March 23, 2017 at 9:15 pm #94368marionsModerator
Natalia….you mentioned CDKN2A/B (it is also possible the presence of ATRX, EPHA5, ERBB2, PDK1, POLE, RAD50, STAT3. Most often these type of labs also identify possible clinical trials you may qualify for. Not sure how it works with American Foundation, but had you looked at their recommendations if indeed the provide this type of information?
The problem with identification of DNA and molecular alterations is that some can be targeted, but it doesn’t necessarily mean that this particular alteration drives tumor growths. That is why targeted drugs are being tested in clinical research studies.
The way I understand your report is that perhaps the physician was not able to obtain clear margins at the surgery site. This happens frequently and not always can it be avoided.
Is there a possibility of consulting with an interventional radiologist? Perhaps the tumor location is suitable for radiation treatment.
Although we don’t have an established second line of treatment, perhaps another chemo combination could be considered.
Please know that I am a research advocate and not a clinician, hence you must make sure to discuss everything with your doctor.
We would really benefit from someone’s experience with failed BRAF inhibitors. Hopefully someone can help us out.
MarionMarch 22, 2017 at 10:44 pm #13123natasha77Member
many many thanks to all who support this site and share any infomation. There are no words to express how valuable it is in all parts of the world.
Sorry for my English, but i try to explain my story. I guess it could be valuable for others and i will be very grateful for any advice.
I knew about my CC in Nov 2015. Never ever liver diseases.
Procedures on 25 November 2015: celiacography, preoperative X-ray endovascular occlusion for left hepatic artery branches.
Surgical treatment on 7 December 2015: Anatomic resection of 2,3 liver segments using radio frequency ablation technique, cholecystectomia, pericardium resection, lymph node dissection from the hepatoduodenal ligament, omentulum, draining the abdominal cavity, pericardium cavity. Resected tumor`s size 12x7x13cm.
PET, CT, and MRI results in January 2016 show further spreading.
February 2 to 10, and February 25 to March 4, 2016, two chemotherapy courses with gemcitabine and oxaliplatin per treatment schema (patient height 170 cm, weight 52-53 kg):
day 1: gemzar 1400 mg intravenous
day 2: oxaliplatin 200 mg i.v.
day 8: gemzar 1400 mg i.v.
PET on 15 March 2016 shows further spreading, the growth has continued. Chemotherapy was stopped.
On 5 April and 5 May 2016 there were held 2 courses of intravenous droppers of pembrolizumab (keytruda, MK-3475) within the clinical trial of Merck – 200 mg intravenously.
MRI, CT in April-May 2016 – negative dynamics, the growth continued (significant numerous metastasizes: in retroperitoneal lymph nodes, hepatoduodenal lymp nodes, lungs, the gate of the liver, near pericardium, abdominal cavity, soft tissues of the feet, hands, etc.), ascites, independent decision to withdraw from the clinical trial.
On April 29, 2016 in connection with mechanical jaundice (bilirubin more than 105 micromolel) there was an emergent decompression of biliary tract – MRCP, bijouterie stenting of the common bile duct.
On April – May 2016 there were received the results of genetic analyses of the Moscow company Evrogen and Amercican Foundation in Cambridge, USA.
Evrogen identified mutation BRAF V600E along with the wild-type allele, the average level of expression of the protein PD-L1.
American Foundation identified BRAF v600e as well, CDKN2A/B (it is also possible the presence of ATRX, EPHA5, ERBB2, PDK1, POLE, RAD50, STAT3).
Staring from 18 May 2016 and till the current moment it is held the target chemotherapy by BRAF inhibitors: tafinlar 75mg/2times a day and mekinist 2mg/a day.
CT as of 15 July 2016 and PET as of 15 September 2016 – positive dynamics,
PET as of 16 December 2016 – lack of negative progression and no active tumor tissue (ALL PRIOR TUMORS DISSOLVED, it was a real miracle).
17 November 2016 stent was removed from the biliary ducts.
PET 7 March 7 2017 – identification of pathological area with hypermetabolism activity of the radiopharmaceutical 1.6×0.7cm (SUV7.00) in magadane seal in scar along middle anterior abdominal wall, the negative dynamics.
On 13 March 2017 puncture of the identified pathological area, results of cytology showed only blood cells.
21 March 2017 MRI with contrast was done.
Based on comparison of the following examinations:
•MRI as of 28 April 2016 (MRCP before stenting, recurrence in peak),
•MRI as of 7 October 2016 (MRCP before stent removal, no active tumor tissue per PET),
•MRI as of 21 March 2017 (hypermetabolism activity of the radiopharmaceutical per PET),
•PET as of 16 December 2016 (no active tumor tissue),
•PET as of 7 March 2017 (hypermetabolism activity of the radiopharmaceutical per PET)
MRI specialists made a conclusion that a number of pathological areas with hypermetabolism activity of the radiopharmaceutical 18 FDG exist. The average size 0.5-0.7 cm, they are located in the areas of prior tumors, recurrence after surgery.
10 March 2017 the blood was taken for analysis of BRAF V600E presence in plasma. The Moscow company Evrogen identified NO existence of this gene mutation in 15th exon of gene BRAF – in DNA of blood plasma.
i will be very grateful for any advice.
i will be very grateful for any information regarding further chemo treatment for patients with resistance on BRAF inhibitor.
two times i was in hell, then absolute disappearing of all tumors on BRAF inhibitor and now it looks like timer is switched on again. i do not know what to do.
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