study all patients received first-line Erbitux but were randomised to receive one of two different chemotherapy regimens in addition - FOLFOX6 or FOLFIRI - both of which proved very effective, according to the investigators. When these patients' tumours were analysed for KRAS gene status, 70% were found to have the wild-type KRAS.
Interim results of CELIM were presented at ESMO by lead investigator Dr Gunnar Folprecht of University Hospital Carl Gustav Carus, Dresden, Germany. Overall, 75% of patients responded to treatment and 42% shrank their tumours sufficiently to undergo surgery, he reported. Of these 35% were left with no residual cancer. In the patients with wild-type KRAS, 79% responded to treatment, 43% were able to undergo surgery and 34% had all traces of cancer removed. "The especially interesting findings of this study were the very high response rates, the good outcome in terms of resectability and the short time it took before patients were able to undergo surgery," he commented. Patients had only 8 cycles of therapy before being evaluated for surgery. If their tumours had not shrunk sufficiently they continued on treatment. But most patients needed only 8 cycles of treatment before they were ready for surgery and the usual time to operation was only five months, he noted.
"I believe these data together with the CRYSTAL data show that Erbitux and one standard chemotherapy provide probably the best option for mCRC where tumours show wild-type KRAS," he concluded.
The growing evidence about the impact of KRAS gene type on the success of Erbitux - shown also in other studies this year such as OPUS and EVEREST - is leading increasingly to a consensus among oncologists that all patients being considered for treatment with EGFR-targeting drugs like Erbitux should first be tested to see whether or not they have the wild-type or mutant KRAS gene. If the mutant KRAS gene is detected, they believe there is no point in these drugs, which are expensive, being prescribed. Although patients tolerate Erbitux well it produces a skin rash and can cause diarrhoea in some. In some European countries, reimbursement for Erbitux treatment is now restricted to use in patients with wild-type KRAS. Diagnostic tests for KRAS are becoming widely available in Europe, according to Professor Van Cutsem, who believes most oncologists should have access to them before the end of the year. "We are truly entering an era of personalised medicine in cancer therapy where treatment is tailored to the individual," he added.
Meanwhile the search goes on for other tumour biomarkers to predict even more accurately what impact a treatment is likely to have. This is happening not just in mCRC but in cancers at other sites, to help identify which treatments work best for particular tumour types. Getting the treatment that is right for them first will give cancer patients the best chance of beating their disease.
hwww.erbitux-international.com
-
Guest
Re: Questions on Erbitux
ps I note you say you are on both Avastin and Erbitux - there have been some findings recently that these two drugs aren't as effective when used together:
Erbitux®/Avastin® Combo Not Effective in Colorectal Cancer http://professional.cancerconsultants.c ... x?id=42262
Researchers affiliated with the CAIRO2 trial reported that the addition of Erbitux® (cetuximab) to Avastin® (bevacizumab), Eloxatin® (oxaliplatin), and Xeloda® (capecitabine) did not provide a clinical benefit and actually reduced progression-free survival in metastatic colorectal cancer. These findings are consistent with results from other trials indicating that the combination of agents targeting the epidermal growth factor receptor (EGFR) and the vascular endothelial growth factor receptor (VEGF) pathways does not provide clinical benefit. These results were recently presented as a late-breaking abstract at the 2008 annual meeting of the American Society of Clinical Oncology (ASCO) in Chicago, Illinois.
Researchers have been hopeful that combining biologic therapies that target different pathways may provide additional benefit for the treatment of various cancers. Because Erbitux and Vectibix target the epidermal growth factor receptor (EGFR) pathway and Avastin targets the vascular endothelial growth factor (VEGF) pathway, and because synergistic activity between the two agents has been noted in laboratory studies, researchers speculated that a combination of the two agents may provide more anticancer activity than either agent used alone in combination with chemotherapy. However, there have been conflicting results regarding the efficacy of the combination of these two targeted agents in colorectal cancer.
The CAIRO2 study was a Phase III trial that was conducted to further evaluate the addition of Erbitux to Avastin-containing regimens in colorectal cancer. The trial, which was conducted by the Dutch Colorectal Cancer Group (DCCG), included 79 Dutch hospitals and 736 patients with metastatic colorectal cancer.1 Patients were ineligible for surgical resection and had not received prior therapy for metastatic disease. The primary endpoint was progression-free survival, with secondary endpoints being overall survival, response rates, toxicity, and translational outcomes.
Patients were randomized to either the control group—which received six cycles of Eloxatin (oxaliplatin, 130 mg/m2 on day one), Xeloda (capecitabine, 1,000 mg/m2 twice daily on days one to 14), and Avastin (7.5 mg/kg on day one), with further cycles including Xeloda (1,250 mg/m2 twice daily on days one to 14) and Avastin (7.5 mg/kg on day one)—or to the group that received the addition of Erbitux (weekly in a 400 mg/m2 loading dose and 250 mg/m2 thereafter) plus the control group regimen. Follow-up was nearly 19 months.
There was no benefit derived among any endpoint for patients treated with the addition of Erbitux; in fact, progression-free survival was significantly reduced among patients treated with Erbitux (9.6 months versus 10.7 months, HR for progression 1.21, P=0.018).
Overall survival was similar between the two groups at approximately 20 months (P=0.21).
Both groups achieved a 44% combined complete and partial response rate (P=0.88).
There was no significant difference between treatment groups in terms of disease stabilization.
Even when KRAS status and the presence of grade 3 rash were included in the statistical analysis, no benefit was noted among the group of patients who received the addition of Erbitux over the control group.
These results are consistent with the results from the analysis of the PACCE (Panitumumab Advanced Colorectal Cancer Evaluation) trial, in which Avastin plus standard Eloxatin or Camptosar® (irinotecan)-based chemotherapy was directly compared with Avastin/chemotherapy and Vectibix as first-line therapy in metastatic colorectal cancer.2 The World Congress on Gastrointestinal Cancer meeting in 2007 was the site of the first public presentation of the PACCE data, which revealed that progression-free survival and toxicities were actually worse in the Vectibix arm, resulting in the discontinuation of treatment with Vectibix in this trial; data collection of PACCE continues despite discontinuation of Vectibix.
Overall, it appears that there is a class effect in which the combination of agents targeted against the EGFR and VEGF provide no clinical benefit and may in fact result in worse outcomes as initial therapy in metastatic colorectal cancer patients. Initial findings from both the CAIRO and PACCE trials were unexpected as preclinical models predicted that the combination of agents targeted against these pathways increased growth inhibition of malignant cells. Further molecular analyses may identify potential subgroups that could derive benefit from this treatment combination or reasons why inhibition of both the EGFR and VEGF pathways through these biologic therapies does not provide improved outcomes for patients with colorectal cancer. The presenter cautioned that EGFR/VEGF treatment combinations such as Erbitux/Avastin should remain in the context of a clinical trial for colorectal cancer at this time.
Reference:
--------------------------------------------------------------------------------
1 Punt CJ, et al. Randomized phase III study of capecitabine, oxaliplatin, and bevacizumab with or without cetuximab in advanced colorectal cancer (ACC), the CAIRO2 study of the Dutch Colorectal Cancer Group (DCCG). ASCO Meeting 2008; Abstract LBA4011.
2 Amgen. Amgen Discontinues Vectibix(TM) Treatment In PACCE Trial Evaluating Vectibix(TM) As Part Of Triple Combination Regimen. Available at: 2007&releaseID=977186. Accessed June 2008.
Erbitux®/Avastin® Combo Not Effective in Colorectal Cancer http://professional.cancerconsultants.c ... x?id=42262
Researchers affiliated with the CAIRO2 trial reported that the addition of Erbitux® (cetuximab) to Avastin® (bevacizumab), Eloxatin® (oxaliplatin), and Xeloda® (capecitabine) did not provide a clinical benefit and actually reduced progression-free survival in metastatic colorectal cancer. These findings are consistent with results from other trials indicating that the combination of agents targeting the epidermal growth factor receptor (EGFR) and the vascular endothelial growth factor receptor (VEGF) pathways does not provide clinical benefit. These results were recently presented as a late-breaking abstract at the 2008 annual meeting of the American Society of Clinical Oncology (ASCO) in Chicago, Illinois.
Researchers have been hopeful that combining biologic therapies that target different pathways may provide additional benefit for the treatment of various cancers. Because Erbitux and Vectibix target the epidermal growth factor receptor (EGFR) pathway and Avastin targets the vascular endothelial growth factor (VEGF) pathway, and because synergistic activity between the two agents has been noted in laboratory studies, researchers speculated that a combination of the two agents may provide more anticancer activity than either agent used alone in combination with chemotherapy. However, there have been conflicting results regarding the efficacy of the combination of these two targeted agents in colorectal cancer.
The CAIRO2 study was a Phase III trial that was conducted to further evaluate the addition of Erbitux to Avastin-containing regimens in colorectal cancer. The trial, which was conducted by the Dutch Colorectal Cancer Group (DCCG), included 79 Dutch hospitals and 736 patients with metastatic colorectal cancer.1 Patients were ineligible for surgical resection and had not received prior therapy for metastatic disease. The primary endpoint was progression-free survival, with secondary endpoints being overall survival, response rates, toxicity, and translational outcomes.
Patients were randomized to either the control group—which received six cycles of Eloxatin (oxaliplatin, 130 mg/m2 on day one), Xeloda (capecitabine, 1,000 mg/m2 twice daily on days one to 14), and Avastin (7.5 mg/kg on day one), with further cycles including Xeloda (1,250 mg/m2 twice daily on days one to 14) and Avastin (7.5 mg/kg on day one)—or to the group that received the addition of Erbitux (weekly in a 400 mg/m2 loading dose and 250 mg/m2 thereafter) plus the control group regimen. Follow-up was nearly 19 months.
There was no benefit derived among any endpoint for patients treated with the addition of Erbitux; in fact, progression-free survival was significantly reduced among patients treated with Erbitux (9.6 months versus 10.7 months, HR for progression 1.21, P=0.018).
Overall survival was similar between the two groups at approximately 20 months (P=0.21).
Both groups achieved a 44% combined complete and partial response rate (P=0.88).
There was no significant difference between treatment groups in terms of disease stabilization.
Even when KRAS status and the presence of grade 3 rash were included in the statistical analysis, no benefit was noted among the group of patients who received the addition of Erbitux over the control group.
These results are consistent with the results from the analysis of the PACCE (Panitumumab Advanced Colorectal Cancer Evaluation) trial, in which Avastin plus standard Eloxatin or Camptosar® (irinotecan)-based chemotherapy was directly compared with Avastin/chemotherapy and Vectibix as first-line therapy in metastatic colorectal cancer.2 The World Congress on Gastrointestinal Cancer meeting in 2007 was the site of the first public presentation of the PACCE data, which revealed that progression-free survival and toxicities were actually worse in the Vectibix arm, resulting in the discontinuation of treatment with Vectibix in this trial; data collection of PACCE continues despite discontinuation of Vectibix.
Overall, it appears that there is a class effect in which the combination of agents targeted against the EGFR and VEGF provide no clinical benefit and may in fact result in worse outcomes as initial therapy in metastatic colorectal cancer patients. Initial findings from both the CAIRO and PACCE trials were unexpected as preclinical models predicted that the combination of agents targeted against these pathways increased growth inhibition of malignant cells. Further molecular analyses may identify potential subgroups that could derive benefit from this treatment combination or reasons why inhibition of both the EGFR and VEGF pathways through these biologic therapies does not provide improved outcomes for patients with colorectal cancer. The presenter cautioned that EGFR/VEGF treatment combinations such as Erbitux/Avastin should remain in the context of a clinical trial for colorectal cancer at this time.
Reference:
--------------------------------------------------------------------------------
1 Punt CJ, et al. Randomized phase III study of capecitabine, oxaliplatin, and bevacizumab with or without cetuximab in advanced colorectal cancer (ACC), the CAIRO2 study of the Dutch Colorectal Cancer Group (DCCG). ASCO Meeting 2008; Abstract LBA4011.
2 Amgen. Amgen Discontinues Vectibix(TM) Treatment In PACCE Trial Evaluating Vectibix(TM) As Part Of Triple Combination Regimen. Available at: 2007&releaseID=977186. Accessed June 2008.
Re: Questions on Erbitux
I started out on Fulfox plus Avastin plus cetuximab (erbitux). It got me from un-operable to operable, and from there to NED, so I think it worked for me. 5-Fu does the heavy lifting, but Avastin and cetuximab add to it. As for the rash...Kaiser sent me to the dermatologist to help me deal with it. He gave me an antibiotic and something called metrolotion, and that helped a lot. I would wash with a very gentle soap in the morning, and an apricot scrub at night. The grainy scrub was surprisingly gentle, and got off the makeup and all the dead skin that builds up. Clinique makes a foundation aimed at people who have rosasea (the rash is chemo-induced rosasea) that is pale green. It covers the red and gives an appearance of beige. You can use it alone, or add your usual makeup. The rash clears up soon after you go off it. Susan
Dx 5/07 Stage IV 59 y/o
6 mos Folfox, Avas., erb.
Surg. for colon, liver mets 1/08
Folfox & Avas. 2/08-8/08
Liver met 10/09, Iri 11/09 - 7/10
SBRT 4/10, 12/10
30-40 lung mets 4/11
Irin./erbitux 5/11-8/11
xeloda/avastin 8/11-2/12
xeloda/erb 2/12/-4/12
6 mos Folfox, Avas., erb.
Surg. for colon, liver mets 1/08
Folfox & Avas. 2/08-8/08
Liver met 10/09, Iri 11/09 - 7/10
SBRT 4/10, 12/10
30-40 lung mets 4/11
Irin./erbitux 5/11-8/11
xeloda/avastin 8/11-2/12
xeloda/erb 2/12/-4/12
Re: Questions on Erbitux
My dad has been on Erbitux and Folfox and he had a bad rash all over his body. He has been using a cold compress and lots of coconut oil to get relief from the dry flaking of acne/rash which causes severe itching. You could get this oil at any Indian Store.
ritu
ritu
dad 68 Dx stage 4
mCRC 02/09
solitary met to lung
resection rectum 5/09
liver lung brain mets 5/10
cyberknife lung gammaknife brain
chemo xeloda/oxi/erbitux
mCRC 02/09
solitary met to lung
resection rectum 5/09
liver lung brain mets 5/10
cyberknife lung gammaknife brain
chemo xeloda/oxi/erbitux
-
DebbieBale
Re: Questions on Erbitux
I get bouts of acne, but it comes and goes, redness in the face also that comes and goes from the Eurbitix. I get the acne on my chest too. And the clinque product does work, I used it this morning. I also use Aveeno face scrub at night. It really helps with skin tone and is very mild. Drink prenty of fluids! I've been buying flavored water and it is a nice change from plain water. I find if I pour the water in a glass instead of drinking out of the bottle, I get less gas.
( No gulping)
( No gulping)
Re: Questions on Erbitux
drtrudi wrote:Just found out that my colon cancer (stage IV - peritoneal mets) was the "wild" type genetically.... I started Erbitux about a month and a half ago.... I have broken out with the worst acne of my life.... Now I am 43 and I am not complaining, especially since fulfori whipped my butt for almost a year... I am now on folfox, avastin, and erbitux..... My onc says the acne is a good sign - it means the erbitux is helping, but my understanding of this drug is that it keeps the cancer from getting worse and has no killing abilities.... I am on tetracycline and am going to pick up some clindamycin ointment prescribed by the onc now.... My question is what were your side effects (if any) on erbitux, what you did for it, how long it lasted and did it help you in your battle with colon cancer..... Thanks in advance!!!! trudi
If you just have peritoneal mets, has your oncologist suggested a "hot chemo" wash called HIPEC?
viewtopic.php?f=1&t=5149
Re: Questions on Erbitux
Thank you all so much!!!!! To the guest1: yes, my doctor has spoken to me regarding the surgery and chemo "wash" - right now, due to my weight and last summer having 2 bouts of sepsis from IV lines (one PICC line and one port), one was mrsa, they say I'm not a candidate.... so, I am losing weight, thinking that by the time I have the 12 folfox treatments (around October) I might have enough weight off to have surgery.....
Diagnosed April Fool's Day 2008 with Grade 4 mucinous adenocarcinoma of the sigmoid colon with peritoneal mets
4/23/08 colon resection
May 08 - folfiri
Nov 08 - irinotecan and avastin
April 09 - changed to folfox, erbitux, and avastin
CTC currently 0
4/23/08 colon resection
May 08 - folfiri
Nov 08 - irinotecan and avastin
April 09 - changed to folfox, erbitux, and avastin
CTC currently 0
Re: Questions on Erbitux
drtrudi wrote:Thank you all so much!!!!! To the guest1: yes, my doctor has spoken to me regarding the surgery and chemo "wash" - right now, due to my weight and last summer having 2 bouts of sepsis from IV lines (one PICC line and one port), one was mrsa, they say I'm not a candidate.... so, I am losing weight, thinking that by the time I have the 12 folfox treatments (around October) I might have enough weight off to have surgery.....
It's a pretty gruesome surgery and goes by the nickname MOAS - mother of all surgeries - due to the size of the incision and the length of time it takes to perform the cytoreduction and HIPEC (12 hours for some people).
Re: Questions on Erbitux
About Erbitux, here's a good article about the side effects and so forth...
http://www.cancerworld.org/CancerWorld/ ... px?id=1707
http://www.cancerworld.org/CancerWorld/ ... px?id=1707
Daughter of Dad with Stage IV CC
Re: Questions on Erbitux
Had my 3rd round of Vectibix today. Erbitux and V. are closely related, as you probably know. I have a grade 3 skin reaction (acne-like), mainly chest and back, with face and scalp involvement, as well. I asked my onc for a derm referral 2 wks ago. Here's what came of it:
Derm concurred that doxycycline is best choice for antibiotic. She also Rx'd triamcinolone for chest and back, and hydrocortisone 2.5% along with clinamycin lotion for above neck only. The hydro ointment and clind. lotion can be mixed together for application. She mentioned that there is a concern about c. diff that prohibits use of topical clindamycin in a body-wide fashion (!)
Both my onc and the derm referenced a Dr. Lacouture, a derm from Northwestern U. as the leading figure for opinion on treatment of EGFR related skin reactions. Check out this link I found, paper authored by Dr. Lacouture:
http://www.skintherapyletter.ca/stl/2007/12.6/1.html
Good luck with your therapy. A year of Folfiri....whoa, I hated my 4 rounds of that stuff!
Derm concurred that doxycycline is best choice for antibiotic. She also Rx'd triamcinolone for chest and back, and hydrocortisone 2.5% along with clinamycin lotion for above neck only. The hydro ointment and clind. lotion can be mixed together for application. She mentioned that there is a concern about c. diff that prohibits use of topical clindamycin in a body-wide fashion (!)
Both my onc and the derm referenced a Dr. Lacouture, a derm from Northwestern U. as the leading figure for opinion on treatment of EGFR related skin reactions. Check out this link I found, paper authored by Dr. Lacouture:
http://www.skintherapyletter.ca/stl/2007/12.6/1.html
Good luck with your therapy. A year of Folfiri....whoa, I hated my 4 rounds of that stuff!
Last edited by tomh7 on Fri Jun 05, 2009 10:53 pm, edited 2 times in total.
Tom, age 51, appendix cancer, dx 3/07
Rt. colon resect 4/07, 5/10 LN, FOLFOX 6, 12 txs, 6-12/07
Liver met dx 7/08, Lap. liver resect, 8/08
Mets in liver, pancreas, 1/09
Folfiri + Avastin, 4 txs, 2-4/09, progression
Vectibix 5/09 -6/09, progression
Rt. colon resect 4/07, 5/10 LN, FOLFOX 6, 12 txs, 6-12/07
Liver met dx 7/08, Lap. liver resect, 8/08
Mets in liver, pancreas, 1/09
Folfiri + Avastin, 4 txs, 2-4/09, progression
Vectibix 5/09 -6/09, progression
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Lifes2short
- Posts: 549
- Joined: Mon Oct 30, 2006 10:54 pm
- Location: Salt Lake City, UT
Re: Questions on Erbitux
Tom, thanks for the link. I have just started Erbitux and I found that article very helpful. My doc gave me a prescription for doxycyclin and an oral corticosteroid called Medrol. According to the article, the oral steroid would be used only for a very severe rash. I will ask my doctor to prescribe the topical medication first.
FWIW, my clinic gave me a two page "skin care" write up done by a former patient. He recommended Sween Cream by Coloplast for full body moisturizing and Green Tea shampoo by Paul Mitchell.
FWIW, my clinic gave me a two page "skin care" write up done by a former patient. He recommended Sween Cream by Coloplast for full body moisturizing and Green Tea shampoo by Paul Mitchell.
Age 45; Stage IV, mets to liver, nodes and bones.
Dx 12/05; Chemoradiation, surgery, Folfox, Folfiri, Folfiri, Folfiri, Folfiri
Intrathecal pain pump 3/09 (works great!)
Irinotecan / Erbitux 5/09 - ?
Two wonderful kids ages 7 and 5
Dx 12/05; Chemoradiation, surgery, Folfox, Folfiri, Folfiri, Folfiri, Folfiri
Intrathecal pain pump 3/09 (works great!)
Irinotecan / Erbitux 5/09 - ?
Two wonderful kids ages 7 and 5
Re: Questions on Erbitux
Thank you all so much..... It has been quite the year and I just found out from my onc, that when I get through my 12th treatment of Folfox, he still wants me to stay on some form of chemo.... I thought that I'd be done, but he says he's going to give me a 4 month break... Oh well..... don't think he has much hope of a cure/NED for me...... 
Diagnosed April Fool's Day 2008 with Grade 4 mucinous adenocarcinoma of the sigmoid colon with peritoneal mets
4/23/08 colon resection
May 08 - folfiri
Nov 08 - irinotecan and avastin
April 09 - changed to folfox, erbitux, and avastin
CTC currently 0
4/23/08 colon resection
May 08 - folfiri
Nov 08 - irinotecan and avastin
April 09 - changed to folfox, erbitux, and avastin
CTC currently 0
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Lifes2short
- Posts: 549
- Joined: Mon Oct 30, 2006 10:54 pm
- Location: Salt Lake City, UT
Re: Questions on Erbitux
drtrudi, is the chemo working for you? Are the mets still there? Smaller? Still growing? I'm kind of surprised to see that your doc has had you on chemo non stop for more than a year. That's a whole lot of harsh meds. How are you doing? Does your doctor think he can erradicate the cancer completely and permanently with the ongoing chemo? If not, I don't understand why he's throwing all the available drugs at you all at once. I have worked with my doctor to maximize my quality of life and to make the chemo drugs effective for as long as possible. When we have proof that the chemo is working and the cancer has receded or stopped growing, I stop treatment and enjoy life. When the cancer becomes active again I start chemo again. My doc and I had a long discussion recently about whether to add Erbitux to my Irinotecan now or save it for when I really need it. I like his way of thinking. I decided to hit the Irinotecan/Erbitux combo in hopes of faster and more pronounced response. But I hope that I'll be able to stop the chemo before the Erbitux stops working on me. I'd like to think that I have at least one more shot at chemo after this.
I know this is kind of a unique approach and I don't know if it would work for anyone else. But it has been good for me and I'm very glad that my doctor has supported me in doing this. Please note that my cancer is so widespread that I am not a candidate for any type of resection. For those who have mets confined just to the liver or lungs (or both) it makes sense to stay on the chemo and try to shrink the tumors to a point where they are resectable. But if your diagnosis is terminal, I would highly recommend talking to your doctor about balancing quality of life with treatment.
I know this is kind of a unique approach and I don't know if it would work for anyone else. But it has been good for me and I'm very glad that my doctor has supported me in doing this. Please note that my cancer is so widespread that I am not a candidate for any type of resection. For those who have mets confined just to the liver or lungs (or both) it makes sense to stay on the chemo and try to shrink the tumors to a point where they are resectable. But if your diagnosis is terminal, I would highly recommend talking to your doctor about balancing quality of life with treatment.
Age 45; Stage IV, mets to liver, nodes and bones.
Dx 12/05; Chemoradiation, surgery, Folfox, Folfiri, Folfiri, Folfiri, Folfiri
Intrathecal pain pump 3/09 (works great!)
Irinotecan / Erbitux 5/09 - ?
Two wonderful kids ages 7 and 5
Dx 12/05; Chemoradiation, surgery, Folfox, Folfiri, Folfiri, Folfiri, Folfiri
Intrathecal pain pump 3/09 (works great!)
Irinotecan / Erbitux 5/09 - ?
Two wonderful kids ages 7 and 5
Re: Questions on Erbitux
Lifes2short wrote:drtrudi, is the chemo working for you? Are the mets still there? Smaller? Still growing? I'm kind of surprised to see that your doc has had you on chemo non stop for more than a year. That's a whole lot of harsh meds. How are you doing? Does your doctor think he can erradicate the cancer completely and permanently with the ongoing chemo? If not, I don't understand why he's throwing all the available drugs at you all at once. I have worked with my doctor to maximize my quality of life and to make the chemo drugs effective for as long as possible. When we have proof that the chemo is working and the cancer has receded or stopped growing, I stop treatment and enjoy life. When the cancer becomes active again I start chemo again. My doc and I had a long discussion recently about whether to add Erbitux to my Irinotecan now or save it for when I really need it. I like his way of thinking. I decided to hit the Irinotecan/Erbitux combo in hopes of faster and more pronounced response. But I hope that I'll be able to stop the chemo before the Erbitux stops working on me. I'd like to think that I have at least one more shot at chemo after this.
I know this is kind of a unique approach and I don't know if it would work for anyone else. But it has been good for me and I'm very glad that my doctor has supported me in doing this. Please note that my cancer is so widespread that I am not a candidate for any type of resection. For those who have mets confined just to the liver or lungs (or both) it makes sense to stay on the chemo and try to shrink the tumors to a point where they are resectable. But if your diagnosis is terminal, I would highly recommend talking to your doctor about balancing quality of life with treatment.
Good plan. My father followed something similar and enjoyed great quality of life for 3 1/2 years before complications set in. That said, he has had great success "recycling" chemotherapies. When one regimen stops working, he goes on a maintenance cycle to let his body recover or tries a different regimen. When that regimen stops working, he tries the old regimen again 6 months or a year later.
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