Adenocarcinoma of the Esophagus: Understanding Your Pathology Report

by Catherine Forse MD FRCPC and Jason Wasserman MD PhD FRCPC
July 29, 2026

Adenocarcinoma of the esophagus is a type of cancer that develops from the gland-forming cells lining the esophagus, the muscular tube that carries food from the mouth to the stomach. The word adenocarcinoma means the cancer arose from glandular cells, the cells that normally make and release mucus.

This cancer almost always starts in the lower part of the esophagus, close to where it joins the stomach, in an area called the gastroesophageal junction. In some cases it extends into the uppermost part of the stomach. It is the most common type of esophageal cancer in North America, Europe, and Australia, and its frequency has risen substantially over the past several decades.

This article will help you understand the findings in your pathology report, what each term means, and why it matters for your care.

What causes adenocarcinoma of the esophagus?

Most adenocarcinomas of the esophagus develop in people who have Barrett esophagus, a change in the lining of the lower esophagus. In Barrett esophagus, the normal flat squamous cells that line the esophagus are gradually replaced by glandular cells resembling those found in the intestine, including goblet cells. This change is called intestinal metaplasia, and it develops because long-standing gastroesophageal reflux disease (GERD) allows stomach acid and bile to damage the esophageal lining over and over again.

Over years, these abnormal glandular cells can accumulate further genetic damage and progress to dysplasia, a precancerous change in which the cells look increasingly abnormal under the microscope. Dysplasia in Barrett esophagus is classified into two levels:

Low-grade dysplasia — The cells look mildly abnormal. The risk of progressing to cancer is real but relatively low, and the finding is usually managed with close monitoring or endoscopic treatment.
High-grade dysplasia — The cells look markedly abnormal and disorganized. The risk of progressing to invasive cancer is much higher, and this change is often found alongside or next to an early adenocarcinoma.

If your report mentions dysplasia near the tumor, it supports the conclusion that the cancer developed through the Barrett esophagus pathway. With large or deeply invasive tumors, the surrounding Barrett esophagus and dysplasia may have been overgrown by the cancer and may no longer be visible in the specimen. Its absence does not change the diagnosis.

Other factors that raise the risk of adenocarcinoma of the esophagus include obesity, particularly weight carried around the abdomen, smoking, male sex, older age, white European ancestry, and a family history of Barrett esophagus or esophageal adenocarcinoma. This cancer is several times more common in men than in women and most often occurs in people over 60.

What are the symptoms of adenocarcinoma of the esophagus?

The most common symptom of adenocarcinoma of the esophagus is difficulty swallowing, called dysphagia, which typically begins with solid foods such as bread or meat and progresses over time to softer foods and liquids. This happens because the growing tumor narrows the opening of the esophagus.

Other symptoms include unexplained weight loss, pain or discomfort in the chest or upper abdomen, pain on swallowing, heartburn or reflux that has changed in character, nausea, and vomiting. Some people are diagnosed after investigation of anemia, a low red blood cell count caused by slow bleeding from the tumor surface. A smaller number of cancers are found before any symptoms appear, during a surveillance endoscopy in someone already known to have Barrett esophagus, or incidentally during an endoscopy or imaging test done for another reason.

How is the diagnosis made?

The diagnosis of adenocarcinoma of the esophagus is made only after tissue from the esophagus is examined under a microscope by a pathologist. The tissue is obtained during an upper endoscopy, also called a gastroscopy, in which a thin flexible tube with a camera is passed through the mouth into the esophagus. Small tissue samples, called biopsies, are taken from any abnormal-looking area. For very early tumors, the abnormal lining may instead be removed in one piece by endoscopic mucosal resection or endoscopic submucosal dissection.

Under the microscope, the pathologist looks for abnormal gland-forming cells that have broken out of the surface lining and are growing into the tissue beneath, a process called invasion. The glands are irregular, crowded, and often fused together; the cells show atypia with enlarged and dark-staining nuclei, and the surrounding tissue often reacts by becoming dense and scar-like, a change called desmoplasia. The report may describe the way the cancer cells are arranged using terms such as tubular, papillary, mucinous, or signet ring cell. Tubular is the most common, and more than one pattern is often present in the same tumor. These are descriptions of growth pattern rather than separate diseases, although tumors made up largely of signet ring cells or of mucin pools tend to behave less favorably.

Immunohistochemistry, a test that uses antibodies to detect specific proteins inside cells, may be performed when the diagnosis is not straightforward on a small biopsy. Adenocarcinoma of the esophagus usually shows cytokeratin 7 (CK7) and often CDX2, and lacks the squamous markers p40 and p63. This pattern helps separate adenocarcinoma from squamous cell carcinoma, the other main type of esophageal cancer, and helps confirm that a cancer found elsewhere in the body started in the esophagus or stomach. These stains identify what the tumor is; they are different from the biomarker tests described later, which guide the choice of drug therapy.

Once cancer is confirmed, imaging is used to determine how far it has spread before treatment is planned. This usually includes a CT scan of the chest and abdomen, a PET scan, and endoscopic ultrasound, which uses sound waves from inside the esophagus to estimate how deeply the tumor has grown and whether nearby lymph nodes look abnormal.

Tumor location and the gastroesophageal junction

Because adenocarcinoma of the esophagus usually arises at the lower end of the esophagus, your report will state exactly where the center of the tumor was located. This matters because the same tumor is staged differently depending on which side of the gastroesophageal junction its center sits.

Under the current staging rules, a tumor whose center lies in the esophagus, at the gastroesophageal junction, or no more than 2 cm into the upper stomach is staged as an esophageal cancer. A tumor whose center lies more than 2 cm into the stomach is staged as a stomach cancer, even if it grows upward into the esophagus. Some reports also use the Siewert classification, which divides junctional tumors into types I, II, and III based on how far above or below the junction the center of the tumor lies.

This is a technical rule about which staging system applies, not a statement about how serious the cancer is. If your report and your medical team seem to describe the tumor differently, as esophageal in one place and gastric in another, this rule is usually the reason.

Histologic grade

Histologic grade describes how closely the cancer cells in an adenocarcinoma of the esophagus resemble the normal gland-forming cells they came from. The pathologist assigns the grade by estimating how much of the tumor still forms recognizable glands.

Grade 1 (well differentiated) — More than 95% of the tumor forms well-organized glands. These tumors most closely resemble normal tissue.
Grade 2 (moderately differentiated) — Between 50% and 95% of the tumor forms glands.
Grade 3 (poorly differentiated) — Less than 50% of the tumor forms glands, and in some areas no gland formation is seen at all. The cells look markedly abnormal.
GX — The grade could not be assessed, usually because the sample was too small or too altered by prior treatment.

Grades 1 and 2 are often grouped together as low grade, and grade 3 as high grade. Higher-grade tumors tend to grow more quickly and are more likely to have spread to lymph nodes at the time of diagnosis. For early esophageal adenocarcinomas that have not spread to lymph nodes, grade also feeds directly into the final stage group, so the same depth of invasion can produce a different stage depending on the grade. Grading a small biopsy can be difficult, and the grade is sometimes revised after the full surgical specimen is examined.

Depth of invasion

Depth of invasion describes how far an adenocarcinoma of the esophagus has grown into the wall of the esophagus, and it is one of the most important findings on the report. The esophageal wall is built in layers:

Mucosa — The innermost lining, where adenocarcinoma begins. It contains the surface epithelium, the lamina propria (a thin supportive layer), and the muscularis mucosae (a thin band of muscle at its base).
Submucosa — A supportive layer just beneath the mucosa that carries the larger blood vessels and lymphatic channels. Once a tumor reaches this layer, the risk of spread to lymph nodes rises sharply.
Muscularis propria — The thick muscle layer that contracts to push food toward the stomach.
Adventitia — The outermost connective tissue that anchors the esophagus in the chest.

Unlike most of the digestive tract, the esophagus has no serosa, the smooth outer membrane that elsewhere acts as a barrier. This is one reason esophageal cancers can grow into neighboring structures such as the windpipe, the aorta, or the lining around the heart. The deepest layer the tumor reaches determines the pathologic tumor stage (pT), described further below.

Lymphovascular invasion

Lymphovascular invasion means that cancer cells from the adenocarcinoma were seen inside a small blood vessel or lymphatic channel within or around the esophageal wall. It is reported as present or absent.

These channels carry fluid and cells away from the esophagus, so tumor cells inside them may travel to nearby lymph nodes or, through the bloodstream, to distant organs. Lymphovascular invasion is one of the strongest predictors of lymph node involvement in esophageal adenocarcinoma. Its presence may influence whether chemotherapy or radiation is considered in addition to surgery, and in very early tumors it often shifts the discussion away from endoscopic treatment alone.

Perineural invasion

Perineural invasion means that cancer cells were seen surrounding or growing into a nerve. Nerves run through the tissue in and around the esophageal wall, and cancer cells that reach them can use them as a pathway into nearby tissue. Your report will state whether perineural invasion is present or absent.

Perineural invasion is associated with a higher risk that cancer will return near the original site and with poorer outcomes overall. It is one of several findings the treatment team weighs when deciding whether additional treatment after surgery should be discussed.

Treatment effect

Many people with adenocarcinoma of the esophagus receive chemotherapy, or chemotherapy combined with radiation, before surgery. This is called neoadjuvant therapy, and it is given to shrink the tumor, treat cancer cells that may have already spread, and improve the chance that surgery removes everything. When the esophagus is removed after this treatment, the pathologist assesses how much living cancer remains and assigns a treatment response score, most often using the modified Ryan scheme:

Score 0 (complete response) — No living cancer cells remain anywhere in the specimen. This is the most favorable result and is associated with the best long-term outcomes.
Score 1 (near-complete response) — Only single cancer cells or rare small clusters remain. Nearly all of the tumor was destroyed.
Score 2 (partial response) — Residual cancer is present, but there is clear evidence that treatment shrank the tumor, such as scarring or pools of mucin where the tumor used to be.
Score 3 (poor or no response) — Extensive cancer remains with little or no evidence that the tumor responded.

Because treatment can leave scattered surviving cells behind, the pathologist examines the entire area where the tumor was, called the tumor bed, and often takes additional tissue sections before concluding that no cancer remains. Pools of mucin or scarring without living cancer cells do not count as residual tumor. When the specimen was removed after neoadjuvant therapy, the stage on the report carries a “y” in front of it, written as ypT and ypN. A complete or near-complete response is associated with a substantially better prognosis, and the score is always interpreted alongside the stage and the other findings on the report.

Surgical margins

A margin is the cut edge of the tissue removed during surgery for adenocarcinoma of the esophagus. The pathologist inks these edges and examines them under the microscope to determine whether cancer cells reach the cut surface. Several margins are examined and reported separately:

Proximal margin — The upper cut end of the removed esophagus, closest to the mouth.
Distal margin — The lower cut end, closest to or within the stomach.
Radial (circumferential) margin — The outer soft tissue surface surrounding the esophagus. This is the margin most often involved by tumors that have grown deeply through the wall, and it is the one most closely linked to cancer returning at the surgical site.

The results are reported as follows:

Negative margin (clear or uninvolved) — No cancer cells reach the inked edge. The report usually also gives the distance in millimeters between the tumor and the closest margin.
Positive margin (involved) — Cancer cells are present at the inked edge, meaning cancer may remain in the body. This finding is one of the factors the team weighs when considering additional treatment after surgery.

Two different conventions are used internationally for calling the radial margin positive. Some laboratories require the tumor to touch the inked surface, while others call the margin positive when the tumor lies within 1 mm of it. Your report will state which measurement was used, and the distance in millimeters is given so the result can be interpreted either way.

Lymph nodes

Lymph nodes are small immune organs found throughout the body, including alongside the esophagus and in the upper abdomen. Cancer cells that enter lymphatic channels can become trapped in them, and cancer found in a lymph node is a form of metastasis. During surgery for adenocarcinoma of the esophagus, the surgeon removes the nearby lymph nodes so the pathologist can examine them.

Your report will state how many lymph nodes were examined and how many contained cancer. A node is described as positive if cancer is found in it and negative if it is not. Examining an adequate number of nodes matters for accurate staging, and current guidelines suggest that at least 15 nodes be assessed when surgery is performed without prior chemotherapy or radiation. Fewer nodes are often found after neoadjuvant therapy, because treatment shrinks them.

If cancer is present in the nodes, the report may also describe extranodal extension, meaning cancer cells have broken through the outer capsule of a node into the surrounding fat, and tumor deposits, which are separate collections of cancer cells in the surrounding tissue without any recognizable lymph node. Both are associated with poorer outcomes. The number of positive nodes determines the nodal stage (pN) and is among the strongest predictors of outcome in esophageal cancer.

Biomarker and molecular testing

Biomarkers are proteins or genetic changes measured in tumor tissue that predict whether an adenocarcinoma of the esophagus is likely to respond to a particular drug. Biomarker testing is a standard part of managing this cancer, and for advanced or metastatic disease it directly determines which drugs can be offered. Current practice is to test every advanced esophageal or gastroesophageal adenocarcinoma for four things at minimum: mismatch repair status, HER2, PD-L1, and claudin 18.2.

Most of these tests are performed by immunohistochemistry, which detects proteins in the tissue, or by next generation sequencing, which reads many genes at once. For early-stage tumors that are removed and cured surgically, some or all of these tests may not be performed, because they guide drug therapy rather than surgery.

HER2

HER2 (human epidermal growth factor receptor 2) is a protein on the cell surface that signals cells to grow and divide. In some esophageal adenocarcinomas, the ERBB2 gene is amplified, meaning extra copies are present, so the tumor cells make far too much HER2 protein. Roughly 10% to 20% of esophageal and gastroesophageal adenocarcinomas are HER2-positive. Testing begins with immunohistochemistry:

HER2 0 or 1+ (negative) — Little or no HER2 protein is present, and HER2-targeted drugs are not expected to work. No further HER2 testing is done.
HER2 2+ (equivocal) — An intermediate amount of protein is present. In situ hybridization, usually FISH, is then performed to count copies of the ERBB2 gene and classify the result as amplified (positive) or not amplified (negative).
HER2 3+ (positive) — A strong amount of HER2 protein is present, and no confirmatory test is needed.

A positive result indicates eligibility for HER2-targeted therapy in advanced disease. Options include trastuzumab combined with chemotherapy in the first-line setting, with pembrolizumab added when the tumor also expresses PD-L1, and trastuzumab deruxtecan for disease that progresses afterward. The scoring rules for esophageal and gastric tumors differ from those used in breast cancer, allowing staining along only part of the cell membrane to count, so a HER2 score cannot be compared across cancer types. HER2 can also differ from one part of a tumor to another, which is why testing is sometimes repeated on a different sample.

PD-L1

PD-L1 is a protein that some tumors display on their surface to switch off immune cells that would otherwise attack them. Immunotherapy drugs called checkpoint inhibitors, including pembrolizumab and nivolumab, block this signal. PD-L1 is measured by immunohistochemistry and reported as a Combined Positive Score (CPS), which counts the tumor cells and nearby immune cells showing PD-L1 for every 100 tumor cells.

CPS less than 1 (negative) — Very few cells show PD-L1. Since 2025, the approvals for pembrolizumab and nivolumab in esophageal and gastroesophageal cancers exclude this group, because trials showed no meaningful added benefit.
CPS 1 or higher (positive) — Enough cells show PD-L1 to meet the minimum threshold for checkpoint inhibitor eligibility.
CPS 5 or higher, or CPS 10 or higher — Higher scores predict greater benefit. Some drug approvals and treatment pathways use these higher cut-offs, and which one applies depends on the drug and the treatment setting.

PD-L1 also guides decisions after surgery. For people who received chemotherapy and radiation before surgery and still had cancer remaining in the specimen, adjuvant nivolumab is an option when the tumor is PD-L1 positive.

Mismatch repair (MMR) and microsatellite instability (MSI)

Mismatch repair is the system a cell uses to correct copying errors in its DNA. Four proteins do most of this work: MLH1, PMS2, MSH2, and MSH6. Immunohistochemistry is used to check whether each one is present in the tumor cells.

MMR proficient (pMMR) — All four proteins are present. Your report may describe them as retained, intact, preserved, or showing no loss of nuclear expression. The equivalent molecular result is microsatellite stable (MSS). This is the normal result and by far the most common one in esophageal adenocarcinoma.
MMR deficient (dMMR) — One or more of the four proteins is absent, described as loss of expression. The equivalent molecular result is microsatellite instability-high (MSI-high).

Mismatch repair deficiency is uncommon in esophageal adenocarcinoma, affecting only a small percentage of cases, but it carries two important implications. First, it indicates eligibility for immunotherapy: pembrolizumab is approved for dMMR or MSI-high cancers regardless of where in the body the cancer started, and response rates in these tumors are high. Second, it raises the possibility of Lynch syndrome, an inherited condition that increases the lifetime risk of colorectal, endometrial, and several other cancers, and that affects blood relatives. When MLH1 and PMS2 are the proteins lost, testing for MLH1 promoter methylation is usually performed first, because this non-inherited change explains most cases. If an inherited cause remains possible, referral for genetic counseling is offered.

Claudin 18.2

Claudin 18.2 is a protein that helps seal the junctions between the cells lining the stomach. It is not normally found in the esophagus, but adenocarcinomas arising at or near the gastroesophageal junction often produce it. It is measured by immunohistochemistry, and the result depends on both how many tumor cells stain and how strongly.

Claudin 18.2 positive — At least 75% of tumor cells show moderate to strong staining around their outer edge. This indicates eligibility for zolbetuximab, an antibody given with chemotherapy for advanced HER2-negative gastric and gastroesophageal junction adenocarcinoma.
Claudin 18.2 negative — Fewer than 75% of tumor cells stain at that intensity. Zolbetuximab is not expected to be effective, and other treatment pathways are considered.

Roughly a third of advanced gastroesophageal adenocarcinomas are claudin 18.2 positive. When a tumor is positive for both claudin 18.2 and PD-L1, the treatment team weighs which pathway to pursue first, and the PD-L1 score is usually part of that discussion.

Other findings on molecular testing

When comprehensive molecular testing is performed on an adenocarcinoma of the esophagus, the report may list additional genetic changes. Most are not yet linked to an approved drug for this cancer, but some open the door to tumor-agnostic treatments or clinical trials. The most commonly reported are:

NTRK gene fusions — Very rare in this cancer, but a positive result indicates eligibility for larotrectinib or entrectinib, drugs approved for NTRK-fusion cancers regardless of where they started.
Tumor mutational burden (TMB) — A count of how many mutations the tumor carries. A high result, usually defined as 10 or more mutations per megabase of DNA, indicates eligibility for pembrolizumab across cancer types.
TP53, KRAS, and other mutations — Frequently found in esophageal adenocarcinoma. These do not currently change treatment for most people, but they may identify clinical trials.

Not every case requires every one of these tests. A report that lists only some of them is not incomplete; which tests are ordered depends on the stage of the cancer and the decisions being made. You can read more about these and other tests in our Biomarkers and Genetic Testing section.

Pathologic stage (pTNM)

Pathologic stage describes how far an adenocarcinoma of the esophagus has grown and whether it has spread. It uses the TNM system of the American Joint Committee on Cancer (AJCC), 8th edition, which remains the current edition for cancers of the esophagus. T describes how deeply the tumor has grown into the wall, N describes how many nearby lymph nodes contain cancer, and M describes spread to distant organs. The letter p means the stage was determined by examining tissue under the microscope, and M is usually determined by imaging rather than by pathology. If chemotherapy or radiation was given before surgery, the stage is written with a “y” in front, as ypT and ypN.

Tumor stage (pT)

pTis — High-grade dysplasia. Abnormal cells are confined within the glands and have not begun to invade.
pT1a — The tumor has grown into the lamina propria or the muscularis mucosae, the thin layers just beneath the surface lining. This is also called intramucosal adenocarcinoma.
pT1b — The tumor has grown into the submucosa.
pT2 — The tumor has grown into the muscularis propria, the main muscle layer of the esophageal wall.
pT3 — The tumor has grown through the muscle layer into the adventitia, the outermost connective tissue.
pT4a — The tumor has grown into a neighboring structure that can usually still be removed surgically, such as the pleura lining the lung, the pericardium around the heart, the azygos vein, the diaphragm, or the peritoneum.
pT4b — The tumor has grown into a structure that generally cannot be removed, such as the aorta, a vertebral body, or the airway.

Nodal stage (pN)

pN0 — No cancer was found in any of the lymph nodes examined.
pN1 — Cancer was found in one or two lymph nodes.
pN2 — Cancer was found in three to six lymph nodes.
pN3 — Cancer was found in seven or more lymph nodes.
pNX — No lymph nodes were submitted or they could not be assessed.

The pT and pN results are combined into an overall stage group from I to IV. For esophageal adenocarcinoma removed without prior treatment, the histologic grade is also used in assigning the stage group for early, node-negative tumors. Specimens removed after neoadjuvant therapy use a separate set of stage groupings, which is one reason a stage given before treatment may differ from the one on the final report.

What is the prognosis for adenocarcinoma of the esophagus?

The prognosis for adenocarcinoma of the esophagus depends most of all on the pathologic stage, particularly how deeply the tumor grew into the esophageal wall and how many lymph nodes contain cancer. For esophageal cancer overall in the United States, five-year relative survival is approximately 49% when the cancer is still confined to the esophagus, 28% when it has reached nearby lymph nodes or tissues, and 5% when it has spread to distant organs, with all stages combined at approximately 22%. Adenocarcinoma tends to do somewhat better than these combined figures suggest, and because these numbers come from people diagnosed several years ago, they do not yet reflect the newer chemotherapy and immunotherapy regimens now in use.

Outcomes at the earliest end of the spectrum are much better than these averages. A tumor confined to the mucosa (pT1a) with no lymph node involvement is often cured, with long-term cancer-specific survival exceeding 90%.

The following findings on your pathology report are associated with poorer outcomes:

Deeper invasion into the esophageal wall — Outcomes worsen at each step from pT1 through pT4.
A greater number of positive lymph nodes — The single strongest predictor of outcome after depth of invasion.
Positive surgical margin — Particularly the radial margin, which is linked to cancer returning at the surgical site.
Lymphovascular or perineural invasion — Both are associated with a higher risk of recurrence.
Poorly differentiated (grade 3) tumor — Associated with faster growth and a higher chance of lymph node involvement.
Poor response to neoadjuvant therapy — A treatment response score of 2 or 3 carries a less favorable outlook than a score of 0 or 1.
Extranodal extension or tumor deposits — Both indicate more extensive local spread.

Biomarker results also matter. HER2-positive, PD-L1-positive, claudin 18.2-positive, and mismatch repair deficient tumors all have treatment options that were not available a decade ago, and these have meaningfully improved survival in advanced disease. Your treatment team will weigh all of these findings together, alongside your age, overall health, and how the cancer responds to treatment, when discussing what to expect.

What happens after this diagnosis?

Once adenocarcinoma of the esophagus is confirmed, the pathology report is reviewed alongside imaging and endoscopy findings by a multidisciplinary team that typically includes gastroenterology, thoracic surgery, medical oncology, radiation oncology, radiology, pathology, and dietetics. The findings on the report guide which options the team considers.

For a very early tumor confined to the mucosa (pT1a) with no lymphovascular invasion, negative margins, and low grade, endoscopic removal followed by ablation of the remaining Barrett esophagus may be sufficient, without an operation on the esophagus.

For tumors that have grown deeper or reached lymph nodes but have not spread to distant organs, treatment usually combines drug therapy with surgery. Chemotherapy given before and after surgery, most often the FLOT regimen, has been shown in a large randomized trial to produce better survival than chemotherapy combined with radiation before surgery for esophageal adenocarcinoma, and guidelines have shifted toward this approach for people fit enough to receive it. Chemoradiation before surgery remains an appropriate option in many situations. Since late 2025, the immunotherapy drug durvalumab has also been approved for use with FLOT before and after surgery in resectable gastric and gastroesophageal junction adenocarcinoma. When chemoradiation was given before surgery and cancer still remained in the specimen, adjuvant nivolumab may be considered if the tumor is PD-L1 positive.

For cancer that has spread to distant organs, treatment is directed by the biomarker results on the report. HER2-positive tumors open the option of trastuzumab-based therapy and later trastuzumab deruxtecan; PD-L1-positive tumors open the option of pembrolizumab or nivolumab added to chemotherapy; claudin 18.2-positive, HER2-negative tumors open the option of zolbetuximab; and mismatch repair deficient tumors open the option of immunotherapy alone.

Whatever the treatment path, supportive care is an important part of managing this cancer. Swallowing difficulty and weight loss are common, and a dietitian is usually involved early. A stent or other endoscopic procedure may be used to keep the esophagus open. Follow-up after treatment includes regular clinical review and CT imaging, with endoscopy when Barrett esophagus remains, and involvement of a palliative care team alongside active treatment is common and is aimed at symptom control rather than signaling that treatment has stopped.

Questions to ask your doctor

What is the pathologic stage of my cancer (pT and pN), and what does that mean for me?
How deeply did the cancer grow into the wall of my esophagus?
How many lymph nodes were examined, and how many contained cancer?
Were all of the surgical margins negative, including the radial margin, and how close was the tumor to the nearest edge?
Was lymphovascular or perineural invasion present?
What was the histologic grade of my tumor?
Was the center of my tumor in the esophagus or in the stomach, and which staging system was used?
If I had chemotherapy or radiation before surgery, what was my treatment response score, and what does it mean?
What were my HER2, PD-L1, mismatch repair, and claudin 18.2 results?
Do any of my biomarker results make me eligible for targeted therapy or immunotherapy?
Should I be referred for genetic counseling based on my mismatch repair result?
Is additional treatment recommended after surgery, and what would it involve?
Are there clinical trials open to someone with my stage and biomarker profile?
What follow-up tests and imaging will I need, and how often?