beach sunrise wrote:Also, not sure what its all about but some use "Care Oncology" for support. Maybe others will let you know more about it.
beach sunrise wrote:Also, not sure what its all about but some use "Care Oncology" for support. Maybe others will let you know more about it.
rp1954 wrote:1. We stopped spread and most growth with modified Japanese immunochemo and ADAPT approaches with lots of alternative extras early on, with a lot of effort on targets and trials to identify good components and dosages specific for my wife.
2. Then we were able to get surgery when several mets reached ~2cm and were trying to breakout (extracapsular penetrations with fine root-like extensions). Normally various drs figured she was done for when they saw the initial spread early on but didn't say so too loudly to us. Doing extra everything continuously she contained her mets for a year, until the second surgery. The trick is to find a surgeon with the proven ability for the particular surgical task, the inclination AND stroke to get it done. Most wouldn't. Your mom's sites are bigger leagues.
3. My point of view is to do amped up mild chemo versions to stop cancer spread soonest and then chip out the worst chemo resistant sites surgically, if possible.
4. We found ADAPT+++ formulas for her, but that doesn't mean ADAPT (oral chemo + celecoxib) can be made to work everybody'. However even the basic ADAPT approach does have a lot of amazing cases including advanced spreads. ADAPT/ADAPT+++ probably needs extra skills and effort to maximize success.
One person on the forums did 7 surgeries, mostly repeats, finally doing the stuff to stop the spread on the 7th surgery...
The met record for successful surgery(s) I've read of, is about 100 mets.
The problem is that the "pros" are stuck about any idea of stopping new mets with mild off label formulas AND doing multiple surgeries (inoperable) because they "know" it can't possibly work. Also they need to protect themselves from criticism and lawsuits.
The longer you don't do a **successful** chemical formula, the harder it gets for true NED.
DIfferent patients have different situations as to what any given data can do for them, but without more data, you don't get meaningful choices.
Constraining (y)our data set to some average or below yokel's view, didn't make sense for us - we wanted to be ready for comparison with all research groups' papers if possible, precisely to not be cornered into average treatment (guidelines) with predetermined failures (and toxicity).
Sometimes conventional chemo may be best (e.g. simple PD1 inhibitors, when data show they can work on a clear target). Data, data, data...
catstaff wrote:The genetic information you posted indicates KRAS G12D (glycine, the normal amino acid, substituted by aspartic acid at a particular location) in at least some of the cells. This is the most common KRAS mutation in colorectal and pancreatic cancer and some others. This is like my husband's; he is also negative for HER2 and the other common mutations you mentioned, as well as microsatellite proficient (MSS).
Your mother's spread is also very similar to my husband's. He had distal retroperitoneal lymph node involvement when he was diagnosed, so it's no surprise where his recurrence came from, but once it's in the lymph nodes at all it can spread through the lymphatic system. It is, however, not the most typical spread for colorectal cancer (it may be more common for rectal than for colon), which usually goes to the liver or lungs.
Once it's disseminated through the lymphatic system it is regarded as incurable because they can't remove the lymphatic system. Thus the conventional wisdom that surgery doesn't do any good, so chemo only. If the small tumor is causing hydronephrosis, though, I'm surprised they weren't amenable to it since they've indicated for my husband they'll take out isolated lymph nodes and such if they're "causing a problem" and that seems to be causing a problem in your mother's case. However, even removing all the known sites would not cure the cancer because you can be certain that it's distributed through the lymphatic system now.
He is currently about to start cycle 4 of FOLFIRI plus bevacizumab. His CEA has gone down quite a bit already, though we'll learn tomorrow whether the trend will continue. This combination can be pretty effective (knock wood) on small mets. This is the standard second-line treatment for metastatic colorectal cancer. Our oncologist is very open to clinical trials and we tried to get him into one before starting folfiri but he was rejected. However, we're going to see how long the folfiri works and whether they'll consider removing the recurrence in his low pelvis, especially if he's able to have his colostomy reversal so he'd be having surgery anyway. I don't get to talk to the oncologist much since I can't accompany my husband to the infusions still, but he'll have a CT in about a month and I will be there for that discussion one way or another. He is finding this chemo pretty tolerable so far, which matches with the experiences many participants here have said about themselves or their family member. It's been much better than FOLFOX (which was a failure anyway).
PD1 inhibitors don't work by themselves for MSS cancers except in fairly unusual cases of particularly high mutation burden, which doesn't sound like the case here. Hence the trials pairing them with various vaccines. The clinical trial you linked looked interesting but would probably work best if your mother's cancer cells were strong CEA secretors--does her CEA go up with the growth of the mets?
rp1954 wrote:Sounds like your mom was not offered a compelling chemo and followup monitoring option, conventional or otherwise.
e.g. risk based biomarkers that highly predict who recurs without correct molecular treatments, no matter how unimpressive the molecule (cheap, lower toxicity, registered for other conditions), or more aggressive blood monitoring.
A compelling marker pair is the basis of adding cimetidine early on, for heavily CA199+CSLEX1 biomarked stage II/III patients, do it or die in the heavy marker cases despite an otherwise very favorable prognosis. CSLEX1 staining is not readily available in the US, but CA199 covers a lot of the probability.
This is one example of a possible treatment-marker/test pairing to add near initial diagnosis. I am not thinking cimetidine so much at this late date, especially w/o CA199 but if serum CA199 is high, in your shoes I might pursue the tissue stains in some circumstances, and CA199 has other implications.
There are many such pregnant possibilities with even less documentation - aspirin, celecoxib, PSK, vitamin C, D3, K2, flavonoids.
Your mom may be concerned of about treatment toxicity - conventional options are usually pretty intimidating.
We certainly were concerned about chemo but had the advantage of knowing after the first month, from surgical pathology, her supplemental package had worked. So we combined a mild daily chemo strategy added to the already demonstrated supplements and slowly tested more, based on papers or individual drs. The trick is to get enough immune and chemo activity without the big side effects for daily, long term use.
You need to be aware of overall options and that many non conventional options are not offered with full one stop shopping.
Or even offered at all, if decades have expired with their researcher. We parcel out our medical support and fill gaps at home.
Your mom's conventional options are probably:
Folfox + biological (Avastin or Erbitux/Vectibix);
Folfiri + biological (Avastin or Erbitux/Vectibix);
a Xeloda variant of the above;natural
or maybe, a PD1 inhibitor.
Patients often add some natural support during this time period, but may have tensions between their oncologist and their natural medicine support.
We had tissue work that suggested 5FU + the alternatives could actually beat oxi-, gem- or irinotecan combinations, as well as be used daily.
One somewhat popular mCRC/stage 4 option here that has no obvious major medical provider right now is ADAPT or "ADAPT+++",
(chronomodulated) UFT or Xeloda + celecoxib + aimed adjuncts/supplements
After 2+ years of daily chronomodulated UFT+cimetidine+aimed supplements, we did chronomodulated UFT + celecoxib + aimed supplements for years without the degradation and breakdown by normal chemo, precisely to stop circulatory and lymphatic spread. Your mom has much more serious lymphatic spread now than my wife and is harder to control. UFT is not approved in the US. Also the hydronephrosis is a complication that may or may not resolve with treatment.
Because of coxibs' noteriety I was reluctant about celecoxib until necessity favored it, and it worked but my wife also had episodes of hypercoagulability that had to be timely identified and dealt with, whether coxib related or not. Very definitely a skill - risk - benefit - QoL balance required there.
From my point of view, the best and quickest first estimate is post a CBC differential and a superchemistry (Chemo 20+++, LDH with CA199, more inflammation markers) up for discussion, fragility, and comparison. Incomplete bloodwork is a common problem that has to directly resolved by the patient, we can literally die waiting for agreement from insurance and drs.
Beza1422 wrote:How was the report for his CEA? I sent a private message to you and would like to further discuss a few things if you have the time of some clinical trials that are pending and what your husband has tried if that would be ok? I’m also confused on the typing KRAS G12D vs G12A (which was on my mom’s report today)?
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