CraiginPA

That is sad news. I hope it was less distressing for her than it might have been if it had spread elsewhere. Once things settle down I hope you can begin to adapt to your loss and resume your own life. Best hopes, Craig

Debbie, I am so sorry to hear of your loss, but as a stage IV cancer fighter I do understand his preferences as you described and it sounds like it was a good end though unexpectedly soon. Thank you for sharing your news. I wish you your own healing as you adapt to continuing on without him except in spirit. Best hopes, Craig

Jackie (JocelynM), FYI, I'm still waiting to see published or presented results from the phase 1/phase2 trials of Talon's menadione (synthetic vitamin K3) lotion. The briefest of info is given here: http://www.talontx.com/pipeline.php?divid=trialsummary and the status of their development pipeline for this is graphically shown here: http://www.talontx.com/pipeline.php I've seen other clinical trials exist or existed for vitamin K1 (as found some foods) for EGFR inhibitor rash, but don't know their results. Per prior lab research, K3 is supposed to be much more potent at neutralizing EGFR inhibitors than K1, yet as a lotion it was hoped that too little would be absorbed to neutralize the Tarceva effect on the cancer inside the body. Apparently the research trials continue. Best hopes, Craig

And so would every researcher in the world. They are trying. As far as I can see, cancer is complicated. It may be driven by one mutation but there's usually others that help it and hide it from natural defenses (like DNA repair or self-destruction, etc.). And animal cells are pretty adaptive already -- over millions(?) of years living cells have learned all sorts of adaptations and backup mechanisms for coping with changes in their environment, changes in available resources, and unfavorable environmental toxins or poisons. Unfortunately, cancer cells know these same adaptive tricks, too. Then you are a far better person than I. My mother would never have wanted me to sacrifice my career to help her fight against the cancer that took her life. My father and a local care managing service company working with her doctors meant she didn't need any other help. She didn't even have me take a brief "family leave." She preferred to just talk with us by phone and have us visit as often as we could when she could handle it a visit. (I have known a few good professionals in their 50's in whom a career lapse of a couple of years during a recession meant they could not find similar employment ever again; in a couple of cases they or their family never recovered from the financial hardship it led to. A leave of absence might be better than resigning, if possible. Of course, if jobs are more plentiful where you are for what you do, that might not be an issue.)Best hopes, Craig

https://www.google.com/#q=FWIW I'd guess it's the 3rd most common abbreviation in email messages after FYI and BTW, and more common than IMHO (or IMO). Best hopes, Craig

I'm still doing well. (No progression seen on last month's CT scan. Next one isn't for 3 more months unless I show signs suggesting a need to move up the date.)FWIW, I haven't said much lately on this discussion because I didn't have anything useful to add and I don't have experience with the stage of treatment your Mom is getting. I'm keeping an eye on the discussion, though. You've been in good hands and good company. Best hopes, Craig

P.S. -- another way to try to determine the kind of primary is gene profiling, as described in this trial: http://jco.ascopubs.org/content/early/2 ... 12.43.3755 That describes a new tool used in that trial that enabled them to pick a specific cancer type in 98% of the cases. Whether or not they were correct isn't provable, but it did improve treatment outcomes so it probably was better than not knowing at all. Best hopes, Craig

P.S. -- I never had a cough. Just a crackling sound when I lay down to sleep at first. Later it grew to be fluid that spilled up my windpipe when I bent over -- my only noticeable symptom. I didn't start coughing at all until after my bronchoscopy, and not even much then. Lucky for me, treatment has been able to relieve that for 15 months so far. Best hopes, Craig

Wylie, Sorry to hear about your Dad. I can't make a valid guess as to which type of lung cancer. If I remember correctly, a long smoking history (esp. if he didn't quit long ago) does significantly increase the chances it could be small cell lung cancer, squamous cell lung cancer, or an adenocarcinoma with a not-so-useful KRAS driving mutation (as opposed to a more useful one), but there are some smokers who even have a rare very rare, usually-useful (for a number of months) ALK- or ROS1-driven adenocarcinoma (rare regardless of smoking status, and with 90% of it occurring in younger never-smokers). The type of lung cancer would be one of the first things the pathologists will try to determine once he's gotten a biopsy sample taken (and a biopsy is usually done ASAP within days of seeing there's a tumor in there, at least here in the USA). FYI, if they said his cancer was inoperable, that might be either because they've seen it spread away from the original site (i.e., it's migrating through the body or across the lungs) in which case they might call it Stage IV, or it might be in a place they can't usually eradicate it from (pleural lining, which would also make it be called Stage IV), or it might be in a location too dangerous to use surgery or radiation on (e.g., around the heart or aorta). Best hopes, Craig

Thanks, Erika. The most common driving mutation for a smoker's lung adenocarcinoma is KRAS, so getting that tested could be one clue as to whether it is from the lung (although adenocarcinoma's from elsewhere can also be KRAS). It would be better, though, if it weren't the not-so-useful-yet KRAS-driven, because that would open up the possibility that the driving mutation might be a more useful one like EGFR. (ALK, ROS1 or RET might also have a chance, but those are much less likely in a smoker, though still possible.) There are other IHC (immunohistochemistry) tests that might give them a clue as to the source. I thought TTF1, CK7, and CK20 are the usual ones a lab would check to confirm whether it might be an adenocarcinoma from the lungs. Did they do those tests to help them decide? Here's a paper describing how such things (and others) are sometimes used: http://www.aaomp.org/annual-meeting/doc ... andout.pdf Best hopes, Craig

Erika, I'm sorry to hear your Dad's situation, but glad you are reaching out to others. Do they know what specific type it is? Adenocarcinoma? Squamous cell? Large cell? Small cell? Best hopes, Craig

Hospital or cancer center social workers tend to know the ins & outs of the available forms of assistance with the costs of cancer treatment. Is that service available in your area? You could also call your county government -- they sometimes have programs that fill a gap between state programs and Medicare/Medicaid. If you're willing to talk about it, how is the testing and treatment planning coming along? Have they determined the specific type of lung cancer? Adenocarcinoma? Squamous cell? Large cell? something else? (NSCLC is a pretty large category, and the specific type can change testing and treatment options.) Best hopes, Craig in PA

Re: Lung transplants for lung cancer: I read up on discussions about lung transplant after hearing about the possibility in one case. Unfortunately, it isn't a reasonable option, except for a very lucky few. 1. If you have an early stage cancer that hasn't spread, your remaining lung capacity after surgery should be sufficient to survive a long time. If after surgery the cancer had silently already spread to the other lung (undetectably), replacing the lungs wouldn't help as described next: 2. If you have cancer that has already spread elsewhere, the cancer cells are presumed to be wandering about your body, so replacing lungs won't help because the cancer cells will just float back to the lungs and start the cancer again. Chemo sometimes eradicates such cancer, but the odds are too small to risk wasting a donor's lung vs. giving it to someone who has good odds of getting 20 years out of it. 3. There is one potential exception. The BAC (bronchioloalveolar carcinoma) subtype of adenocarcinoma often (not always) stays confined to the lungs and progresses slowly, so if the lungs are removed cancer might not re-seed the lungs so easily. From what I've read, the odds are about 50% that the cancer will return. That is not good enough for some lung transplant surgeons who would like the donor lungs to last many years in someone. From the point of view of the BAC patient, it's a "win-win" because if the BAC doesn't return they live years and even if it does return the BAC might progress so slowly that they might get as much as 4 years out of those lungs. Even so, I know someone who searched nationwide for a lung transplant surgeon who would was willing to do the procedure of his wife with BAC. He only found two (after screening dozens). Unfortunately, lung transplant surgery is pretty risky, and although her transplant was initially successful, she died a couple of days later. Someday when lungs can be grown from stem cells, we might have unlimited spare parts made to match our own tissues. (It's a shame that some politicians blocked government-sponsored stem cell research.) Then the problem is treating mets elsewhere, but in an ideal BAC case that shouldn't be an issue for years. There's also the possibility of a mechanical device that might be better than nothing, if it doesn't cause blood clots (strokes & heard attacks), e.g.,: http://news.cnet.com/8301-27083_3-20083 ... re-oxygen/ I sure wish they'd hurry up with that -- it could be a life-extender for people who's front-runner cancer issue was lung impairment. Best hopes, Craig

FYI, I read somewhere a doctor wrote that the right amount of biopsy material to get these days is a "boatload." Obviously an exaggeration, but when I had my 2nd bronchoscopy biopsy, 24 samples were taken, which was 2 or 3 times as much as from the first. Best hopes, Craig

Correct -- the Stage IV can be due to the cancer spreading to other parts of the lungs, i.e., not just near the original site. That is why I'm stage IV -- cancer was seen on CT scans in every lobe of both lungs (although just tiny spots in the left lung, but confirmed by a 2nd biopsy later). No cancer was seen elsewhere or in nodes. If it really is BAC, there's a fair chance that a PET scan would show nothing outside the lungs and would not show the cancer that looks like GGO (ground glass opacity) or haze except where it has consolidated into a mass. I say that because that was my situation, and it caused the local doctors to mistakenly assume I had no cancer beyond what they could see on the PET scan, i.e., early stage cancer and surgically operable. Fortunately, a 2nd opinion from more experienced university doctors read the CT correctly so I could stop the pointless surgery in the nick of time. My personal experience has been that for my mBAC (assuming it remains confined to the lung as it often does) PET isn't very useful; CT is the important one. If the cancer responds well to the chemo, that would be a wonderful thing. Chemo offers a chance of cure, however small those odds might be in stage IV lung cancer. Mucinous BAC, though, has a anecdotal reputation of being less responsive than average to chemo but there are enough exceptions (and no good statistical studies) to doubt that. My oncologist mentioned an mBAC patient of hers who did very well with Alimta for a while, for example. I recognize Alimta (premetrexed) and Cisplatin. That combo has higher-than-average odds of working well in never-smokers. I am not familiar with other supportive drugs that are given to control side-effects. The side-effects from the initial infusion or two might not be very difficult. They are likely to get stronger as the chemo has a cumulative effect. Hopefully that will give enough time There is enough research supporting the idea of treating with an EGFR inhibitor drug as the 1st line of treatment *if* it is known that a person's lung cancer is driven by an EGFR mutation (and not one of the already-known drug-resistant variants of EGFR). An EGFR inhibitor sometimes works in patients who don't have an EGFR mutation, but then the odds for chemo would be better than for the inhibitor drug, so chemo would be the better first option. Sometimes in the USA, when a patient needs to start treatments ASAP, they start chemo before they know the EGFR test result. If the test comes back positive for an EGFR mutation (and not a known-resistant variant) then the would either finish the chemo first or switch to the EGFR inhibitor and come back to that chemo later. (I think there's usually a preference to finish a line before moving on, on the same assumption as for antibiotics.) In Asia, the probabilities favor EGFR in never-smoking women so heavily that doctors might be inclined to assume EGFR until proven otherwise, and act accordingly, but I don't know. The data I know is East Asia and I've seen something similar for India to make me think EGFR was almost as common there, too. But if you Mom has been elsewhere, it's hard to know how whether being in a different cultural environment with different behaviors changes the odds or whether it might be driven by inherited genes. FYI, if it were me, and if I did have the EGFR mutation, I'd want to ask if I could get some kind of scan (or even an ordinary x-ray) to try to measure the effect of the chemo before starting an EGFR drug so I'd know if it might be worth going back to finish more of that chemo later. I do hope you find that she does have some kind of drug-targetable driving mutation (EGFR, ALK, ROS1, RET, ...?) that offers her an additional drug or track of experimental drugs that might have a good chance of extending her life. Best hopes, Craig ________ P.S. -- If you need research citations for anything I described, let me know. I'm just too tired right now -- need some sleep.

To support your thinking: http://www.ijcep.com/files/IJCEP704003.pdf supports the use of TTF-1+ and CK7+ to try to identify lung adenocarcinoma. And the article also says . . . "CK7+ / CK20- profile is not restricted to lung cancers .... The differential diagnosis for CK+ / CK20+ adenocarcinomas also includes neoplasms with origins in the pancreas, . . ." From http://www.aaomp.org/annual-meeting/doc ... andout.pdf (a very good paper on dx of cancers of unknown origin): CK7+ and CK20+ is common in pancreatic carcinomas, but elsewhere it mentions . . . "In my own experience, I have seen . . . a [TTF-1] positive pancreatic carcinoma . . . ." I do not think the term "focally positive" relates to cancer in any specific organ. It seems to mean that only some cells showed a positive result and some didn't. (Small clusters? Thin layer? I don't know.) My impression is that it might mean an ambiguous result, but you really need a doctor to interpret those words. You could ask a specific question like that over on the forums at cancergrace.org . They even have someone there with a lot of pathology lab experience. I don't know more about it than you're able to read yourself, but my guess is that the doctors think it might be bronchioloalveolar carcinoma of the lung and not of the pancreas, but they can't be sure. If it were me, I would ask my doctors if there's any lab test they could do that would definitely rule out other organs of origins. If you want more detail about how these IHC tests look in BAC (bronchioloalveolar carcinoma), read: http://ajcp.ascpjournals.org/content/121/3/350.full.pdf But, in short, it's hard to be definitive because there's plenty of exceptions. For example, in that report 2/3 of mucinous BAC was TTF1-,CK7+,CK20+ but that means 1/3 wasn't that way. FYI, my cancer seems like mucinous BAC based on appearance and behavior (lots of mucus/fluid that stopped by the next day after starting Xalkori, slow metabolism and growth, & confined to lungs thus far), but tested TTF1+, CK7+, CK20- which is typical of ordinary adenocarcinoma and non-mucinous BAC, so I can't be sure. (I'd think differently in an instant if we found it outside lung someday.) Your mother's TTF1 focally+, CK7+, CK20- and observations seems to resemble what those citations say is most common in regular adenocarcinoma or non-mucinous adenocarcinoma of the lung, but maybe being focally positive on TTF-1 means it's a little ambiguous. Does that discussion of IHC testing help? Best hopes, Craig

Beagles3, Until the best plan of action is determined and started, it's a very stressful time. I lost weight and sleep during that period. I don't have much to suggest on how to deal with the emotions of it. To me, it's disappointing to know my life will end sooner than I had hoped, but I never expected to live forever. If sleep or anxiety is an issue, a primary care physician may be able to offer an Rx to help her with those for a while. There are many positive success stories that might feel encouraging and can offset the old statistics. (Statistics that were from the days before certain useful drugs that are available today.) I'm one example: a year and a half ago I thought I'd only have 2 years or so left to live; instead, with the help of a new miracle drug, I'm still walking around like a healthy person with no significant side effects from the pills. (I've been on the drug 14 months so far and it's still holding up, though I'm lucky.) Has her oncologist determined which specific type of cancer it is? Has testing determine which driving mutation is driving the cancer? For some driving mutations, a mutation-targetable inhibitor drug can be an option that usually (not always) is effective for a number of months (and sometimes years, if lucky). I'd like to elaborate, but the odds of something useful depend on which specific type of cancer it is (e.g., adenocarcinoma, and on smoking history. Best hopes, Craig

On the subject of appetite, if weight loss becomes a problem: There is a Rx drug that a doctor can prescribe that stimulates appetite. (For myself, I'd just make myself eat as much as my body needed regardless of mood or bad taste, but many people won't eat unless they feel the urge to.) Best hopes, Craig

Yes, she'll decide based on her values and preferences, regardless what other people might want. I would guess that there probably isn't much difference between treatments available in India vs. South Africa which are effective (as proven by credible published research), but that probably depends on what kind of cancer, type of cancer, & gene mutation driver of cancer she's got vs. what Rx drugs are available or in trials in each location. I would imagine, though, that Rx's that are available in India might be cheaper there. Best hopes, Craig

FYI, where I am brain scans are usually MRI, not CT, but it depends on what they are looking for. MRI's are slower, but don't have the radiation that CT's have. (Radiation has a very small chance of causing cancer, so the more exposures you get the greater the chance of causing a 2nd problem. The risks from CT radiation probably don't matter if a patient isn't expected to live long anyway, but I hope to live more than another year or two so I prefer to avoid unnecessary radiation to my brain. For my chest scans, there's no good alternative to a CT here, although after a year of checking me my doctors changed my scans to a low-dose CT with fuzzier images, but the images are adequate for a radiology expert to see any significant changes.) Best hopes, Craig

AnnieRSA, The additional reports make the picture sound more confusing. The abdominal CT report suggests the contradictory possibility that pancreatic cancer might be the origin of what seemed like lung cancer (i.e., if true, it would mean the cancer in the lungs is not lung cancer but metastatic pancreatic cancer). In contrast, the lung biopsy seems to say lung adenocarinoma, not pancreatic. I cannot sort out a diagnostic question like that; her doctors will need to tell you. It sounds like it is also possible that there's pancreatic adenocarcinoma cancer (independent of the lung cancer or as the cause of the cancer in the lungs), but it might require a biopsy of that pancreatic tissue to determine if it is or isn't. I don't know enough about pancreatic cancer to say much about that subject. But I can tell you that lung adenocarcinoma is not the same thing as pancreatic adenocarcinoma and treatment probably differs. (I think, though, that pancreatic adenocacinoma is more likely to be driven by a not-so-useful KRAS mutation instead of the useful EGFR mutation seen in some lung cancer adenocarcinomas.) BTW, if cancer had spread from an origin ("primary") in the lungs to form metastatic lesions in the pancreas, that would suggest it is more like a regular adenocarcinoma (or mucinous adenocarcinoma) and not very much like mucinous BAC since m-BAC isn't likely to jump to other organs like that. So I'm becoming a bit confused by the conflicting data. Your mother's doctors may need to sort out what is really going on before you'd have a good idea of how to treat her. Is it lung cancer? Pancreatic cancer? Has one spread to the other location, or are both independant primary cancers, or is really there no cancer in the pancreas? And if there is lung cancer (not just pancreatic cancer in the lungs), is its driving mutation a useful one like EGFR? Another thing that is odd is the use of x-ray to try to diagnose lung cancer instead of using a CT scan of the chest. My m-BAC lung cancer didn't even show up on an x-ray. I know that sometimes x-ray is sufficient for a solid tumor or if they know what they are looking for, but I think CT is the best diagnostic tool, esp. when dealing with mucinous BAC. Given the x-ray seemed to see something like infection or thin cancer in both lungs, and given that a biopsy found cancer is present (which makes it more likely that it wasn't infection in the other lung but cancer), it wouldn't surprise me if her doctors suspected stage IV cancer, but you really need to rely on her doctors' knowledge of her case and their experienced judgement about that. A CT might make it more obvious one way or the other, though. If doctors believe cancer has spread far in the body (either from one lung to a distant part of another lung, or from lung to pancreas or pancreas to lung), it indicates cancer cells are migrating through the bloodstream. In the case of lung cancer where cancer has spread far (stage IV), surgery is more likely to reduce the odds of surviving 5 years (which is already very small unless there's a driving mutation that can be inhibited and stays effective for a long time). (Reasons: I've heard the thought that surgery would reduce precious spare lung capacity without stopping the cancer, and the thought that surgery might disrupt blood supply making it harder for drugs to reach all the cancer cells. I don't know the real reason, but a surgeon told me that even in stage III the odds of surviving 5 years are cut in half if surgery is tried before chemo, so he recommended I not consider surgery and he reconfirmed that when an oncologist was able to say I was already stage IV. (When a surgeon tells me to not get surgery, I pay attention.) Why doesn't surgery stop the cancer? Because the cancer cells are already wandering around and may already have set up undetectable spots of cancer that would be missed. Two months after surgery to remove visible cancer those spots could become visible. So instead, when they have a reason to think cancer cells are wandering around, they prefer a systemic treatment like chemo that has a chance of affecting cancer cells wherever they are. FYI - I don't know anything about oxygen concentrator devices. Although there is probably little harm (except to your money and time) in trying non-medical things prior to strarting any medical treatment, it probably wouldn't be wise to rely on anecdotes or promotional sources instead of pursuing medical treatments with proven odds of effectiveness. For example, I don't know of any credible studies indicating effectiveness of the "cancer bush" idea. E.g., see: http://en.wikipedia.org/wiki/Sutherlandia_frutescens (BTW, treatments that "seem" to help might not be, and treatments for one kind of cancer usually won't help another kind.) There is no such thing as lung cancer that is "90% cured." What I think you mean is that a drug made the cancer shrink by 90%. Yes, that sometimes happens with drugs that are targeted to a specific driving mutation, like Tarceva for EGFR-driven cancer I described to you before. (Sometimes chemo can do that too, though the odds aren't as good as knowning you have the right driving mutation and a drug for it.) A treatment like this doesn't apply to every patient, but only patients who have the right driving mutation. (Driving mutation = the gene mutation that is driving the cancer to act like cancer, and if that were inhibited the cancer would behave like a normal cell or even shrink.) Tarceva (for EGFR) and Xalkori (for ALK or ROS1) are not "chemo" and are not "radiation." They have their own side effects, but usually easier to tolerate. Does that help? The new data you shared seems to make the picture more confusing, so I hope that can be sorted out. Best hopes, Craig

AnnieRSA, I can't see anything in that report that suggests it is Stage IV. That seems to be a histology report describing what is seen under a microscope and some test to determine if it is cancer and what type. I see they looked at samples from two lobes -- upper & lower -- so that has me guessing they might be referring to biopsy samples from the two lobes of the left lung, is that correct? I think it is possible to have cancer spread from one lobe to an adjacent one and not be classified as stage IV, but I'm no doctor and can't guess your mom's stage. Spread to lymph nodes is part of the staging calculation, but if she has what I think she has, she might not have any detectable spread to lymph nodes. (BTW, the right lung has 3 lobes -- upper, middle, & lower, while the left lung is divided into just 2 lobes; that's why I guessed this biopsy focused on the left lobe's two lobes.) From that report, it looks like they suspect it might be the mucinous BAC (bronchioloalveolar carcinoma) subtype of adenocarcinoma. I have m-BAC too so I can tell you some of the good and bad about that subtype, although your Mom's cancer is probably a variation driven by a different mutation than the very rare one driving mine so there can be some differences. One of good things about m-BAC is that it often (not always) grows more slowly than an average adenocarcinoma. Mine grows at about half the normal speed, and that gave me time for testing that gave me a new treatment track I wouldn't otherwise have had. It also is usually likely to stay confined to the lungs and not very likely to spread other organs, bones, brain, etc. m-BAC can sometimes change as it cosolidates and then start behaving more invasively and aggressively, but let's hope that doesn't happen. (I'm not expecting that in my own case.) One of the bad things about m-BAC is that it has often already spread undetectably to distant lobes and it can take a sharp-eyed oncologist or radiologist who is experienced with m-BAC to notice evidence of it over there in a CT scan. (If it has a slow metabolism, it probably won't show up on a PET scan except where it's consolidated into a tumor mass.) In those distant locations it might look like just a GGO (ground glass opacity) "haze" or cloudiness. Most of my m-BAC was and still is that cloudiness, and some is too hard for me to see on my CT scans but an expert can using better viewing software. That was my situation -- already spread to both lungs, although it took an expert with more experience than my local doctor to see it and interpret it correctly, saving me from surgery that wouldn't have helped me and would have left me worse off. If it's still in one lung, they might be hopeful it could be III still and they'd try chemo first. If her doctos are saying that surgery is not an option, it is probably at least stage III and maybe they are suspecting it is IV. I think you said her doctors sound like they've given up on your Mom, but do you mean that they don't expect any treatment they try will extend her life, or do you just mean they know the odds of cure are so small that they don't want to offer any false hope? If they know their field well, there should be hope of extending her life a while (at least until proven otherwise). One of the bad things about m-BAC is that there are anecodotal stories suggesting the odds of traditional cytotoxic chemo (poisons) working well on it may be lower than with regular, faster-metabolism adenocarcinoma. Such anecdotes can mislead some doctors into having low expecations for what can be expected from treating m-BAC patients. But such anecdotes are no better than individual case reports -- isolated examples are not reliable indicators of what a good clinical trial with lots of patients would really see. So we don't know if it really has different odds. I do know that some drugs (e.g., Alimta) do sometimes turn out to be useful to some m-BAC patients for a while, but patients vary. However, some m-BAC has a useful driving mutation like the EGFR I mentioned before (or ALK or mine which is ROS1), and something like that makes sense to try if the cancer reaches a point where the doctors consider it incurable. (An inhibitor drug for a driving mutation doesn't eradicate the cancer, it just inhibits it from acting badly; in contrast chemo has a chance of eradicating the cancer, although it's a small chance in late-stage cancer.) My local ocologist was delighted when a referral to a distant expert came back saying I had a useful driving mutation, and even more delighted to see the dramatic improvement I got on the drug very quickly. I think he was expecting only a bad downhill hard road for me with a lifespan of 2 years or so, but instead my clock has been turned back and the expiration date stamped on my butt is too fuzzy to read anymore. BTW, I know an m-BAC patient who has lasted 7 years since diagnosis so far (and she's been through all the hard stuff along the way -- surgery, chemo, 1st generation mutation-targed drug, and 2nd gen experimental mutation-targeted drug. And although the median time to progression for an EGFR-driven lung cancer on Tarceva (or Iressa) is only a number of months (9-10 months?), I've heard of lucky cases where someone is still alive after 7 or more years on the drug for that. That's pretty good given they only gave it to Stage IV patients. From what I hear, India offers most of the advanced medicine that can has been approved elsewhere, sometimes with a lag for the newer treatments (and not as many experimental drugs). India also offers traditional remedies that I haven't seen any clinical trials on. (I mean no trials involving dozens and then hundreds of patients to prove something works for a significant portion of them, and then try to find out who specifically benefits from what, with result published in critically-reviewed medical journals.) Given all the people in the world who promote things that aren't really effective, I can't rely on anything that isn't supported by credible published clinical research trials (or trials-in-progress). It's not worth 000 my life on something without any proof that it should work in me, not when there's something with proven odds of success available. That's my personal opinion and that of most medical doctors; it might one reason her doctors discourage the idea of traveling to India for approaches not grounded in medical research -- if there had been a proven miracle treatment available there for years, her doctors would already know about it, would have proven it in other trials, and would be using it. On the other hand, I'll speculate some doctors in India might be a little more on top of the latest lung cancer research from the USA and Asia than most in South Africa. But if what your Mom needs next is an EGFR test, then she should be able to get that done in South Africa or wherever she is. Re: air travel when one's lungs after surgery might have an issue with the air pressure, you might try to reach out to http://inspire.com/squanch for her thoughts on that. I think she was prevented from traveling for a while for that reason, but I think she's able to fly now. Best hopes, Craig

Unfortunately, it is not unusual for a never-smoker to be told there is nothing serious wrong and then be diagnosed with lung cancer. For example, I was told my x-ray showed no tumor yet a CT scan showed a 6 cm tumor and at least a little spread to all the lobes of both lungs. Either diabetes or cancer can cause weight loss, but not always. I had no weight loss. I am surprised to hear she has both diabetes and lung cancer, if understood you correctly. I wonder if there is any connection. There are many doctors who would be glad to see a patient and offer a 2nd opinion. I don't know any who would do that without seeing the patient, although I think I recall a service that would remotely review and comment on medical records for a big fee. I don't remember who it was, but they had no specialists who focused exclusively on lung cancer. For what it's worth, I am not a believer in promoted remedies that have not yet been proven to be effective in credible clinical trials, regardless how many centuries they have been practiced. If I can't read the research and see it isn't flawed, I assume I can't rely on promoters' claims. I'm also cautious to avoid things that might unknowingly interfere with my medical treatments while I'm getting them. Of course there are many people in India who disagree with my point of view. Best hopes, Craig in PA

AnnieRSA, If it has spread widely within both lungs, there's a good chance it's considered Stage IV. I'd assume that given her age, never-smoker status, gender, and ethnic background, there's a fair chance that she's got an adenocarcinoma, and then maybe the EGFR mutation. In the USA, a couple of not-for-profit organizations here estimate 15% to 18% of lung cancer is found in never-smokers (different %'s depending on which data they use). One of them believes it is 20% in women (10% in men). It is shame there is so much misperception in the world where most people assume that only smokers get lung cancer when, in reality, all people are at risk even if they seem to have no risk factors. I personally speculate that even if tobacco never existed a large portion of smokers who have lung cancer probably would have gotten it anyway. Best hopes, Craig in PA

Sorry to hear about that. Has a stage (I, II, III, IV) and/or specific type (adenocarcinoma, squamous cell, large cell, small cell, ...) been determined yet? BTW, East Asian never-smoker women with the adenocarcinoma type of lung cancer have something like an 70%-75% chance of having EGFR-driven cancer, and it may be similar in India. (That might be more due to behavioral and cultural factors and exposures than genes, but it's not known.) That can be useful because if it were EGFR-driven cancer, then if it progressed to a stage where it might be considered incurable (usually in Stage IV where it's spread far from the original site), an EGFR inhibitor like Tarceva (erlotinib) or Iressa (gefitinib) might have a good chance (something like 85%+ odds) of controlling EGFR-driven cancer for a number of months. EGFR status is determine by doing a gene mutation test on a biopsy sample. Other useful mutations (more likely in never-smokers) are ALK, ROS1, and a new one is emerging from the research called RET, though these are increasingly rare. Best hopes, Craig in PA (USA)