How fast does adenocarcinoma grow??

Regarding the original question about growth rates:

My primary tumor (adenocarcinoma in head of the pancreas) was about 2.2 cm when totally removed by Whipple (June 15, 2022). It was non-existent on MRI in mid-July of 2022, but with no post-op chemo or radiation, it recurred and grew from nothing to 1.3 cm by the end of October 2022 (3.5 months) and to 2.0 cm on the Dec 2022 MRI 7 weeks later.

Everyone is different, but that seems to have grown pretty fast. 🙁 A similar thing happened while I was off chemo and on a clinical trial for 3 months last year. I don't have the exact before & after dimensions, but my primary tumor grew from "stable / not worrisome" to a complete gastric outlet obstruction (around 3 cm) in that time frame.

Mutations, previous treatment, tumor microenvironment, and whatever nutrients are/aren't available to and used by your cancer cells seem to have a large impact on the growth rates.

One reference [1] I have says, "It is generally believed that once a tumor has reached the size of clinical detectability (1 cm) it has already undergone about 30 doublings (2^30) to reach 10^9 cells. Only 10 more doublings are required to produce a tumor burden of 1 kg (2.2 pounds), which is usually lethal. The average doubling time for breast tumors has been reported to be 180 days while that for small cell lung cancer averages 86 days. (4 references cited internally)"

[1] Cancer Care: The Role of Repurposed Drugs and Metabolic Interventions in Treating Cancer / Paul E. Marik, 2nd edition - Norfolk, VA : Paul Marik Publishing, 2024.

* Yes, I am aware of some of the controversy surrounding Dr. Marik, his book, and the topic of repurposed drugs in general.

My searches for average doubling time of pancreatic adenocarcinoma returned such a wide range of results that I don't want to post them here.

---

Regarding "differentiated" cells: I may be improperly conflating things, but I've been reading and hearing a lot lately about cancer stem cells (CSCs).

I have zero background in biology, so I could be getting a lot wrong here, but... scientists figured out how to extract stem cells from pre-implantation human embryos in 1998. There was all kinds of speculation on the possible use of stem cells to treat various diseases because of their ability to "differentiate" into all the different cells types that comprise a fully developed fetus.

Most of the info below are copy/paste quotes w/o attribution from various Google AI query summaries.

Stem cells can be classified by their potential to differentiate. Totipotent and pluripotent describe embryonic stem cells. Multipotent, oligopotent, unipotent, and nullipotent describe adult somatic stem cells.

Induced pluripotent stem cells (iPSCs) are artificially created pluripotent stem cells from adult somatic cells, like skin or blood cells. This is achieved through genetic reprogramming to make them behave like embryonic stem cells, capable of differentiating into nearly any cell type in the body. Multipotent stem cells, on the other hand, are a type of adult stem cell found in various tissues, with a more limited differentiation potential than pluripotent stem cells.

Cancer cell "dedifferentiation," a process where mature cancer cells revert to a more primitive, stem-like state, is increasingly recognized as a contributor to tumor progression and treatment resistance. This phenomenon, also known as cellular plasticity, allows cancer cells to acquire properties like self-renewal and resistance to therapies, potentially driving tumor recurrence and metastasis.

It's my (untrained!) understanding that cancer stem cells may be harder to detect (thus false-negative biopsies) and harder to treat (chemo resistance) than "mature/differentiated" cancer cells.

I haven't yet found any clear explanations discussing "poorly/highly differentiated cells" on microscope/MRI versus cell differentiation in "stemness/evolution/development/maturity." Hopefully someone who passed a college biology class or two (Are you listening, @stageivsurvivor ? 🙂 ) can chime in and educate us all.

It seems like there is some correlation between the two concepts but also some conflict that could contribute to confusion.

Chiming in here from Lake Tahoe, CA where I am visiting a stage IV patient and getting a better care and treatment plan in place to improve the potential of a better outcome.

In replying to the question about treating actively growing tumor cells and those that are quiescent and have a "stemness" to them, chemotherapy works by various drug agents breaking DNA and intercalating into the damaged DNA. This shuts down vital processes of the cell. Each agent works at a specific point of the cell-either in the G2 growth phase, the synthesis phase where new DNA is being synthesized or during the phase of Mitosis where the tumor cell splits and becomes two daughter cells with equal amounts of DNA.

Tumor cells can go into a quiescent phase having a stem-like quality. They are in a G0 phase-essentially in a steady state of no growth or synthesizing new DNA. So it is for this reason that standard of care chemo regimens are not effective. The concern I had when I was under treatment was in trying to eliminate any minimal residual disease (MRD) and allow cells to reach this quiescent state. I never had a break, pause or delay in treatment. Low WBC counts were immediately addressed with Neulasta. Doing full-dose Folfirinox of 24 cycles and 22 cycles of 5-FU in groups of six may have eliminated most if not all MRD.

What oncologists feel was the "tipping point" who have familiarity with my case feel that the excessive amount of oxaliplatin converted the immunologically cold pancreatic tumors to immunologically hot tumors. This means the oxaliplatin component caused the tumor cells to express neoantigens (new protein clusters) on the cell surface making them visible to one's immune system cells such as macrophages, dendritic cells, antigen presenting cells and tumor infiltrating lymphocytes TIL's).

The TIL's develop long-term memory. Using dendritic cell vaccine therapy works in similar fashion whereby TIL's recognize these new proteins and have long-term memory. Researchers have discovered that tumor conversion can be achieved using cytokines and chemokines. This is much easier on the patient than massive amounts of oxaliplatin. Dendritic cell therapy is on the verge of now being effective in pancreatic cancer because of the discovery in how to convert immunologically cold tumors to hot ones. Keep an eye open for trials using dendritic cell therapy. PennMedicine/Abramson Cancer Center at the Hospital of the University of Pennsylvania is likely going to become a leader in this area.

This is off topic, sorry. But since cancer centers were mentioned - could I ask a question?
I don’t see MD Anderson, Houston, mentioned very often with these posts on PC. Is it known to have less of a focus on care in this area?

Tiny pancreatic cysts (2-3 mm) were found on a MRI while confirming left adrenal enlargement, June 2025 at Baylor Scott & White. Radiology reported they reflected BD IPMNs.
An abdominal CT scan at MD Anderson looking for tamoxifen related uterine cancer from 2024 did not show any pancreatic issues . . .but again, tiny cysts. I’m already a 2022 breast cancer patient at MD Anderson; I’m 3.5 hrs away from the center.

I have an October appt at MDA with a gastroenterologist to review the scan. I expect the recommendation will be for another scan in 2026 as this is so small.

However, if I need treatment in the future I’d want to be where the best care is and if I’m traveling it doesn’t matter the direction.

You can reach out to PanCAN.org for pancreatic centers of excellence; based mainly on volume of treatment I believe. MD Anderson is highly regarded in this field and many others. They may be one of the top facilities in terms of clinical trials. We don’t discuss facilities as much here, as we do managing symptoms and next steps. I hope that helps!

Wow, @stageivsurvivor, I feel like I'm in the university bio classes again ( which I never studied real well when I was in college)! We are so grateful that you have this level of understanding of cell behavior and can share that with us. It sounds promising. I found out I have a peritoneal nodule abutting the appendix and will ask oncologist today if we can just abstract the appendix. I'm somewhat concerned about the idea of mutated cell transferrence or spreading of cancer cells to healthy areas once you are fiddling with procedures in the body- what is your opinion of the risk of this type of spread? Does it make sense to do a noninvasive procedure like appendectomy to remove the nodule. I feel like my current oncologist has checked out" and is not really watching the candy store anymore.

When you say back pain, exactly where is the back pain?

I just stumbled across a good paper with some good references on growth rates. I can't write a proper summary at the moment, but include some quotes and links below:

The paper: https://pmc.ncbi.nlm.nih.gov/articles/PMC4520782/

Quotes:

"Evidence based on mutational analysis predicts that pancreatic cancers are confined to the pancreas for many years, perhaps a decade or more before spreading beyond the pancreas."

"Clinical experience indicates that most patients with advanced stage pancreatic cancer progress rapidly."

"We find, after adjusting for factors associated with age at diagnosis, the average age differences of patients with larger versus smaller T stage tumours is small and often not statistically significant, suggesting that most pancreatic cancers rapidly progress from lower to higher T stages."

"We estimate that the average T1-stage pancreatic cancer progresses to T4 stage in just over 1 year."
[ Good reference on tumor sizes (T1-T4) using the TNM scale at: https://www.cancer.org/cancer/types/pancreatic-cancer/detection-diagnosis-staging/staging.html ]

"This undetectable period of growth may represent the majority of the overall time to progression, since a founding cancer cell has to undergo many tumour doublings to become a detectable tumour (a 1 cm diameter tumour contains ∼1 billion cells), but only a few more doublings to grow into an advanced-stage tumour. The most relevant timeframe for early detection purposes is the time from when a cancer first becomes detectable by diagnostic tests up until it begins to progress beyond stage I disease. Although pancreatic cancer has a poor prognosis overall, patients with small stage I cancers have a better outcome than most patients with resectable cancers (mostly stage IIB)."

"Several studies have estimated the growth rate of various cancers using serial tumour marker measurements or serial CT scanning,21 but only limited data of this kind is available for pancreatic cancer. One study that measured serial serum CA19-9 and carcinoma embryonic antigen (CEA) measurements in patients with advanced stage disease estimated the average tumour doubling time of pancreatic cancers to be ∼40–60 days."
[Reference below]

"consistent with the hypothesis that once a pancreatic cancer is detectable by diagnostic tests, its growth and progression to more advanced stage disease is rapid. "

"We also found that larger primary pancreatic ductal adenocarcinomas were more likely to be poorly differentiated. There is evidence that tumour hypoxia which is likely to be greater in larger tumours contributes to the differentiation state of the tumour."

"In conclusion, we find using the adjusted average ages of patients with localised or locally advanced pancreatic cancer at diagnosis that disease progression is rapid, with an average estimated time of 14 months for a T1 pancreatic cancer to progress to the T4 stage."

----------

Reference for the "~40-60 days" tumour doubling time:
https://pubmed.ncbi.nlm.nih.gov/10404129/
Results: The doubling time of CA 19-9 and CEA could be calculated in 90.2% and 58.5% of patients with inoperable pancreatic cancer. CA 19-9 doubling time was clearly associated with survival time in inoperable and palliatively operated cases, but not with sex, age, site of the lesion, or liver metastasis, and was significantly correlated with the tumor volume doubling time.

Conclusions: Examination of CA 19-9 doubling time may be useful in clinical evaluation of the prognosis for patients with pancreatic cancer and could possibly prove valuable in terms of the analysis of the growth process in this disease.

Looking back, I believe this is right on for me. I had GI concerns but I minimized them by changing diet, exercise, and generally distracting myself. I did have ultrasound for pain once, that completely missed any signs.
Anyone in my family that has even mild issues will be screened beginning at 40

My back pain was right in the spinal column directly opposite the bottom
Of the breastbone.

I was diagnosed with Stage IV pancreatic cancer in March, with 6 months to a year left. I am 92, did not opt for treatment. I had a Celiac Nerve Block a month ago and have no pain around the pancreas. However, I am getting a lot of pain in the lower abdomen, which feels like pressure. Could this pressure be caused by the pancreas getting larger and pressing on other organs? My daughter keeps telling me that the pressure might be from som other condition, not the pancreas. But I am convinced that it is caused by the pancreas, as I near the 6 months time since diagnosis. Does anyone have any info about my symptoms? I would appreciate it. Thanks