Has anyone used Tarceva as maintance? I am currently in remission and one onocologist says to take it and the other says not to. How confusing does that get?
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Has anyone used Tarceva as maintance? I am currently in remission and one onocologist says to take it and the other says not to. How confusing does that get?
Cancer Plague Surgery Radiation therapy Head and neck cancer Breast cancer Chemotherapy Pain Tarceva Progesterone Lung cancer
I would love to see the responses you get. My husband was Stage 3A, just finished radiation, and had surgery and chemo prior to that. He is EGFR positive. Sloan Kettering recommended he go on Tarceva as maintenance. He just started on sunday. I am curious to hear why one of your ONCs said not to.......
thanks,
janet
I would post that question on cancergrace.org and let the cancer specialist give their opinions. Good luck and take care, JC
im on tarceva 100mg have been for 8 1/2 mons. started out at 150mg but lowered it because of the severe rash on my face so far so gud my last pet/ct was in may looks like its wrking my last ct was in aug still looked gud my next one is in late nov. im hoping for even better news sum say if it wrks it usually wrks well and for quite sum time the longest ive heard of it wrking was 8yrs. so like i mentioned so far so gud for me except for the side effect of the rash but id rather have rash then cancer everywhere.
Hi Jam:
My Oncologist told me I would be on Tarceva for the rest of my life unless it stops working. I have an appointment with him tomorrow, but I doubt he has changed his mind. I've been on it for 22 months now.
Love to all,
Marylou
Some docs are using maintenance therapy and some are not. I think it is just their own preference. I asked my oncologist about it and for me they didn't feel it necessary. I am in a remission, so they felt why put me on something now if not needed. I guess if I do get the cancer back then it will be given to me. This way I will have a longer time that I could stay alive, and then more chance of longer life if i need to use it, because eventually they told me it might sotp working. Some are on it for maintenance and never would have gotten cancer back again anyway. This is the dilemma with it. And also I think the reason they have 2 different opinions on who to give it too. some are also on it as a first line treatment now also.
Sandy
Tarceva is my first line treatment. My Dr. told me it's going to be my vitamin pill for the rest of my life. I am taking it faithfully and hoping one day I will be off it. The doctor also said: there isn't enough data for any conclusion because it's a new drug. One of her patients has been on it for 8 years and still going strongly; He was one of the clinical trial patients. some patients are taking 25mg every other day and doing well too.
Novo
I've been on tarceva for a year - first line for stage 4 nonsmall cell and it has worked well so far. I started with 150 mg and was reduced at 6 months to 100 mg.
My oncologist said I would be on it until it stops working or some other miracle drug become available.
Hi,
My husband has been diagnosed with Non Small Cell Lung Cancer Stage IV. He was tested at Sloan Kettering for the EGFR mutation and he tested positive. His oncologist, at Sloan Kettering, is starting him on Tarceva as a first line treatment and told him he would have to be on it for the rest of his life or until it stops working. However we are both great believers in good nutrition and healing and staying healthy by strengthening the immune system. So besides the Tarceva we are very careful with his diet and intend to discuss suplements with the doctor, if and when he goes into remission. My own personal, uneducated, opinion, from the gut, is that if you can sustain remission without a medication, then you should. But you have to be willing to alter your lifestyle and food habits if they are not compliant with preventing cancer.
Good Luck and Good Health
Nili
Thanks everyone for your insight. The one onocologist is old fashioned and didn't order pet scans or bone scans. My surgeon ordered ct of the chest . What was missing was mri of the brain. I got brain met . I had sterotatic surgery Dec of 08. That turned into a jelly substance and they removed July 09. I since then went to another onocologist. She said to take it. I was so confused and need to get copy of EGFR test results. I know there were five mutations. I just glanced quickly but one was positive. I know the Kras was negative and for the remainder I just don't know. The difference between the two onocologists is that one more aggressive. She believes in testing to catch things early and he has the attitude wait for symtoms. Survival is the same. She believes it will be standard protocol in the future. I just want to add the first onocologist said it may work but why take somthing if you wasn't sure . Isn't this cancer? The uncertainty?
Some oncologists may think (for good reason) it is not necessary to take Tarceva as maintenance, after remission. Although this targeted thearpy may be initially effective, the drug may eventually stop working, and a tumor may begin to grow again.
This is called acquired or secondary resistance. The change of a single base in DNA that encodes the mutant EGFR protein has been shown to cause drug resistance. This is different from primary resistance, which means the drug never worked at all.
Initially, tumors have the kinds of mutations in the EGFR gene that were previously associated with responsiveness to this type of drug. But, sometime tumors grow despite continued therapy because an additional mutation in the EGFR gene, strongly implies that the second mutation was the cause of drug resistance.
Biochemical studies have shown that this second EGFR mutation, which was the same as before, could confer resistance to the EGFR mutants normally sensitive to these drugs. Secondary resistance is very different from primary resistance.
gpawelski - I always appreciate and enjoy your posts because you are so knowledgeable and we really need that. In the above post, are you saying that if the doctor puts you on Tarceva and the tumor starts growing again that other chemos will not work? Basically you are without effective chemo? Please explain as I am simple minded in some areas. Thanks.
sticktogether. You are grasping the understanding of cancer and cancer cells. I'd give you more credit for asking the vital questions.
Tumors are highly complex in their behavior and don't necessarily need a gene mutation to alter their behavior. A chemo-induced gene mutation can happen when the original chemo received does not work. The cancer comes back. When it does this, the cancer comes back more aggressively.
The mutagenic (changing) effects of the wrong chemotherapy on a genetically-unstable tumor, drives the tumor into a state of more aggressive behavior. You might kill off a whole lot of cancer, only to cause a mutation in the remaining cancer, such that the remaining cancer behaves in a more aggressive fashion.
Patients would certainly have a better chance of success had their cancer been chemo-sensitive rather than chemo-resistant, where it is more apparent that chemotherapy improves the survival of patients.
And in the case of Tarceva (the same for Erbitux and Iressa), a change of a single based in DNA that encodes the mutant EGFR protein has been shown to cause acquired or secondary drug resistance.
EGFR (epidermal growth factor receptor) expression is associated with a poorer prognosis for many patients with solid tumors. EGFR expression is for Tarceva. In some cancer cells, EGFR triggers uncontrolled cell division.
Testing patients for EGFR to determine which patients would benefit from targeted therapies such as Tarceva, Erbitux and Iressa, was limited only to those patients whose tumors were determined to be EGFR protein positive.
There are rare patients that respond very well. However, cancer cells evolve resistance to Tarceva by multiple mechanisms related to genetic alterations both within the EGFR gene and at other sites.
Will the fact that EGFR negative patients not benefit from Tarceva and limit its usage? The FDA approved indication for Tarceva does not limit prescirbing specifically to EGFR positive patients. In the drug's registration trial, determining response based on EGFR was not a major endpoint of the study.
The growth of lung cancer appears to depend upon a variety of different growth factors. If the growth of the tumor is not entirely dependent on EGFR, an anti-angiogenic therapy directed to that growth factor alone, may not be effective.
If there are a number of different growth factors with different influences on different tumors, then you must either isolate the predominant growth factor very specifically, or use a variety of anti-angiogenic drugs to combat various methods of tumor growth.
Cancer cells are smart too. Patients sometimes become resistant to targeted therapies as cancers mutate in ways that make drugs ineffective. Cancer cells will find ways around therapy if you don't get rid of them.
A goal would be to choose therapies so they target the precise proliferation pathways the cancer is using. We have the ability to profile tumors so that oncologists would know not to use one particular drug (or combinations of drugs) because it won't help, but utilized some other particular drug (or combination) because it shows that it is synergistic (cooperative) to the cancer cells (killing them).
A functional profiling assay can assess the activity of a drug (or combinations of drugs) upon combined effect of "all" cellular processes, using several metabolic (cell metabolism) and morphologic (structural) endpoints, measuring the "profile" of the whole cell (it's entire genome). It is analogous to measuring thousands of genes before and after drug exposure.
O.K. Now you got me on the last paragraph...Is this in reference to the biopsy or sample of the tumor to be tested to see which chemos work? Do you know of a way to get this information without the sample?
A functional profiling assay can assess the activity of a drug (or combinations of drugs) upon combined effect of "all" cellular processes, using several metabolic (cell metabolism) and morphologic (structural) endpoints, measuring the "profile" of the whole cell (it's entire genome). It is analogous to measuring thousands of genes before and after drug exposure.
sticktogether
I think think the ultimate goal is to profile one genes but we are not there yet. We have some tools and there has been some progress , but bottom line there is no complete answer. I think it is a shot in the dark. Why do some do well on certain chemos and others do not? Is it worth a shot if the onocologist says so, I think so. The problem I had is one doc said it may work but why take somthing if you weren't sure, The other doc said it would be favorable for me to take it. In the world of cancer whats for sure.
jam
I think what jam is saying may be true. The ultimate goal is to profile ones genes, but we are not there yet with molecular profiling. When it comes to drug selection genomics (molecular profiling) is far too limited in scope to encompass the vagaries and complexities of human cancer biology. Efforts to administer targeted therapies in randomly selected patients often result in low response rates at significant toxicity and cost.
While researchers continue to develop molecular probes to select candidates, the cell culture analysis platform serves as a functional profile capable of examining the nuances of cellular response to drugs. To exploit the full potential of targeted anticancer therapies, physicians will need laboratory tests that match patients to specific drugs.
Cell culture assays are able to accurately predict how an individual patient's cancer cells will respond to an array of drug combinations. It is able to quantify synergistic drug combinations and individually tailor treatment.
Molecular profiling tests cannot do this. These are the reasons.
In chemotherapy selection, molecular profiling examines a single process within the cell or a relatively small number of processes. The aim is to tell if there is a theoretical predisposition to drug response.
Functional profiling examines not only for the presence of the molecular profile but also for their functionality, for their interaction with other genes, proteins, and processes occurring within the cell, and for their response to anti-cancer drugs.
The goal of molecular testing is to look for patterns of normal and abnormal gene expression which could suggest that certain proteins might or might not be produced within a cell. However, just because a gene is present, it does not mean that an associated protein has been produced.
Protein testing goes one step further by testing to see if the relevant protein actually has been produced. However, even Protein testing cannot tell us if a protein is functional or how it will interact with other proteins in the presence of anti-cancer drugs.
Gene and protein testing involve the use of dead, formaldehyde preserved cells that are never exposed to chemotherapy drugs. Gene and protein tests cannot tells us anything about uptake of a certain drug into the cell or if the drug will be excluded before it can act or what changes will take place within the cell if the drug successfully enters the cell.
Gene and protein tests cannot discriminate among the activities of different drugs within the same class. Instead, gene and protein tests assume that all drugs within a class will produce precisely the same effect, even though from clinical experience, this is not the case. Nor can gene and protein tests tell us anything about drug combinations.
Functional tumor cell profiling tests living cancer cells. It assesses the net result of all cellular processes, including interactions, occurring in real time when cancer cells actually are exposed to specific anti-cancer drugs. It can discriminate differing anti-tumor effects of different drugs within the same class. It can also identify synergies in drug combinations.
Although gene and protein testing currently are limited in their reliability as clinical tools for drug selection, the tests can be important in research settings such as in helping to identify rational targets for development of new anti-cancer drugs.
As you can see, just selecting the right test to perform in the right situation is a very important step on the road to personalizing cancer therapy.
And yes, sticktogether, a live "fresh" tumor sample is needed. Tissue, blood, bone marrow, and ascites and pleural effusions are possibilities, providing tumor cells are present, and only live cells can be used. At least one gram of fresh tru-cut biopsy tissue is needed.
Hi,
My wife is stage IW NSCLC and using Tarceva 150mg daily as first line for almost six months- no chemo. She responds well to medicines but struggling with nutritions. Is there anything you can advise? Please do cause I have so much difficult in finding food with calories to keep her weight plus don't know what is good or bad food? Some doctors say no limit for cancer patients. what is/are the right way(s)?
Thanks
Braided
I've had the very same problem with my wife - lack of wanting to eat. With the trush and other factors, it was very hard to develop good eating habits. I put her on Megace (extremely expensive) in order to put back two-thirds of all the weight she lost. It has about a 50-50 chance of success. You won't exactly know if it will work unless you try it.
A study by researchers at Wake Forest University Baptist Medical Center and colleagues showed that a drug originally used to treat breast cancer may help combat the severe weight loss that can plague patients undergoing radiation treatment for lung and head and neck cancer.
"The drug clearly reduced weight loss and improved quality of life in study patients," said Michael Farmer, M.D., who presented his results to the American Society for Therapeutic Radiology and Oncology (ASTRO).
The research involved megestrol acetate (Megace), a synthetic form of the female hormone progesterone. The drug was originally used as an anti-hormonal treatment for breast cancer and was found to induce weight gain as a side effect. Later studies showed the drug's effectiveness as an appetite stimulant for patients with HIV, chronic diseases and cancer cachexia, a "wasting syndrome" in which fat and muscle are lost because of the presence of a cancerous tumor.
Weight loss can also be a problem in patients undergoing radiation treatment for lung cancer and cancers of the head and neck, such as cancer in the mouth or throat. The high doses of radiation used to treat these cancers can cause decreased appetite and weight loss, nausea and painful swallowing. These patients typically receive radiation alone or a combination of radiation and chemotherapy, which can worsen the side effects of treatment, particularly nausea.
"Due to the pain and nausea, it is very difficult for patients to eat sufficient quantities of food and drink proper amounts of fluid during treatment," said Farmer. "It is a critical time to maintain adequate food intake and hydration, yet one of the most frequent complaints from patients during this type of therapy is a decreased appetite."
Farmer said the expected mean weight loss among these patients is about 12 pounds after eight weeks of radiation therapy and that weight loss is a significant predictor of how well patients fare.
"Weight loss is correlated with decreased overall survival, decreased quality of life and decreased response to treatment," he said. "In addition, if the weight loss is severe enough, it can lead to breaks in treatment that may decrease the effectiveness of therapy."
The study involved 38 patients with lung cancer or cancer of the head and neck who were treated at Wake Forest Baptist or through four other centers. Twenty patients received megestrol acetate daily during eight weeks of radiation treatment and for 12 weeks afterwards. The remaining 18 patients received an inactive placebo during the same time period.
The mean weight for patients receiving megestrol acetate did not change significantly. However, the group receiving placebo had a mean weight loss of 11 pounds after 20 weeks.
Previous studies with megestrol acetate in cancer patients focused on patients with advanced cancer who were already receiving radiation or chemotherapy and had already begun to lose weight. In the current study, patients were given megestrol acetate from the start of treatment, to prevent weight loss.
"While we know that weight loss is associated with a poorer outcome, we don't know for certain that preventing weight loss will improve survival," said Farmer. "This issue has not been well studied and warrants more attention," Farmer said.
The safety of megestrol acetate has been well-documented in the previous studies. Farmer said, however, that patients should be screened for a risk of developing blood clots.
"While there is a small increased risk of blood clots in advanced cancer patients who take megestrol acetate, we did not observe this in our study patients," he said.
The research was conducted by the Comprehensive Cancer Center of Wake Forest University Research Base, a National Cancer Institute funded network of 93 community cancer centers in 19 states working with Wake Forest to conduct clinical trials in cancer patients. Wake Forest is one of only six NCI-designated Cancer Center Research Bases in the nation performing community-based cancer clinical trials.
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