Colorectal Cancer: Understanding Your Pathology Report After Surgery

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Colorectal cancer is a cancer that starts in the lining of the large intestine, which includes the colon and the rectum. Almost all of these cancers begin in the gland-forming cells that line the inside of the bowel and grow outward into the wall. Pathologists call growth beyond the lining invasion. Once it happens, the cancer can reach nearby lymph nodes and, less often, spread to other parts of the body, which is called metastasis.

This article explains the pathology report created after surgery to remove a colorectal cancer, an operation that may be called a colectomy, a low anterior resection, or an abdominoperineal resection. It covers every item your pathologist is required to report, in the order you will find them, and it applies to all types of colon and rectal cancer. Reading it will help you understand what each term means and why it matters for your care.

Why your pathology report looks like a checklist

Most colorectal cancer pathology reports include a section that looks like a list of headings, each followed by a short answer. This is called a synoptic report, and it follows a standard checklist published by the College of American Pathologists (CAP) and used by laboratories across North America, Europe, and much of the world. The checklist makes sure that every feature known to affect treatment decisions is reported for every patient, in the same words, no matter which laboratory examined the tissue.

One checklist covers colon and rectal cancers together, so your report may list items that do not apply to your situation. Several items apply only to rectal cancers, and a report on colon cancer will mark them “not applicable.” When any item does not apply, the report will say something like “not identified,” “not applicable,” or “cannot be determined.” Seeing those phrases does not mean something was missed. It usually means the feature was looked for and wasn’t there, or that the removed tissue didn’t include the structure being asked about.

This particular checklist is used for cancer removed by an operation. A polyp removed during a colonoscopy is reported using a different checklist, and so are slow-growing neuroendocrine tumors (carcinoid tumors), lymphoma, and sarcoma. If your report does not match the items described here, it may have been written from one of those other checklists. Our guide to the colonoscopy biopsy report covers samples taken during a colonoscopy.

How is the diagnosis made?

A pathologist diagnoses colorectal cancer by examining a tissue sample under a microscope. In almost all cases, the first sample is a biopsy or a polyp removed during a colonoscopy, a procedure in which a flexible camera is passed through the bowel and tissue is taken from any abnormal area. Surgery follows, and the report described in this article comes from that surgical specimen.

The wall of the colon and rectum is built in layers. The innermost layer, the mucosa, contains the glands that line the bowel and sits on a thin sheet of muscle called the muscularis mucosae. Below that is the submucosa, then a thick muscle layer called the muscularis propria, then fat, and in some parts of the bowel an outer surface called the serosa. Under the microscope, the pathologist looks for tumor cells that have broken through the muscularis mucosae into the submucosa. That is the point at which a colorectal tumor is called invasive, because the submucosa is the first layer containing blood vessels and lymphatic channels large enough for cancer cells to travel through. Tumor cells confined to the mucosa are called intramucosal carcinoma or high-grade dysplasia and are not expected to spread.

Most colorectal cancers can be diagnosed based on tissue appearance alone. When the tumor is difficult to classify, the pathologist may perform immunohistochemistry, a test that uses colored stains to show specific proteins in tissue. Stains for CDX2 and CK20 help confirm that a tumor started in the colon or rectum rather than spreading there from somewhere else, and stains for synaptophysin, chromogranin, and INSM1 are used when a neuroendocrine carcinoma is suspected. After colorectal cancer is confirmed, imaging is performed to assess how far the disease has spread. This usually includes a CT scan of the chest, abdomen, and pelvis, and for rectal cancer, an MRI of the pelvis. A blood test for carcinoembryonic antigen (CEA) is often measured before surgery. The pathology report describes what was found in the removed tissue; imaging describes the rest of the body.

The operation that was performed

The first item on a colorectal cancer pathology report names the operation, which tells you which part of the large intestine was removed and sent to the laboratory as the specimen. Surgeons remove a length of bowel rather than just the tumor, because the blood vessels that supply that segment carry the lymph nodes that must be examined.

Right hemicolectomy — Removal of the first part of the colon, including the cecum and the ascending colon, and usually the last few inches of the small intestine.
Transverse colectomy — Removal of the section of colon that crosses the upper abdomen.
Left hemicolectomy — Removal of the descending colon on the left side of the abdomen.
Sigmoidectomy — Removal of the sigmoid colon, the S-shaped segment just above the rectum.
Low anterior resection — Removal of the rectum, or part of it, with the two cut ends joined together so that bowel function through the anus is preserved.
Total abdominal colectomy — Removal of the whole colon. This is performed when there is more than one cancer, or when the rest of the colon is diseased or at high risk.
Abdominoperineal resection — Removal of the lower rectum together with the anus, performed when a cancer sits too low for the bowel to be rejoined. This operation leaves a permanent colostomy.
Other, or not specified — Used when the operation does not match one of the categories above, or when the request form did not name it. The report will then describe what was received.

The report may also note that additional organs or tissue were removed with the bowel, or that lymph nodes were submitted as a separate specimen.

Tumor site: where in the bowel the cancer started

Tumor site names the part of the colon or rectum the colorectal cancer arose in. The pathologist selects every subsite the tumor involves so that a large cancer may have more than one name.

Right side — The cecum, the ileocecal valve, the ascending colon, and the hepatic flexure.
Middle — The transverse colon and the splenic flexure.
Left side — The descending colon, the sigmoid colon, the rectosigmoid junction, and the rectum.
Colon, not otherwise specified — The tumor is in the colon, but the exact segment could not be determined from the specimen or the information supplied.
Cannot be determined — The site could not be established, and the report explains why.

Cancers of the rectum are managed differently from cancers of the colon, and several items on this checklist are completed only for them. Which side of the bowel a cancer started on also carries real information. Cancers on the right side more often have a faulty DNA repair system, more often produce mucus, and respond differently to some drugs, while cancers on the left side more often respond to a class of treatments called anti-EGFR therapy. Your oncologist uses the site alongside the molecular results described later in this article.

For rectal cancers only, the report also states where the tumor sits relative to a fold of tissue called the anterior peritoneal reflection: entirely above it, entirely below it, straddling it, or not specified. This matters because the rectum is only partly covered by the smooth membrane that lines the abdomen. A tumor below the reflection is surrounded by fat rather than that membrane, which changes how surgeons assess margins and which treatments they consider before surgery.

Quality of the mesorectum (rectal cancer only)

The rectum sits inside an envelope of fat called the mesorectum, which contains the lymph nodes that drain it. In modern rectal cancer surgery, the surgeon removes that envelope intact, an operation called total mesorectal excision. After removing the rectal cancer, the pathologist examines the outer surface of the specimen before cutting into it and grades how completely the envelope was removed. Reports on colon cancers mark this item “not applicable.”

Complete — The mesorectum is bulky and smooth, with no defect deeper than 5 millimeters.
Near complete — The surface is irregular with defects deeper than 5 millimeters, but none reaching the muscle wall of the rectum.
Incomplete — There is little bulk to the mesorectum, and defects reach down to the muscle wall.
Cannot be determined — The specimen could not be assessed, and the report explains why.

The whole specimen is graded by its worst area. A complete mesorectum is associated with a lower chance of the cancer returning in the pelvis, and this item is one of the few places in pathology where the report describes the operation itself rather than the disease. A near-complete or incomplete result may be considered when radiation and follow-up are discussed.

Types of colorectal cancer (histologic type)

Histologic type describes what the colorectal cancer looks like under the microscope. Pathologists assign the type using the World Health Organization (WHO) classification of digestive system tumors. For most patients, the type is conventional adenocarcinoma, and the stage, the grade, and the molecular results carry more weight in treatment decisions than the type alone. A few of the types below behave differently enough that naming them changes how we understand the cancer.

Adenocarcinoma

Adenocarcinoma is by far the most common type of colorectal cancer, accounting for roughly 85 to 90 out of every 100 cases. It develops from the gland-forming cells that line the inside of the bowel. Under the microscope, the tumor cells form irregular glands and tubes that push through the wall, and the surrounding tissue often reacts by becoming dense and scar-like, a change called desmoplasia. Most of these cancers grow out of a precancerous polyp over a period of years, which is the reason colonoscopy screening prevents cancer rather than only detecting it.

When your report says adenocarcinoma with no further qualifier, it means the tumor shows the usual pattern and does not meet the criteria for one of the named types below. This is the expected result and not a sign that the tumor was hard to classify.

Mucinous adenocarcinoma

Mucinous adenocarcinoma is the second most common type, making up roughly 5 to 15 out of every 100 colorectal cancers. It is diagnosed when more than half of the tumor is made up of pools of mucin, the slippery substance normally produced by the lining of the bowel, with tumor cells floating in it. Mucinous cancers are more common on the right side of the colon and more often have a faulty DNA repair system, which is why the mismatch repair testing described later in this article matters particularly here. When a tumor contains mucin but less than half of it is mucinous, the report usually describes it as an adenocarcinoma with mucinous features rather than assigning the mucinous type.

Uncommon and rare types

Each of the following accounts for a small share of colorectal cancers, usually fewer than 5 out of every 100. Every one of them appears on the checklist, so your report may name a type you have never heard of.

Signet-ring cell carcinoma — More than half of the tumor is made of cells filled with mucin that pushes the nucleus to one side, so the cell resembles a ring with a stone. This type tends to spread earlier and carries a less favorable outlook than conventional adenocarcinoma of the same stage.
Poorly cohesive carcinoma — The tumor cells grow as scattered single cells rather than sticking together to form glands. It is closely related to signet-ring cell carcinoma and behaves similarly.
Medullary carcinoma — Sheets of large tumor cells surrounded by numerous immune cells. Although it looks high grade, it behaves as a low-grade cancer and carries a better outlook than its appearance suggests. It is strongly associated with a faulty DNA repair system and sometimes with Lynch syndrome.
Serrated adenocarcinoma — The tumor glands have a saw-toothed edge, and the cancer is thought to arise from a serrated polyp rather than a conventional adenoma.
Micropapillary adenocarcinoma — Small, tight clusters of tumor cells sitting in empty-looking spaces. It is frequently found alongside conventional adenocarcinoma and is associated with vessel invasion and spread to lymph nodes.
Adenoma-like adenocarcinoma — An invasive cancer whose surface looks like a benign adenoma, which can make it difficult to recognize on a small biopsy. It generally carries a favorable outlook.
Adenosquamous carcinoma — The tumor contains both gland-forming areas and areas made of flat, skin-like squamous cells.
Undifferentiated carcinoma — The tumor cells form no glands and produce no mucin, and they show no features that would place them in another category.
Carcinoma with a sarcomatoid component — Part of the tumor is made of spindle-shaped cells that resemble a soft tissue tumor rather than a carcinoma.
Large cell neuroendocrine carcinoma — A poorly differentiated neuroendocrine carcinoma made of large cells. It grows quickly and is treated differently from adenocarcinoma.
Small cell neuroendocrine carcinoma — A poorly differentiated neuroendocrine carcinoma made of small cells with very little cytoplasm. Like its counterpart in the lung, it grows quickly and is usually treated with chemotherapy regimens designed for neuroendocrine cancers.
Mixed neuroendocrine-non-neuroendocrine neoplasm (MiNEN) — A tumor containing both a carcinoma and a neuroendocrine carcinoma, with each part making up at least 30 percent. The report names both components, and treatment usually follows the neuroendocrine part.

If your tumor does not fit any listed category, the report will say “other histologic type” and describe what was seen. If the tissue was too damaged or too poorly preserved to classify, it will say “carcinoma, type cannot be determined.” Some reports add a histologic type comment, which is free text the pathologist uses to explain an unusual feature or a mixture of patterns.

Slow-growing, well-differentiated neuroendocrine tumors, sometimes called carcinoid tumors, are reported on a separate checklist and are not covered by the items in this article.

Histologic grade

Histologic grade describes how closely the colorectal cancer cells resemble the normal glands of the bowel. It is based on how much of the tumor forms recognizable glands, and it is reported on a four-tier scale.

G1, well differentiated — More than 95 percent of the tumor forms glands.
G2, moderately differentiated — Between 50 and 95 percent of the tumor forms glands. This is the most common result.
G3, poorly differentiated — Less than 50 percent of the tumor forms glands.
G4, undifferentiated — The tumor forms no glands and produces no mucin.
GX, cannot be assessed — There was not enough tumor left to grade reliably, which happens most often after treatment given before surgery.
Not applicable — Grading is not used for this tumor. Neuroendocrine carcinomas are classified by type rather than graded, and the report will say so.

Many oncologists group these four grades into two: G1 and G2 together are called low grade, and G3 and G4 together are called high grade. High-grade cancers are more likely to have spread to lymph nodes and are one of the features considered when adjuvant chemotherapy is discussed for a stage II cancer.

The grading scheme applies to conventional adenocarcinoma and not to the named types above. Medullary carcinoma is the clearest example: it looks poorly differentiated under the microscope but behaves as a low-grade cancer, so grading it in the usual way would be misleading. Pathologists also differ from one another in where they draw the line between grades more than they do for most other measurements, which is one reason grade is weighed alongside stage rather than on its own.

Tumor size

Tumor size is the largest measurement of the colorectal cancer, given in centimeters. Your report gives the greatest dimension and may add a second and third measurement. If the tumor could not be measured, usually because treatment before surgery left only scattered cells in a scarred area, the report says “cannot be determined” and explains why.

Size is recorded for every case, but in colorectal cancer it does not determine the stage. What determines the tumor stage is how deep the cancer has grown into the wall of the bowel, described in the tumor extent section below. A small cancer that has grown all the way through the wall is staged higher than a large one that has not. This surprises many patients, and it is worth checking the depth on your report rather than the measurement in centimeters.

More than one tumor (multiple primary sites)

This item records whether more than one separate colorectal cancer was found. Most reports say “not applicable,” meaning a single cancer was present. When more than one is found, the report says “present” and names the sites, for example, the hepatic flexure and the transverse colon.

Separate cancers in the bowel are staged individually, and the overall stage follows the highest stage rather than adding them together. When each cancer was removed in its own operation, the laboratory completes a separate checklist for each. When two or more are found in a single specimen, the lymph nodes usually cannot be separated, so one report is issued in which each tumor is labeled and described on its own, with shared findings such as margins and lymph nodes reported once. The letter “m” in brackets is added to the tumor stage to show that more than one cancer was present. Finding more than one primary cancer raises the possibility of an inherited condition, and it may prompt a discussion about genetic testing.

Tumor extent: how deep the cancer has grown

Tumor extent describes how far the colorectal cancer has grown through the layers of the bowel wall, from the inner lining outward. It is the single most important measurement on the report, because it determines the tumor stage.

No invasion (high-grade dysplasia) — Abnormal cells are confined to the lining and have not broken through the muscularis mucosae. This result usually appears when a polyp containing cancer was completely removed by polypectomy at colonoscopy, and the operation that followed found only residual high-grade dysplasia.
Invades lamina propria or muscularis mucosae (intramucosal carcinoma) — The tumor cells have moved into the supporting tissue of the lining but have not reached the submucosa. In the colon and rectum,m this is not expected to spread, and it is staged as pTis.
Invades submucosa — The tumor has broken through the muscularis mucosae into the layer beneath, where blood vessels and lymphatic channels run. This is the shallowest depth counted as truly invasive, and it is staged as pT1.
Invades into the muscularis propria — The tumor has reached the thick muscle layer of the bowel wall but has not passed through it. This is staged as pT2.
Invades through muscularis propria into the pericolic or perirectal tissue — The tumor has passed through the muscle layer into the fat surrounding the bowel. This is staged as pT3 and is the most common finding in operations performed for colorectal cancer.
Invades visceral peritoneum — The tumor has reached the smooth outer membrane covering parts of the bowel, either directly or through an area of inflammation. This is staged as pT4a.
Directly invades or adheres to adjacent structures — The tumor has grown into a neighboring organ or structure, which the report names. This is staged as pT4b. When the tumor was stuck to a neighboring organ during the operation but no tumor cells are found in the attachment under the microscope, the stage is based on the depth in the bowel wall instead.
No evidence of primary tumor — No cancer at all remains in the specimen. This result is seen after treatment given before surgery has eliminated the tumor.
Cannot be determined — The depth could not be assessed, and the report explains why.

Not every part of the large intestine has an outer peritoneal covering. The back surfaces of the ascending and descending colon and the lower rectum sit against other tissue rather than in the abdominal cavity, so the pT4a category does not apply there.

Depth of submucosal invasion

When the cancer has reached the submucosa, but not beyond, the checklist asks the pathologist to describe how deep it is. This item applies only to pT1 tumors, and reports on all other cancers mark it “not applicable.” Depth is reported as less than 1 millimeter, between 1 and 2 millimeters, or greater than 2 millimeters, and an exact measurement may be given. Some reports also describe which third of the submucosa the tumor reaches: upper, middle, or lower.

The chance that a pT1 cancer has spread to lymph nodes rises with invasion depth. It is very low when the tumor extends less than 1 millimeter into the submucosa and becomes meaningful at 2 millimeters or more. This measurement matters most when a cancer was found in a polyp removed at colonoscopy, because it is one of the findings used to decide whether an operation is needed at all.

Macroscopic tumor perforation

Perforation means a hole formed through the bowel wall at the site of colorectal cancer, allowing bowel contents to leak into the abdominal cavity. The pathologist records whether a perforation was visible on the specimen with the naked eye. Reports state “not identified,” “present,” or “cannot be determined.”

Perforation is uncommon, occurring in fewer than 1 in 10 patients. When it is present, the tumor is staged as pT4a, and the finding is associated with a higher chance that the cancer will return in the abdomen. Most patients whose report mentions perforation already know it happened, because it is usually the reason emergency surgery was performed.

Lymphatic and vascular invasion

This item records whether colorectal cancer cells were seen inside vessels in or around the bowel wall. Vessels are one route by which cancer reaches lymph nodes and distant organs, so finding tumor cells inside one indicates the cells have gained access to that route. It does not mean the cancer has spread. The checklist separates small vessels from large ones because they carry different information, and the pathologist selects every category that applies.

Not identified — No tumor cells were seen inside any vessel.
Small vessel — Tumor cells are inside thin-walled channels, meaning lymphatics and small blood vessels. This is what most reports mean by lymphovascular invasion, and it is associated with spread to lymph nodes.
Large vessel (venous), intramural — Tumor cells are inside a vein within the wall of the bowel. The significance of this finding alone is less clear than that of the next category.
Large vessel (venous), extramural — Tumor cells are inside a vein beyond the muscle layer, outside the wall of the bowel. This finding, often shortened to EMVI, is associated with a higher risk that the cancer will return and reach the liver. It is one of the features considered when chemotherapy is discussed for a stage II cancer.
Present, not otherwise specified — Vessel invasion was seen, but the type of vessel could not be established.
Cannot be determined — The finding could not be assessed, and the report explains why.

Veins can be difficult to recognize once a tumor has filled and destroyed them, so pathologists sometimes use an elastic stain, which colors the elastic fibers in a vein wall and reveals invasion that would otherwise be missed. Using it can double or triple the number of cases in which venous invasion is found, which is why two reports on similar tumors may differ on this item.

Perineural invasion

Perineural invasion means colorectal cancer cells were seen wrapped around or growing inside a nerve. Nerves run through the wall of the bowel and the fat around it, and they provide another path along which a tumor can extend. The report states “not identified,” “present,” or “cannot be determined.”

Perineural invasion is associated with a higher chance that the cancer will return and with shorter survival, independent of the stage. Like extramural venous invasion, it is one of the high-risk features taken into account when the decision about chemotherapy after surgery for a stage II cancer is finely balanced.

Tumor budding

Tumor budding describes single colorectal cancer cells, or clusters of fewer than five cells, sitting just ahead of the advancing edge of the tumor. The pathologist finds the area with the most buds, counts them within a measured field, and reports both the number and a score.

Low (0 to 4 buds) — The lowest category.
Intermediate (5 to 9 buds) — The middle category.
High (10 or more buds) — Associated with a higher chance of spread to lymph nodes.
Not applicable — Budding is scored only for conventional adenocarcinoma. It is not assessed in mucinous, signet-ring cell, micropapillary, or poorly differentiated tumors unless a conventional component is also present.
Cannot be determined — Inflammation or another feature obscured the tumor edge, and the report explains why.

Budding carries the most weight in two situations: a cancer found in a polyp, where a high score is one of the findings that may lead to an operation, and a stage II cancer, where a high score is treated as a high-risk feature when chemotherapy is discussed.

The polyp the cancer arose in

Most colorectal cancers develop from a precancerous polyp over years. When remnants of that polyp are still visible around the cancer, the pathologist names the type. Many reports say “none identified,” which means the cancer has overgrown and destroyed the polyp it came from.

Tubular adenoma — The most common precancerous polyp, made of crowded abnormal glands.
Villous adenoma — A polyp with long finger-like projections.
Tubulovillous adenoma — A polyp with a mixture of both patterns.
Sessile serrated lesion — A flat polyp with a saw-toothed outline, also called a sessile serrated adenoma or polyp. These are the usual precursor of right-sided cancers with a faulty DNA repair system.
Traditional serrated adenoma — An uncommon serrated polyp, more often found on the left side.
Hamartomatous polyp — A polyp made of a disorganized mixture of the normal tissues of the bowel. These are often associated with an inherited condition, so naming this type may lead to a referral for genetic assessment.
Other — A polyp type not listed above, which the report describes.

Treatment effect after treatment given before surgery

Some patients with colorectal cancer, most often those with rectal cancer, receive chemotherapy, radiation, or both before surgery. This is called neoadjuvant or presurgical therapy. When it has been given, the pathologist describes how much cancer is left and how much the treatment appears to have changed it, using a scoring system known as the modified Ryan scheme.

Score 0, complete response — No living cancer cells remain anywhere in the tumor site.
Score 1, near complete response — Only single cells or rare small groups of cancer cells remain.
Score 2, partial response — Cancer remains, and there is clear evidence that the tumor has shrunk back, but more than single cells or rare small groups are present.
Score 3, poor or no response — Extensive cancer remains with no sign of regression.
Present, not otherwise specified — A treatment effect was seen but was not scored.
No known presurgical therapy — The item does not apply because no treatment was given before the operation. This is what most reports on colon cancers say.
Cannot be determined — The response could not be assessed, and the report explains why.

Two details of this scoring often confuse. Treated tumors frequently leave behind pools of mucin containing no cancer cells at all, and these are counted as eradicated tumor rather than as residual cancer, so they do not raise the stage or count as a positive lymph node. And the response is scored on the main tumor only, not on the lymph nodes. Reports on patients treated before surgery use the letter “y” in front of the stage, written as ypT and ypN, to show that the stage reflects the cancer after treatment rather than before it. A complete response is associated with substantially better long-term outcomes. Tumor regression scoring is also used in some laboratories under other published systems, and your report will name the one it used.

Surgical margins

A margin is the cut edge of the tissue removed at surgery. For colorectal cancer, the pathologist assesses several different margins and measures how close the tumor comes to each. The report first gives a single overall statement, then details.

All margins negative for invasive carcinoma — No cancer cells reach any cut edge. The report usually names the closest margin and gives the distance in centimeters or millimeters, or states that the distance is greater than 1 centimeter.
Invasive carcinoma present at margin — Cancer cells reach a cut edge, and the report names which one.
Cannot be determined — The margins could not be assessed, and the report explains why.

The named margins are the following:

Proximal and distal — The two cut ends of the removed segment of bowel. For a low anterior resection, a distal margin of 2 centimeters is generally considered adequate, and 1 centimeter may be enough for a shallow tumor.
Radial (circumferential) — The surface created where the surgeon dissected the bowel away from the back of the abdomen or the pelvis. This margin matters most in rectal cancer.
Mesenteric — The cut edge of the fat and blood vessels attached to a segment of bowel that is fully wrapped in peritoneum.
Deep and mucosal — Reported for local excisions taken through the anus rather than for a full resection.

The radial margin is treated differently from the others. For rectal cancer, it is counted as positive when tumor is 1 millimeter or less from the inked surface, not only when tumor reaches the surface, because the risk of the cancer returning in the pelvis is similar at either distance. A positive radial margin raises that risk several-fold, which is why the distance is reported separately for every rectal cancer. The smooth outer peritoneal surface of the bowel is not a surgical margin, since the surgeon did not cut through it; tumor reaching it is recorded as pT4a instead.

For rectal cancers, the report gives two distances separately: the distance from the tumor to the radial margin and the distance from the tumor to the distal margin (the cut end below the tumor). If one of these was already given as the closest margin, the report says so rather than repeating the number.

Your report also states the margin status for non-invasive tumor separately, covering high-grade dysplasia, intramucosal carcinoma, and low-grade dysplasia at the cut ends. This matters most in patients with inflammatory bowel disease, whose remaining bowel may carry dysplasia even where there is no invasive cancer. Some reports add a margin comment, which is free text explaining an unusual finding. Similar comment fields exist for the tumor and lymph nodes, and a general comment section at the end of the report lists any test still in progress.

Lymph nodes

Lymph nodes are small immune organs found throughout the body. Colorectal cancer usually reaches the lymph nodes that sit alongside the blood vessels supplying the affected segment of bowel, and those nodes come out with the specimen. Whether cancer is found in them is the strongest single factor in staging colorectal cancer, and it is the main reason a length of bowel is removed rather than just the tumor.

Your report will include:

Number of lymph nodes examined — All the nodes the pathologist found in the tissue submitted. At least 12 is the accepted target, because the chance of missing an involved node falls as more are examined. Fewer than 12 does not mean the operation was inadequate: node counts are lower after radiation, in older patients, and in some individuals simply because of anatomy. When fewer than 12 are found, the pathologist re-examines the specimen for more.
Number of lymph nodes with tumor — An exact number, or “at least” a number when nodes were matted together and could not be separated.
Regional lymph nodes not applicable — No lymph nodes were submitted or found, which happens with small local excisions.

Two size categories are treated differently. Single cells or clusters measuring less than 0.2 millimeters are called isolated tumor cells, and a node containing only these is not counted as involved; the stage stays pN0, and the finding is described in a comment. Deposits between 0.2 and 2 millimeters are called micrometastases, and these nodes are counted as involved.

Extranodal extension, meaning cancer cells that have broken through the outer capsule of a lymph node into the surrounding fat, is not a required item on this checklist. Still, some pathologists describe it in a comment. Where it is reported in colorectal cancer, it is associated with a higher chance of recurrence.

Tumor deposits

A tumor deposit is a separate nodule of colorectal cancer in the fat around the bowel, within the area drained by the tumor, with no recognizable lymph node tissue. The report states “not identified,” “present” with the number found, or “cannot be determined.”

Tumor deposits are counted separately from lymph nodes and from vessel invasion, and the distinction is made by what surrounds the nodule. If the pathologist can identify the remnant of a vein wall around it, it is recorded as venous invasion. If it sits in or around a large nerve, it is recorded as perineural invasion. If it contains lymph node tissue, it is a positive lymph node. Only when none of these is present is it called a tumor deposit, and the nodule’s size and shape do not matter.

When tumor deposits are found, and no lymph node contains cancer, the nodal stage is recorded as pN1c regardless of how deep the tumor has grown, and chemotherapy after surgery is generally considered. When positive lymph nodes are also present, the nodal stage is based on the nodes, and the number of deposits is still recorded. After treatment given before surgery, a nodule of this kind may represent residual main tumor rather than a true deposit, so pathologists apply the term cautiously in that setting.

Distant metastasis

This item records whether colorectal cancer was confirmed under the microscope in a site outside the colon, the rectum, and their regional lymph nodes. It is completed only when tissue from that site was actually examined.

Not applicable — No distant site was sampled. This is what most reports say, because spread to other organs is usually assessed by imaging rather than by the pathologist.
Non-regional lymph nodes — Cancer in lymph nodes outside the drainage area of the affected segment of bowel. For rectal cancer, nodes along the external or common iliac vessels fall into this group.
Liver — The most common site of spread from colorectal cancer, because blood from the bowel travels to the liver first.
Other — Another site, which the report names. The lungs and the peritoneal surfaces are the next most common.
Cannot be determined — The finding could not be established, and the report explains why.

Pathologic stage (pTNM)

Pathologic stage summarizes how far the colorectal cancer had spread at the time of surgery. It is described using the TNM system from the American Joint Committee on Cancer (AJCC), 8th edition, where T describes how deep the tumor has grown, N describes the lymph nodes, and M describes spread to distant organs. The letter “p” in front means the category was determined by examining tissue under the microscope. M is almost always determined by imaging rather than by the pathologist, so most reports leave it blank or mark it not applicable.

Two prefixes may appear before the letters. A “y” means the stage was assigned after treatment given before surgery and describes what was present at the time of the operation rather than at diagnosis. An “r” means the tumor is a recurrence, staged after a period during which no disease was detectable.

The pathologic stage on your report is not the same as the overall stage group (stage I through IV) that your oncologist will discuss with you. The stage group combines the T, N, and M categories into a single number and is assigned by the treating physician using all available information, not by the pathologist. In broad terms, stage I is a cancer confined to the wall of the bowel with no involved nodes, stage II has grown through the wall with no involved nodes, stage III has reached the lymph nodes, and stage IV has spread to another organ. A report that reads pT2 does not mean stage II.

Tumor stage (pT)

The tumor stage for colorectal cancer is based entirely on how deep the tumor has grown into and through the wall of the bowel. The size of the tumor does not enter into it.

pT0 — No cancer remains in the specimen, seen after successful treatment before surgery.
pTis — Cancer confined to the lining, meaning intramucosal carcinoma or carcinoma in situ.
pT1 — The tumor has grown into the submucosa but not into the muscle layer.
pT2 — The tumor has grown into the muscularis propria.
pT3 — The tumor has grown through the muscularis propria into the fat around the bowel.
pT4a — The tumor has reached the visceral peritoneum, the smooth outer surface of the bowel, including through a perforation.
pT4b — The tumor has grown directly into a neighboring organ or structure.
pT4, subcategory cannot be determined — The tumor is pT4, but it could not be established which of the two categories applies.
pT not assigned — The category could not be determined from the material available.

The letter “m” in brackets after the T category means more than one separate cancer was present.

Nodal stage (pN)

The nodal stage is based on how many regional lymph nodes contain colorectal cancer, and on whether tumor deposits were found.

pN0 — No cancer found in the lymph nodes examined.
pN1a — Cancer in one regional lymph node.
pN1b — Cancer in two or three regional lymph nodes.
pN1c — No lymph node contains cancer, but one or more tumor deposits are present in the fat around the bowel.
pN2a — Cancer in four to six regional lymph nodes.
pN2b — Cancer in seven or more regional lymph nodes.
pN not assigned — No nodes were submitted or found, or the category could not be determined.

A node counts as positive when the deposit measures 0.2 millimeters or more.

Metastasis stage (pM)

The metastasis category is completed only when tissue examination confirms spread to a distant site. Otherwise, the report marks it as not applicable.

pM1a — Cancer confirmed in one distant site or organ, with no spread to the peritoneal surfaces.
pM1b — Cancer confirmed in two or more distant sites or organs, with no spread to the peritoneal surfaces.
pM1c — Cancer confirmed on the peritoneal surfaces, alone or together with other sites.
pM1, subcategory cannot be determined — Spread is confirmed, but the pattern could not be established.

Other findings in the colon and rectum

When a segment of bowel is removed for colorectal cancer, the pathologist examines the tissue around the tumor as well and records any additional findings. None of these change the stage, and most are common conditions found by chance. They are recorded because they affect follow-up.

None identified — The surrounding bowel was normal.
Adenomas — One or more additional precancerous polyps elsewhere in the removed segment. The number found influences how soon the next colonoscopy is scheduled. A large number of them raises the possibility of an inherited condition such as familial adenomatous polyposis.
Ulcerative colitis — A long-standing inflammatory condition affecting the lining of the colon and rectum.
Crohn disease — A long-standing inflammatory condition that can affect the full thickness of the bowel wall anywhere in the digestive tract.
Diverticulosis — Small pouches in the wall of the colon. This is very common with age and is unrelated to cancer.
Dysplasia arising in inflammatory bowel disease — Abnormal but non-invasive cells in a colon affected by ulcerative colitis or Crohn disease. This finding shapes decisions about how much bowel to remove and how to monitor the rest.
Other — Any additional finding, which the report describes.

Biomarker and molecular testing

Biomarker testing is part of the workup of every colorectal cancer. These tests measure specific proteins and genes in the tumor to determine which treatments are likely to work, and one also screens for an inherited condition. The results are reported on a separate CAP biomarker template rather than in the resection checklist, so they often arrive days or weeks after the main report, and your report may say that a test is pending. Some are performed on the original colonoscopy biopsy and repeated in the surgical report for completeness.

The biomarker template lists more items than any single patient will have tested. Which ones were performed depends on your cancer stage and your hospital’s practice, so a short biomarker report is not incomplete.

Mismatch repair and microsatellite instability

The mismatch repair system is a set of proteins that find and correct errors made when a cell copies its DNA. When one of these proteins is missing, errors accumulate in short repeated stretches of DNA called microsatellites, and the tumor is described as microsatellite unstable. Every colorectal cancer is tested for this, and it is the most consequential molecular result on the report.

Testing is done in one of two ways, and many laboratories perform both. Immunohistochemistry checks whether four proteins are present in the nuclei of the tumor cells, and each is reported on its own line as intact nuclear expression, loss of nuclear expression, or cannot be determined.

MLH1 and PMS2 — These two proteins work as a pair, and PMS2 is unstable without MLH1, so they are usually lost together.
MSH2 and MSH6 — These two also work as a pair, and MSH6 depends on MSH2 in the same way.
Intact nuclear expression — The protein is present. Staining is often patchy rather than even, and patchy staining still counts as intact.
Loss of nuclear expression — The protein is absent from the tumor cell nuclei.
Cannot be determined — The stain could not be interpreted, and the report explains why.

Your report may also state that the background non-neoplastic tissue, or internal control, showed intact nuclear expression. That line confirms the stain worked. Normal cells on the same slide, such as immune cells and the lining of the surrounding bowel, always carry these proteins, so if they failed to stain, the result in the tumor could not be trusted.

Below the four results, the report gives an interpretation in a full sentence. These are standard wordings, and yours will be one of the following:

No loss of nuclear expression of mismatch repair proteins — All four proteins are present, and the probability that the tumor is microsatellite unstable is low. This is the result in roughly 85 out of every 100 colorectal cancers. It does not completely rule out Lynch syndrome, because a small number of families carry a change that leaves a non-working protein still detectable by the stain.
Loss of MLH1 and PMS2 — Testing for MLH1 promoter methylation, BRAF V600E, or both is indicated to sort out the cause. This is the most common abnormal pattern, and most cases are not inherited.
Loss of MSH2 and MSH6 — High probability of Lynch syndrome, and germline testing of MSH2 may be indicated, followed by MSH6 if that is negative.
Loss of MSH6 only — High probability of Lynch syndrome, and germline testing of MSH6 may be indicated.
Loss of PMS2 only — High probability of Lynch syndrome, and germline testing of PMS2 may be indicated. PMS2 loss carries this meaning only when MLH1 is intact.

The word “probability” in these sentences is doing real work. None of them diagnoses Lynch syndrome. They describe what the tumor stain suggests and what test would answer the question, and only a germline test on a blood or saliva sample can confirm an inherited change. Reports also note exceptions to these interpretations, which is why genetic counseling is offered rather than a conclusion drawn from the stain alone. Prior radiation or chemotherapy can reduce or alter MSH6 staining, a recognized exception.

The second method tests the microsatellites in the tumor DNA directly, usually by polymerase chain reaction, and is reported as follows:

Microsatellite stable (MSS) — No markers show instability. This is the equivalent of intact expression of all four proteins.
Microsatellite instability-low (MSI-L) — One marker, or fewer than 30 percent of the markers tested, shows instability. This is managed in the same way as a stable result.
Microsatellite instability-high (MSI-H) — Two or more markers, or at least 30 percent of the markers tested, show instability. This is the equivalent of loss of one of the four proteins.
Cannot be determined — The test could not be interpreted, and the report explains why.

At least five markers are tested. Your report may name them individually and state whether each was stable or unstable. Two panels are commonly used: a five-marker mononucleotide panel, whose markers are called BAT-25, BAT-26, NR-21, NR-24, and Mono-27, and the older National Cancer Institute panel, which adds markers called D2S123, D5S346, and D17S250. Seeing this list of code names on your report means the laboratory has shown its work.

A deficient or unstable result carries three consequences. It indicates eligibility for immunotherapy drugs such as pembrolizumab, which work considerably better in these tumors than in others and are approved for this result regardless of where the cancer started. It carries a more favorable outlook in early-stage disease, and it indicates that chemotherapy with fluorouracil alone is unlikely to help a stage II cancer. It may point to Lynch syndrome, an inherited condition that raises the risk of colorectal, uterine, and several other cancers in the person and their relatives. Lynch syndrome accounts for roughly 2 to 3 out of every 100 colorectal cancers, while an acquired cause accounts for around 15 out of 100.

MLH1 promoter methylation

When mismatch repair testing on a colorectal cancer shows loss of MLH1 and PMS2, this test is performed to establish whether the cause was acquired during life rather than inherited. Methylation is a chemical tag that a cell can attach to a gene to switch it off. When the tag builds up on the switch region of the MLH1 gene, the cell stops making the protein even though the gene itself is normal. This happens in ordinary tumors and is not passed to children.

MLH1 promoter hypermethylation present — The loss of MLH1 is explained by an acquired change, and inherited testing is generally not indicated.
MLH1 promoter hypermethylation absent — The loss is not explained, which raises the possibility of Lynch syndrome and generally leads to a referral for germline testing.
Cannot be determined — The test could not be interpreted, and the report explains why.

KRAS and NRAS

KRAS and NRAS are genes that carry growth signals inside colorectal cancer cells. A mutation in either one switches that signal on permanently, so it no longer depends on the receptor above it in the chain. Both genes are tested, and the result matters for one specific treatment decision.

No mutation detected (wild type) — The growth signal still depends on the receptor above it, so drugs that block that receptor, called anti-EGFR therapies, can work. These include cetuximab and panitumumab. About half of colorectal cancers fall here.
Mutation identified — Anti-EGFR therapy is not expected to help, because the signal bypasses the receptor entirely.
Cannot be determined — The test could not be completed, most often because too little tumor was present in the tissue submitted.

When a mutation is found, the report names exactly where it sits in the gene. Four locations, called codons, are tested: 12, 13, 61, and 146. Your report may list which of them were assessed, which is worth checking, because a report that examined only codons 12 and 13 has not excluded a mutation at 61 or 146.

The mutation itself is written in a form that looks forbidding but is simple to read. In “Gly12Asp,” the number is the codon, and the two three-letter abbreviations are the amino acid that should be there and the one that replaced it, so this means that at position 12 a glycine has been replaced by an aspartic acid. The same change is often written as G12D. A version in brackets, such as “GGT>GAT,” gives the underlying change in the DNA letters. All of these describe one finding, not several.

One particular change, KRAS G12C, is now separately targetable in advanced disease, and drugs directed at it are used in combination with an anti-EGFR antibody. If your report names a KRAS mutation, it will also name the specific change, and your oncologist can tell you whether that change opens a treatment pathway.

BRAF

BRAF is another gene in the same growth signaling chain that carries signals inside colorectal cancer cells. The V600E mutation is found in roughly 8 to 12 out of every 100 colorectal cancers, more often in tumors on the right side and in mucinous cancers. It may be reported in two ways. An immunohistochemistry stain detects the abnormal protein directly and is reported as positive, negative, or undetermined. A DNA test is reported as no mutation detected, BRAF V600E detected, another BRAF mutation with the change named, or cannot be determined. Your report may name which changes the laboratory looked for.

This result does three things. In cancer that has spread, a V600E mutation indicates eligibility for a combination of encorafenib, cetuximab, and chemotherapy, which is approved as a first treatment for BRAF V600E colorectal cancer. It carries a less favorable outlook than tumors without the mutation, particularly in advanced disease. And when it is found alongside loss of MLH1, it effectively rules out Lynch syndrome as the cause, because this mutation is not seen in Lynch-associated tumors. A BRAF mutation also predicts that anti-EGFR therapy alone will not work.

PIK3CA

PIK3CA carries growth signals along a different route inside colorectal cancer cells, one that runs beneath both the receptor targeted by anti-EGFR drugs and the KRAS pathway. Almost all mutations sit in one of two regions of the gene, called exon 9 and exon 20, and the report states either that no mutation was detected or which exon the mutation was found in, with the specific change named.

The two locations do not carry the same meaning. Several studies have linked mutations in exon 20 to a poorer response to cetuximab in tumors that are otherwise RAS wild type. In contrast, exon 9 mutations tend to travel alongside KRAS mutations and have not shown an independent effect. The evidence is not settled, so this result is used as supporting information rather than as a decision on its own.

PTEN

PTEN is a brake on the same signaling route as PIK3CA, so losing it has an effect similar to switching that route on. In colorectal cancer, it may be reported by staining or by DNA testing.

Positive expression — The protein is present in the cytoplasm, the nucleus, or both. The brake is intact.
Negative for expression — The protein is absent from both, meaning the brake has been lost. This is reported in somewhere between 19 and 36 out of every 100 colorectal cancers, and the wide range reflects the fact that no standard method for scoring this stain exists.
No mutation detected, or a mutation identified — The DNA result, with the change named where one is found.
Cannot be determined — The test could not be interpreted, and the report explains why.

The role of PTEN loss in choosing treatment is not settled, and it does not currently determine eligibility for a drug on its own.

HER2

HER2 is a protein on the surface of cells that signals them to grow. Roughly 2 to 3 out of every 100 colorectal cancers make far too much of it, usually because the tumor carries extra copies of the HER2 gene. The figure rises to about 5 out of 100 among cancers that are RAS- and RAF-wild type, because HER2 overexpression and RAS or RAF mutation rarely occur in the same tumor. Testing begins with immunohistochemistry, which is scored from 0 to 3+.

Negative (score 0 or 1+) — Little or no HER2 protein is present, and HER2-directed treatment is not expected to help.
Equivocal (score 2+) — The protein result is in between, and a second test decides.
Positive (score 3+) — Strong staining in enough tumor cells. In advanced disease, this indicates eligibility for HER2-directed treatment, including tucatinib combined with trastuzumab in cancers that are also RAS wild-type, and trastuzumab deruxtecan.
Cannot be determined — The stain could not be interpreted, and the report explains why.

Alongside the score, your report may give the strength of the staining, described as none, faint or barely perceptible, weak to moderate, or strong, and the proportion of tumor cells showing staining around the edge of the cell, given as less than 10 percent, 10 to 49 percent, or 50 percent or more. It will also name the scoring system used, because colorectal cancer has no scoring system of its own and laboratories borrow one. The three in use are the breast cancer criteria, the stomach and esophagus criteria, and a set called HERACLES developed for a colorectal cancer trial. They differ mainly in how much of the tumor has to stain, which is why two laboratories can score the same tumor differently, and why the system is named on the report.

An equivocal result may proceed to in situ hybridization, often performed as fluorescence in situ hybridization, which counts gene copies inside individual cells and is reported as amplified (positive) or not amplified (negative). A dual-probe test also counts a fixed landmark on the same chromosome and reports the ratio between the two, along with the average number of HER2 signals per cell. HER2 may instead be assessed on a sequencing panel and reported simply as positive or negative for extra copies or a mutation in the gene.

Multigene expression assays

Some laboratories report a multigene assay that measures the activity of a panel of genes in a colorectal cancer and returns an estimate of the risk that the cancer will return. The result is given as low, moderate, or high risk, and often as a numeric recurrence score. These assays are not part of routine care in colorectal cancer the way they are in breast cancer, and where one has been performed, your oncologist can explain what weight it carried in the plan.

Other results on a molecular panel

Many patients with colorectal cancer that has spread have their tumor tested on a large next-generation sequencing panel that examines dozens or hundreds of genes at once. Several results from such a panel may appear on your report even though they are not items on the CAP biomarker template.

NTRK fusions — A rare finding in colorectal cancer, seen in fewer than 1 in 100 cases and most often in tumors that are mismatch repair deficient. A fusion indicates eligibility for larotrectinib or entrectinib, which are approved for this result regardless of where the cancer started.
Tumor mutational burden — A count of how many mutations the tumor carries, expressed as mutations per megabase. A high result, generally 10 or more, indicates eligibility for pembrolizumab across cancer types. In colorectal cancer, a high count almost always accompanies a mismatch repair deficient result.
POLE mutations — Rare, and associated with an unusually large number of mutations and a favorable outlook.
TP53, SMAD4, and RET — TP53 and SMAD4 changes are common in colorectal cancer and are reported for completeness rather than to determine a treatment. RET fusions are rare and may open a treatment or trial pathway.

How the testing was done

The biomarker report for colorectal cancer usually ends with a section describing the methods, so another laboratory can judge how much weight to give the result. A patient can use two items in it.

The first is the percentage of tumor cells in the tested sample, sometimes called cellularity. Sequencing tests need a minimum proportion of tumor cells to detect a mutation reliably, so a low percentage usually explains a result reported as cannot be determined. The second is the dissection method, which describes how the tumor was separated from surrounding normal tissue before testing: cut out under a microscope by the pathologist, cored from the block, or tested as a whole section with no separation. Both are recorded because they affect how confident the laboratory can be in a negative result. The section also names the specific test, antibody, or instrument used for each marker, and it may record how the tissue was preserved and how long it sat before preservation, since delays degrade the DNA.

You can read more about the tests described here in the Biomarkers and Genetic Testing section of this website.

What is the prognosis?

Prognosis is the expected course of a disease. For colorectal cancer, the outlook depends far more on how far the cancer had spread when it was removed than on any other single feature. When the cancer is still confined to the wall of the bowel, roughly 90 out of every 100 people are alive five years later. When it has reached nearby lymph nodes, that figure is about 73 out of 100. When it has spread to distant organs, it is closer to 15 out of 100, although this figure has been improving as surgery for liver spread and newer drug treatments have become more widely used. Across all stages combined, roughly 65 out of every 100 people diagnosed with colorectal cancer are alive five years later.

These figures describe large groups of people diagnosed years ago and cannot predict what will happen to any one person. Your own outlook depends on the combination of findings in your report, above all the following:

Lymph node status — The strongest single factor. Outcomes are best when no cancer is found in the nodes, and risk rises with the number involved.
Depth of invasion — Cancers confined to the wall of the bowel carry a lower risk of recurrence than those that have grown through it or reached a neighboring organ.
Tumor deposits — Their presence is associated with a higher risk of recurrence, even when every lymph node is negative.
Extramural venous invasion — Associated with a higher risk that the cancer will return in the liver.
Perineural invasion — Associated with a higher risk of recurrence and shorter survival, independent of stage.
Histologic grade — High-grade cancers recur more often than low-grade cancers of the same stage.
Margin status — A positive margin, and in rectal cancer a radial margin of 1 millimeter or less, raises the risk of the cancer returning at the operation site.
Mismatch repair status — A deficient result carries a more favorable outlook in stage II disease and identifies patients who respond well to immunotherapy when the cancer is advanced.
BRAF V600E — Associated with a less favorable outlook, mainly in cancers that have spread.
Number of lymph nodes examined — Outcomes in stage II disease are better when more nodes were examined, because the stage is more likely to be accurate.
Response to treatment given before surgery — Where presurgical treatment was given, a complete response is associated with substantially better long-term outcomes.

What happens after this diagnosis?

The pathology report for colorectal cancer is the document your treatment team uses to plan what comes next. A group that typically includes a surgeon, a medical oncologist, a radiation oncologist, a pathologist, and a radiologist coordinates care and often reviews reports together at a tumor board meeting.

The findings on your report shape several decisions:

Chemotherapy after surgery — Considered when lymph nodes contain cancer, and considered for a stage II cancer when high-risk features are present, such as growth through the wall to the peritoneal surface, perforation, a positive margin, high-grade histology, extramural venous invasion, perineural invasion, high tumor budding, or fewer than 12 lymph nodes examined. A mismatch repair deficient result generally weighs against chemotherapy with fluorouracil alone in stage II disease.
Radiation — Considered for rectal cancer, and usually given before surgery rather than after. If it was not given beforehand and the margins or nodes indicate higher risk, radiation after surgery may be discussed.
Further surgery — A positive margin may lead to a discussion about removing more tissue. When a cancer found in a polyp shows deep submucosal invasion, high tumor budding, vessel invasion, or a positive margin, an operation is generally considered.
Immunotherapy — Considered when the cancer is mismatch repair deficient and has spread or cannot be removed. Approaches that use immunotherapy instead of surgery in mismatch repair deficient rectal cancer are being studied in clinical trials.
Targeted therapy — Considered in advanced disease based on the KRAS, NRAS, BRAF, and HER2 results on your report.
Genetic assessment — Considered when the tumor is mismatch repair deficient without an acquired explanation, which raises the possibility of Lynch syndrome; when many adenomas were present, which raises the possibility of familial adenomatous polyposis; and when more than one primary cancer was found, when a hamartomatous polyp was identified, when the cancer was diagnosed at a young age, or when there is a family history.
Follow-up — Usually a colonoscopy within the first year after surgery, then at intervals based on what is found, along with CEA blood tests and CT scans for several years. Patients with a stoma also receive support from a specialist nurse.

If any part of your report is unclear, your treating physician can request the full report from the laboratory and go through it with you, and a second opinion on the pathology can be arranged if you would like one.

Questions to ask your doctor

What type of colorectal cancer do I have, and what does that type mean for me?
What does the tumor extent line on my report mean, and how deep did the cancer grow into the wall of my bowel?
What was the histologic grade, and is my cancer considered low grade or high grade?
How many lymph nodes were examined, and how many contained cancer?
Did the report find any tumor deposits, and what does that mean for my treatment?
Does my report mention lymphatic or vascular invasion, and was it small vessel or extramural venous?
Did you find perineural invasion, and what was my tumor budding score?
Were all my margins negative, and for a rectal cancer, how far was the tumor from the radial margin?
What are my mismatch repair or microsatellite instability results, and what do they mean for immunotherapy and for my family?
If my report says loss of nuclear expression of a mismatch repair protein, has MLH1 methylation or BRAF testing been done, and should I be referred for germline testing?
What are my KRAS, NRAS, BRAF, and HER2 results, and what treatments do they make available to me?
What is my overall stage group, and how does it relate to the pT and pN categories on my report?
If I had treatment before surgery, what was the treatment effect score, and what does it mean for my outlook?
What is the follow-up plan, and when will my next colonoscopy be?