2000miler

Percy – There are a lot of explanations on the web (Wikipedia, You Tube, etc.) concerning the “95% confidence interval,” “null hypothesis,” and p-value, but they generally involve statistical terms and numbers and are not representative of survival analysis.

The survival curves I’ve plotted so far are based on samples of cholangiocarcinoma.org data and the SEER data. Both of these databases are themselves only a sample of all the cholangiocarcinoma cases in the cholangiocarcinoma universe, which would be the world for cc.org and the USA for the SEER data. The curves are all approximate, since I’m working with a sample and not the whole universe. If I used another sample of the same size, I would get a different curve. If I had 100 samples, each the same size, I would get 100 different curves. On average, 95 of these curves would lie between an upper curve and a lower curve. This is the 95% confidence interval. The R statistical software I use plots the 95% confidence interval for each curve and I will do that for my corrected SEER IHCC curves to better illustrate this. I haven’t shown them in the past because they clutter up the plot.

The “null hypothesis” assumes there is no relationship between two measured phenomena. For example, in my last plot, the “null hypothesis” assumes that survival will be be the same with 0 or 1 positive node. If this was the case, the curves would lie on top of each other, but they could be separated solely because they are two independent samples. The question, are they separated because they are just two different samples, or are they separated because survival is dependent on positive nodes. The answer is in the p-value, which gives the probabilitiy that they are different because they are just two independent samples. Generally researchers would use a p-value equal to or less than 0.05 as evidence that the difference is because survival is dependent on positive nodes (>=95%) and not just different samples (<=5%) Bruce

Below are histology codes and malignant tumors found in SEER which are not intrahepatic cholangiocarcinoma but are considered as intrahepatic bile duct cancers.

8000/3: Neoplasm, malignant
8001/3: Tumor cells, malignant
8010/3: Carcinoma, NOS
8012/3: Large cell carcinoma, NOS
8020/3: Carcinoma, undifferentiated type, NOS
8031/3: Giant cell carcinoma
8032/3: Spindle cell carcinoma
8033/3: Pseudosarcomatous carcinoma
8041/3: Small cell carcinoma, NOS
8046/3: Non-small cell carcinoma
8050/3: Papillary carcinoma, NOS
8070/3: Squamous cell carcinoma, NOS
8124/3: Cloacogenic carcinoma
8140/3: Adenocarcinoma, NOS
8141/3: Scirrhous adenocarcinoma
8161/3: Bile duct cystadenocarcinoma
8180/3: Combined hepatocellular ca. & cholangiocarcinoma
8240/3: Carcinoid tumor, malignant
8246/3: Neuroendocrine carcinoma
8260/3: Papillary adenocarcinoma, NOS
8310/3: Clear cell adenocarcinoma, NOS
8440/3: Cystadenocarcinoma, NOS
8453/3: Intraductal papillary-mucinous carcinoma, invasive
8470/3: Mucinous cystadenocarcinoma, NOS
8480/3: Mucinous adenocarcinoma
8481/3: Mucin-producing adenocarcinoma
8490/3: Signet ring cell carcinoma
8500/3: Infiltrating duct carcinoma, NOS
8560/3: Adenosquamous carcinoma
8800/3: Sarcoma, NOS
8980/3: Carcinosarcoma, NOS
9100/3: Choriocarcinoma
9120/3: Hemangiosarcoma

Bruce

I haven’t done the extrahepatic CC cases yet, but I should be able to do those.

I was hoping to find SEER data to do the two components of extrahepatic cc separately. These two components are refererred to in the 7th edition of the AJCC as perihilar (aka Klatskin) and extrahepatic (aka distal).

CS Schema v0204 shows bile duct data as Bile Ducts Intrahepatic (11,789 patients), Bile Ducts Perihilar (13,099 patients) and Bile Ducts Distal (387 patients). Most of the Bile Ducts Distal data is from 2010, which was the year the 7th edition of the AJCC became effective and extrahepatic cc was divided into perihilar and distal. For 2010, bile duct data in CS Schema v0204 is divided into intrahepatic (881, 51.0%), perihilar (510, 29.5%), & distal (337, 19.5%). The distribution for extrahepatic cc is, perihilar (60.2%) and distal (39.8%). Using 39.8% for distal, I would have expected to see about 5,367 cases of distal bile duct cancer in CS Schema v0204, instead of the very small 387 cases that are there, so something is definitely wrong with the process in which pre-2010 cases of extrahepatic cc has been divided into perihilar and distal.

Bruce

This post was first postesd on 6/1/13 and edited on 6/4/13 to correct for the inclusion of Klatskin and other tumor data that was contained in the SEER Bile Duct – Intrahepatic file, but was not intrahepatic cholangiocarcinoma. This data has been eliminated in this revised analysis. Also, some surgery cases where the surgery could not be specifically identified as a resection were included in the previous analysis. These were mostly pre-1998 data where surgical codes were not included in SEER. These were also eliminated in this analysis.

This is my first analysis using SEER (Surveillance Epidemiology and End Results) data. I requested a CDROM when I submitted my application to SEER, but just received a username and password to their online data, so I just used that in this analysis.

SEER has several databases and sites containing cholangiocarcinoma data, some of which is duplication, and some of which is not. I used the database “Incidence – SEER 18 Regs Research Data + Hurricane Katrina Impacted Louisiana Cases, Nov 2012 Sub (1973-2010 varying)” and the Site and Morphology “CS Schema v0204” The SEER 18 database has the latest data which goes through 12/31/2010. I found Intrahepatic CC patients in three ofther Site and Morphology sections, but the CS Schema v0204 had the most, a total of 11,789.

The survival curves below show that a single postive node substantially reduces survival for patients who have resected intrahepatic cholangiocarcinoma.

In the analysis, I eliminated those patients with mutiple cancers, patients who had non-resection surgery, and patients who died from causes other than intrahepatic cc or its complications. A total of 355 patients were used in the analysis. These patients were diagnosed with intrahepatic cc from 1998 – 2010, median 2006. Their ages ranged from 17 – 84, median 59 years.

Median survival is 3.42 years for 0 positive LNs and 1.33 years for 1 positive LN. Statistical parameters for the analysis are Chsq = 33.9, 1 degree of freedom, p = 5.78 e-09. I wanted to do this analyis from the start using the posted Cholangiocarcinoma Foundation data, but never could find sufficient data to get a statistically significant comparison. However, I will add those to the plot in a later post to show comparison between those from the boards and SEER’s.

Bruce Baird

Marion – I think the secret is just keeping the vows made when we got married. Of course, my wife’s vow contained the word “obey.”

Bruce

Marion asked me on another board how my wife was doing, so I’ll respond here where I have her story.

In my last post on 1/30/13, I mentioned that, because of the fevers my wife had while she was on chemo, the oncologist decided to continue the chemo on a day by day basis, and to cancel plans for any radiation. Well, that all changed. My wife finished all four 2 wk on, 1 wk off, cycles of GemCis on 2/4/13. She started 25 M-F radiation treatments with 5FU on 2/25 and ended on 4/1/13, the day after Easter. She would have finished on Good Friday but Ochsner Radiation was closed on that day.

Since then she has gotten her life back, dancing 4 times/wk, playing bridge 3-4 times/wk, researching waste and corruption in Jefferson Parish politics and making presentations at the Jefferson Parish council meetings and other public meetings. We traveled to Michigan to see our granddaughter graduate from Michigan State University earlier this month, are having a big birthday party for her and her twin sister this June where our 4 children and 7 of our 8 grandchildren are coming to New Orleans, and are planning a cruise to the Panama Canal this October.

Bruce

A member asked me the following question off-line and my answer may be of interest to other members.

Qustion:
How does it look for someone with CC to be opened up by a surgeon and then be closed because of spread that the scans didn’t pick up?

My Answer:
I have compiled data for 557 members so far. Of these 557 members, I have 159 patients who had surgery to perform a resection. Of these 159, a total of 25 (15.7%) of these surgeries failed mostly because the cancer had spread and the spread had not been detected by prior scans and other tests.

Bruce Baird