TORADOL (ketorolac) linked to Recurrence Prevention
Comments
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Here is the graph I was talking about.
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Retsky referencing. the Reduction Mammo study. "But, as in surgeries with "raw" surface areas, such major plastic surgeries are associated with greater difficulties in hemostasis than lumpectomy (often performed on a day-case basis) or mastectomy. "
Me-- Raw areas--surgical words for capillary bleeding. A dry field is good. Depending on the type of surgery, cauterization or burning of bleeders is a consideration. Too much cauterization isn't good. Having just a bit of bleeding is good for wound healing. It's a line. It's not an absolute. Each surgeon knows how they like a wound bed to look at closure.
In the RED. MAMMO study it involved 4 PS's that worked in two hospitals. They came to anesthesia and said "We don't want anesthesia to use Toradol to be used on our patients" Genesis of the study. Study has it 's merits. No one studied the PS's surgical techniques. Could they have improved something?
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What would happen in the 36 - 48 month time frame if a patient was routinely taking an NSAID post op? Makes me go hmmmmm.....
Unfortunately there was no reference to NSAIDS post op in the study. -
123 is that the schematic
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What??? They call me Abby Normal 😀
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The point of the study was directed at only the perioperative use of Toradol with it's impact on interrupting the inflammatory cascade. If the studies hold true. A single use of a drug at pre-incison can change the course of recurrence.
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123. you posted a schematic . It was small I went to the study and found what looked like your pic Is that it?
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Forget et al. data were updated September 2011 and shown in hazard form but not smoothed as in fig. fig.7.7. Patient data are presented in the table. Patients included in this figure were less than 80 years of age, tumor less than 9 cm diameter and disease free survival greater than 2 months. It can be seen that relapses in months 9 -18 accounted for the major difference between ketorolac and non-ketorolac patients.
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123, still there?
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All the words in the world and then we look at a bar graph.............................and have a no chit moment
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Still here....
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In the bar graph what's happening in the Keto group between months 24-48? It looks like a higher recurrence for that group in that time period.
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Were those graphs the ones you were refrring too?
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Well no1 then I added the second.
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Yes that's the graph I was referring to.
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Getting close to DBF being home. Glad you got us to posting the graphs. I realize I like the bar graph versus the smooth graph. It brings to a point your question about the 36 -48 month in more graphic display. no clue what it means. Your question . Put it on the list to ask Retsky. Great question. Go girl
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123, shucks anyone looking at those graphs , either smooth or bar, and doesn't consider the value Toradol has a perioperative drug. Hmmm
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We need to continue this thread but you need to enjoy time with DBF! To be continued....
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Hugs 123, He just walked through the door and rubbed my shoulders
...................................to the pool....................... -
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123,
hope for la de da in the pool -
So....
Could the bump in the Keto group between 24 - 48 months be do to
1) non-compliance with hormone therapy
2) secondary inflammatory response
3) angiogenesis from wound healing
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Don't know, but write it in your question list to ask Retsky. 123, when the goal is to talk to the researcher, your focus needs to get more intense. The more intense you get, the more you analyse the work. Previous post I said, if you wanted me to talk to the researcher I would have to change my focus. I'm very happy to guide you to talk to him. You will totally love it. But preparation is everything to accomplish a good phone call. Say he turns out to be a total egotistical self absorbed analpore and he shut's you down. It's still fun. For the times I've done it, even including the CDC gal that said 'You have 5 minutes", it was a great learning experience. All but her were really nice folks.
Will look at your specific questions tomorrow and see if it's addressed in his study.
The first time I did it. I was intense about how EMT"s /paramedics were being trained in patient assessment. I called a guy that was on the national scene. We talked . He drew me into the national discussion. Ended up because of that initial phone call, I became involved in writing a book that changed the world. It was a great way to start LOL. But I went into that call immersed in what was, and what I believed it needed to be.
So, have faith that your preparation in calling Retsky will be fun and fruitfull.
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Lol! Working full time and doing rads the earliest I can pencil Retsky or anyone else will probably be some time in 2016! 😜
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okay that's off the discussion list
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Blood vessel cells help tumors evade the immune system
Date:
August 24, 2015
Source:
Karolinska Institutet
Summary:
A new study is the first to suggest that cells in the tumor blood vessels contribute to a local environment that protects the cancer cells from tumor-killing immune cells. The results can contribute to the development of better immune-based cancer therapies.
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FULL STORY
A study by researchers at Sweden's Karolinska Institutet is the first to suggest that cells in the tumour blood vessels contribute to a local environment that protects the cancer cells from tumour-killing immune cells. The results, which are being published in the Journal of the National Cancer Institute, can contribute to the development of better immune-based cancer therapies.
Immune-based antitumour therapies, that strengthen the body's own ability to fightcancer, have attracted great attention in recent years and achieved interesting success rates, especially in malignant melanoma. However, many patients still do not respond to immune-based therapies.
The results from the current study imply that tumour pericytes, a cell that is part of the tumour blood vessels, critically manipulate the tumour environment, helping the cancer cells escape immune surveillance.
"Understanding the interplay between tumour pericytes, malignant cells, and the immune system might help in designing more personalised and effective therapeutic approaches," says Principal Investigator Guillem Genové at the Department of Medical Biochemistry and Biophysics at Karolinska Institutet.
Tumours evade the immune system by a variety of mechanisms, one of them being the recruitment of so called 'myeloid-derived suppressor cells' (MDSC). MDSCs suppress the ability of killer T-cells to destroy cancer cells. It is known that the more MDSCs present, the worse the prognosis or therapy response of the patient. Tumours secrete signal molecules such as interleukin-6 (IL-6) that help in recruiting MDSCs, but the mechanisms behind IL-6 tumour secretion are quite unknown.
The researchers found that the higher the number of pericytes, the more "normal" the tumour environment looked like. On the contrary, diminished pericyte numbers altered the microenvironment and correlated to higher IL-6 expression from the malignant cells and more MDSCs. They also identified a subset of breast cancer patients who had fewer pericytes and increased MDSCs, correlating to a worse prognosis and more aggressive characteristics of the tumour.
"Our work suggests that ways to increase the numbers of pericytes could potentially decrease IL-6 expression. This could improve cytotoxic T-cell activity and result in better antitumour effect," says Dr Genové.
The research was supported by grants from, among others, the Swedish Cancer Foundation, the Strategic Cancer Research Program (StratCan) and BRECT Breast Cancer Theme Centrum at Karolinska Institutet, and the Swedish Research Council-supported STARGET Linneus Center of Excellence.
Story Source:
The above post is reprinted from materials provided by Karolinska Institutet. Note: Materials may be edited for content and length. -
Wonder if this is part of the explanation for the 24 - 48 month increase in recurrence ....
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Retsky
Using Computer Simulation to Analyze Bimodal Relapse Pattern
Based on computer simulation, to explain the 10 month peak we postulated that induction of angiogenesis at the time of surgery provoked sudden exits from dormant avascular phases to active growth and then to detection. That mode is quite sharp and most often seen among premenopausal patients with axillary lymph node involvement (N+). We suggested the remainder of relapses within the first 40 or so months to be surgery-induced growth of previously dormant single malignant cells. We proposed that the broad late peak relapses result from steady stochastic progressions from single dormant malignant cells to avascular micro-metastases and then on to growing deposits with no apparent synchronization to the time of surgery.
Most Important Finding – Early Relapses are the Result of Something that Happens at Surgery
The most important finding of this early work is that something happens at or about the time of surgery to accelerate or induce metastatic activity that results in early relapses. These early relapses comprise over half of all relapses. Surgery-induced angiogenesis of dormant avascular micrometastases and surgery-induced activity of single malignant cells are implicated. Late relapses are apparently not accelerated by surgery but the shallow peak at 5 years occurs as a result of shedding from primary ceasing after primary removal. We have been vigilantly looking for new data with which we can learn more about surgery-induced tumor activity and that perhaps will also lead to improved outcomes. As we describe here, there has been an important development.
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Interesting! Very interesting!
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