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Living with cancer· Appointment prep

Appointment sheet: KRAS G12C-mutant pancreatic ductal adenocarcinoma

One page to bring and write on: your details, the questions for KRAS G12C-mutant pancreatic ductal adenocarcinoma plus your own, the words you may hear, what to bring, the treatments the standard of care names, and room for the answers and agreed next steps. What you type stays in this browser. Print it or save it as a PDF. New to all this? Start with the first 60 days. Orientation, not medical advice.

Tick the questions to print

All of this cancer's questions start ticked. Untick what does not apply; ticks are kept in this browser. .

Your own questions

Shared with the prep pack, so questions you add there appear here too.

Print or save as PDF

Use (or Ctrl+P, Cmd+P on a Mac). To keep a copy, choose Save as PDF as the destination in the print dialog. Only the sheet prints; the controls stay on screen. Your typed notes print where you typed them; empty fields print as ruled lines to write on.

Appointment sheet

KRAS G12C-mutant pancreatic ductal adenocarcinoma

Prepared with OnCo (onco.cc/prep/kras-g12c-pdac/). Orientation, not medical advice; your team knows your case.

My details

Name
Date of appointment
Hospital and clinician
Who is coming with me

What I know, what is unclear, changes to discuss

Saved in this browser
What I know so far
What is unclear to me
Changes since last time

My questions

17 on the sheet
Newly diagnosed
  1. 1.What is my exact diagnosis, stage, and grade, and which tests established them?
  2. 2.Which biomarkers have been tested on my tumour (for example KRAS G12C by tissue or plasma next-generation sequencing, Co-alterations in TP53, CDKN2A and SMAD4, Acquired KRAS mutations, KRAS amplification or receptor tyrosine kinase bypass at progression, CA 19-9 for response monitoring, Liver enzymes on a G12C inhibitor), and what were the results?
  3. 3.Which subtype is my cancer, and does that change the recommended treatment?
  4. 4.Is germline (inherited) genetic testing recommended for me or my family?
First line
  1. 5.For my situation (first line), which of the standard options do you recommend and why?
  2. 6.Am I a candidate for FOLFIRINOX / mFOLFIRINOX, NALIRIFOX (liposomal irinotecan + oxaliplatin + 5-FU/LV), Gemcitabine + nab-paclitaxel, and what side effects should I expect?
After first-line chemotherapy
  1. 7.For my situation (after first-line chemotherapy), which of the standard options do you recommend and why?
  2. 8.Am I a candidate for Daraxonrasib, Sotorasib, Adagrasib, and what side effects should I expect?
  3. 9.How do the results of RASolute 302 apply to someone like me?
Clinical trials
  1. 10.For my situation (clinical trials), which of the standard options do you recommend and why?
  2. 11.Am I a candidate for Elironrasib, Olomorasib, Glecirasib, and what side effects should I expect?
  3. 12.How do the results of Study of Elironrasib and Daraxonrasib as Monotherapies and Combination Therapy in Participants With Advanced KRAS G12C Mutant Solid Tumors and Study of LY3537982 in Cancer Patients With a Specific Genetic Mutation (KRAS G12C) apply to someone like me?
Any stage
  1. 13.Are there clinical trials I could join, for example of Elironrasib, Study of Elironrasib and Daraxonrasib as Monotherapies and Combination Therapy in Participants With Advanced KRAS G12C Mutant Solid Tumors, Olomorasib, Study of LY3537982 in Cancer Patients With a Specific Genetic Mutation (KRAS G12C)?
  2. 14.Would a second opinion at a high-volume centre change anything, and can you help arrange it?
  3. 15.What supportive care (symptom control, nutrition, exercise, mental health, financial help) is available from the start?
  4. 16.I read that “Responses to G12C-selective inhibitors are shallower and shorter in the pancreas than in the lung”. How does that affect my plan?
  5. 17.I read that “Neither sotorasib nor adagrasib has a pancreatic indication, so access depends on off-label use and trials”. How does that affect my plan?

The words I may hear

  • Oncogene: A gene that, when over-activated by mutation or extra copies, pushes a cell to grow and divide.
  • KRAS mutation subtypes (G12C, G12D, G12V): KRAS, the most commonly mutated cancer gene, comes in flavours named by the exact amino acid change.
  • CA 19-9: A sugar molecule shed into the blood by most pancreatic cancers; useful to follow treatment, not to screen.
  • Drug resistance (primary and acquired): Why cancer drugs stop working: the tumour either never depended on the target or evolves around the block.
  • Driver mutation: One of the few mutations in a tumour that actually causes it to grow.

Tests and results to bring

Biomarker results to ask for: KRAS G12C by tissue or plasma next-generation sequencing (about 1 to 2 percent of pancreatic adenocarcinomas), Co-alterations in TP53, CDKN2A and SMAD4, Acquired KRAS mutations, KRAS amplification or receptor tyrosine kinase bypass at progression, CA 19-9 for response monitoring, Liver enzymes on a G12C inhibitor.

Scans and tests linked to this cancer: Comprehensive genomic profiling, Liquid biopsy (ctDNA).

Bring copies of scan reports, pathology and blood results, and a list of every medicine and supplement.

The treatments I may be offered

From the standard of care recorded for this cancer; which apply depends on your stage and biomarkers. Ask which the team recommends and why.

Answers and next steps

Saved in this browser
What I was told
Agreed next steps, dates and who to call