Adenocarcinoma of the Stomach: Understanding Your Pathology Report

by Jason Wasserman MD PhD FRCPC
July 31, 2026

Adenocarcinoma is the most common type of stomach cancer, accounting for roughly 90% to 95% of all cases. It begins in the glandular cells that line the inside of the stomach, the cells that normally produce mucus and digestive juices. In adenocarcinoma, these cells grow in an uncontrolled way and form a tumor that can grow into the deeper layers of the stomach wall and spread to other parts of the body.

Your report may name a specific type, such as tubular adenocarcinoma or poorly cohesive carcinoma, and may also use terms from an older system such as intestinal type or diffuse type. All of these are forms of adenocarcinoma of the stomach, and the section on histologic type below explains how they relate to one another.

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 stomach?

Adenocarcinoma of the stomach usually develops over many years through a sequence of changes in the stomach lining, driven by a combination of infection, environment, and inherited factors.

Chronic Helicobacter pylori infection — This bacterium damages the stomach lining and causes long-standing inflammation. Over decades, this can progress through thinning of the normal glands, called atrophy, then intestinal metaplasia, in which the stomach lining is replaced by cells resembling those of the intestine, then dysplasia, and finally cancer. This is the most important preventable cause of stomach cancer worldwide, and treating the infection reduces risk.
Epstein-Barr virus (EBV) — Found in roughly 10% of stomach adenocarcinomas. These tumors have a distinct biology, described further in the biomarker section.
Diet and lifestyle — Diets high in salt-preserved, pickled, or smoked foods and low in fresh fruits and vegetables increase risk, as does tobacco use.
Previous stomach surgery, pernicious anemia, and autoimmune gastritis — All associated with long-term changes in the stomach lining that raise risk.
Inherited conditions — A small but important number of stomach cancers are caused by an inherited gene change. Changes in the CDH1 gene cause hereditary diffuse gastric cancer, in which affected family members have a high lifetime risk of poorly cohesive (signet ring cell) stomach cancer. Lynch syndrome, familial adenomatous polyposis, juvenile polyposis, and Peutz-Jeghers syndrome also increase risk to varying degrees.

Genetic counseling is generally offered when a report shows poorly cohesive or signet ring cell carcinoma in a younger person, when mismatch repair deficiency is found, or when there is a family history of stomach or related cancers, because the implications extend to blood relatives.

What are the symptoms of adenocarcinoma of the stomach?

Many people with early adenocarcinoma of the stomach have no symptoms at all, which is one reason the cancer is often found at a later stage in countries without screening programs. When symptoms do appear, they are often vague and easily attributed to indigestion.

Common symptoms include persistent stomach pain or discomfort, feeling full after only a small amount of food, bloating, nausea, vomiting, loss of appetite, and unexplained weight loss. Difficulty swallowing can occur when the tumor is near the top of the stomach. Bleeding from the tumor surface may cause black tarry stools or blood in vomit, and slow blood loss over time causes anemia, a low red blood cell count that leads to fatigue, weakness, and breathlessness.

How is the diagnosis made?

The diagnosis of adenocarcinoma of the stomach is made only after tissue from the stomach is examined under a microscope by a pathologist. The tissue is usually obtained during an upper endoscopy, in which a thin flexible tube with a camera is passed through the mouth into the stomach so the lining can be inspected and small tissue samples called biopsies taken from any abnormal area.

Under the microscope, cancer is identified when the normal glands of the stomach lining are replaced by malignant cells that grow in a disorganized pattern and invade the tissue beneath. The pathologist records the histologic type, the grade, the depth of invasion, and whether features such as lymphovascular or perineural invasion are present.

Some tumors are harder to detect on biopsy than others. Poorly cohesive and signet ring cell cancers spread as scattered single cells through the wall rather than forming a mass, so the overlying lining can look almost normal at endoscopy and biopsies may be repeatedly negative. When the stomach wall appears thickened or stiff on imaging or endoscopy, additional or deeper biopsies are often taken for this reason. Immunohistochemistry, a test that uses antibodies to detect specific proteins, may be used to highlight scattered tumor cells or to confirm that a poorly differentiated tumor is an adenocarcinoma rather than another cancer type.

Once cancer is confirmed, imaging determines how far it has spread. This usually includes CT scans of the chest, abdomen, and pelvis. Endoscopic ultrasound may be used to assess depth of growth into the stomach wall, and a PET-CT scan is sometimes performed. A laparoscopy, a small operation to look inside the abdomen directly, is often done before planning surgery, because deposits on the surface of the abdominal lining are frequently too small to see on a scan.

Histologic type

Histologic type describes how the cancer cells of a stomach adenocarcinoma are arranged when viewed under the microscope. Two different classification systems are in use, and your report may name a type from either or from both, which can be confusing if the terms are read as if they were alternatives.

The current World Health Organization system names the type based on the pattern the tumor forms:

Tubular adenocarcinoma — The most common type. The cancer cells form irregular tube-like glands. These tumors usually form a visible mass and are most often found in people with a history of H. pylori infection and intestinal metaplasia.
Papillary adenocarcinoma — The cancer cells grow along finger-like projections of supporting tissue called papillae. This type is uncommon, tends to occur in older people and in the upper stomach, and often appears well differentiated. Despite that, it can spread to the liver and to lymph nodes more readily than its appearance suggests.
Poorly cohesive carcinoma — The cancer cells lose their attachments to one another and spread individually or in small clusters through the stomach wall without forming glands. Because the cells scatter rather than form a mass, this type can be difficult to see at endoscopy, can be missed on biopsy, and can thicken and stiffen a large area of the stomach wall, an appearance historically called linitis plastica. It tends to occur in younger people and more often in women than the other types.
Poorly cohesive carcinoma, signet ring cell type — A form of poorly cohesive carcinoma in which most of the tumor cells contain a large droplet of mucus that pushes the nucleus to one edge, producing the appearance of a signet ring. Current classification reserves this label for tumors in which signet ring cells make up more than half of the tumor. When this type is found in a younger person or where there is a family history, hereditary diffuse gastric cancer caused by a CDH1 gene change is considered.
Mucinous adenocarcinoma — More than half of the tumor consists of pools of mucus with cancer cells floating within them. These tumors are often found at a more advanced stage than tubular tumors.
Mixed carcinoma — The tumor contains a substantial amount of more than one pattern, most often a gland-forming component together with a poorly cohesive component. Mixed tumors tend to behave more like the poorly cohesive component.

Several uncommon types are also recognized. Adenocarcinoma with lymphoid stroma, sometimes called medullary carcinoma, consists of sheets of cancer cells surrounded by dense immune cells; most of these tumors are EBV-positive or mismatch repair deficient, and they generally have a better outlook than other stomach cancers. Hepatoid adenocarcinoma contains cells resembling liver cells and often produces a protein called alpha-fetoprotein that can be measured in blood. Micropapillary carcinoma grows as small clusters of cells sitting in empty spaces and is associated with a higher rate of lymph node involvement.

An older system, the Laurén classification, divides stomach adenocarcinoma into two main groups and remains widely used because it is a useful shorthand. Intestinal type tumors form glands, correspond mostly to the tubular and papillary types above, and typically arise from the H. pylori and intestinal metaplasia sequence. Diffuse type tumors do not form glands and correspond to poorly cohesive and signet ring cell carcinoma. Tumors with features of both, or of neither, are called mixed or indeterminate. If your report gives a Laurén type and a World Health Organization type, they are two descriptions of the same tumor rather than two separate findings.

Tumor grade

Grade describes how closely the cancer cells of a stomach adenocarcinoma resemble normal stomach cells. The pathologist assigns the grade based on how much of the tumor still forms recognizable glands.

Grade 1 (well differentiated) — More than 95% of the tumor forms glands and closely resembles normal stomach 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.
GX — The grade could not be assessed, usually because the sample was too small or too altered by previous treatment.

Poorly cohesive and signet ring cell carcinomas are classified as poorly differentiated by definition, since their cells do not form glands at all. For these tumors, the grade adds little information beyond the type itself, and the type is the more meaningful finding. Higher grade tumors tend to grow faster and are more often associated with spread to lymph nodes at the time of diagnosis.

Depth of invasion

Depth of invasion describes how far a stomach adenocarcinoma has grown into the wall of the stomach, and it is among the most important findings on the report. The stomach wall is built in layers:

Mucosa — The innermost lining, where adenocarcinoma begins. It includes the surface and glandular cells, a supportive layer called the lamina propria, and a thin band of muscle called the muscularis mucosae.
Submucosa — A supportive layer beneath the mucosa carrying the larger blood vessels and lymphatic channels. Once a tumor reaches this layer, the risk of spread to lymph nodes rises substantially.
Muscularis propria — The thick muscle layer that contracts to mix food and move it onward.
Subserosa — A thin layer of connective tissue just beneath the outer surface.
Serosa — The smooth outer covering of the stomach, facing the abdominal cavity. Once a tumor breaks through this surface, cancer cells can shed directly into the abdomen.

Tumors confined to the mucosa or submucosa are described as early gastric cancer regardless of whether lymph nodes are involved, and this group has a substantially better outlook and may be eligible for endoscopic rather than surgical treatment. In advanced cases the tumor can grow directly into neighboring structures such as the spleen, pancreas, colon, liver, or abdominal wall. The deepest layer reached determines the pathologic tumor stage (pT).

Lymphovascular invasion

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

These channels carry fluid and cells away from the stomach, so tumor cells inside them may travel to nearby lymph nodes or, through the bloodstream, to distant organs such as the liver. Lymphovascular invasion is one of the strongest predictors of lymph node involvement, and its presence may influence whether additional treatment is discussed. In an early tumor being considered for endoscopic removal, finding lymphovascular invasion usually shifts the discussion toward surgery.

Perineural invasion

Perineural invasion means that cancer cells were seen surrounding or growing into a nerve. Nerves run through the stomach wall and the surrounding tissue, and cancer cells that reach them can use them as a pathway to extend beyond the main tumor. 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 found more often in deeply invasive and poorly cohesive tumors, and it is one of several findings the treatment team weighs when deciding whether treatment beyond surgery should be discussed.

Treatment effect

Many people with adenocarcinoma of the stomach receive chemotherapy before surgery, called neoadjuvant chemotherapy, to shrink the tumor, treat cancer cells that may already have spread, and improve the chance that surgery removes everything. When the stomach is removed afterward, 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.
Score 2 (partial response) — Residual cancer is present, but there is clear evidence that treatment shrank the tumor, such as scarring or pools of mucus where tumor used to be.
Score 3 (poor or no response) — Extensive cancer remains with little or no evidence of response.

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 none remains. Pools of mucus 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 is written with a “y” in front, as ypT and ypN.

Surgical margins

A margin is the cut edge of the tissue removed during surgery for adenocarcinoma of the stomach. 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 specimen, toward the esophagus.
Distal margin — The lower cut end, toward the small intestine.
Radial (circumferential) margin — The outer soft tissue surface, particularly relevant when the tumor lies along the back wall of the stomach close to adjacent structures.
Omental margin — The edge of the omentum, the apron of fatty tissue attached to the stomach that is removed with the specimen.

The results are reported as follows:

Negative margin — 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 — 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 further surgery or additional treatment.

Two conventions are used internationally for calling the radial margin positive. Some laboratories require tumor to touch the inked surface, while others call it positive when tumor lies within 1 mm. Your report will state which was used, and the distance in millimeters is given so the result can be interpreted either way. Margins matter particularly in poorly cohesive tumors, whose scattered cells can extend well beyond the visible edge of the tumor, which is why the cut ends are sometimes checked during the operation itself.

Lymph nodes

Lymph nodes are small immune organs found throughout the body, including around the stomach and along the blood vessels that supply it. 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 the nearby lymph nodes are removed so the pathologist can examine them.

Your report will state how many lymph nodes were examined and how many contained cancer. Examining an adequate number matters for accurate staging, and current guidelines recommend that at least 16 nodes be assessed, with more than 30 preferred in some centers. Fewer nodes are often recovered after chemotherapy, because treatment shrinks them.

If cancer is present, 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 a 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.

Biomarker and molecular testing

Biomarkers are proteins or genetic changes measured in tumor tissue that predict whether a stomach adenocarcinoma is likely to respond to a particular drug. Biomarker testing directly determines which drugs can be offered in advanced disease, and current practice is to test every locally advanced or metastatic stomach adenocarcinoma for at least four things: mismatch repair status, HER2, PD-L1, and claudin 18.2. For a small early tumor removed and cured surgically, some or all of these may not be performed.

Testing is done by immunohistochemistry, which detects proteins in the tissue, by in situ hybridization, which detects genes or viral material, or by next generation sequencing, which reads many genes at once.

HER2

HER2 is a protein on the cell surface that signals cells to grow and divide. In some stomach cancers the ERBB2 gene is amplified, meaning extra copies are present, so the tumor makes far too much HER2 protein. Roughly 10% to 20% of stomach adenocarcinomas are HER2-positive, and this is more common in intestinal-type tumors and in those near the top of the stomach. 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.
HER2 2+ (equivocal) — An intermediate amount of protein is present. In situ hybridization, usually FISH, is 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: 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 stomach tumors differ from those used in breast cancer, allowing staining along only part of the cell membrane to count. HER2 can also vary 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 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 stomach 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, and some approvals and treatment pathways use these higher cut-offs depending on the drug and setting.

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 checks whether each is present.

MMR proficient (pMMR) — All four proteins are present. Your report may describe them as retained, intact, or showing no loss of nuclear expression. The equivalent molecular result is microsatellite stable (MSS). This is the normal and most common result.
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). This occurs in roughly 8% to 10% of stomach cancers.

A deficient result carries three implications. It predicts strong benefit from immunotherapy, and pembrolizumab is approved for dMMR or MSI-high cancers regardless of where the cancer started. It is associated with a better outlook stage for stage. And it raises the possibility of Lynch syndrome, an inherited condition affecting 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. Many stomach cancers continue to produce it. It is measured by immunohistochemistry, and the result depends on 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 stomach 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 stomach 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.

Epstein-Barr virus (EBV)

Epstein-Barr virus is present in the tumor cells of roughly 10% of stomach adenocarcinomas. It is detected by a test called EBER in situ hybridization, which finds viral genetic material inside the cancer cells.

EBV positive — The virus is present in the tumor cells. These tumors are often surrounded by dense immune cells, usually show high PD-L1, are less likely to involve lymph nodes, and generally carry a better outlook than EBV-negative tumors.
EBV negative — The virus is not present. This is the usual result.

A positive result does not mean the cancer is contagious or that a recent infection caused it. Most adults carry this virus harmlessly for life; in a small number of people it becomes incorporated into cells that later become cancerous.

Other findings on molecular testing

Comprehensive molecular testing may list additional genetic changes. Most do not currently change treatment, but some open the door to tumor-agnostic drugs or clinical trials:

Tumor mutational burden (TMB) — A count of how many mutations the tumor carries. A high result, usually 10 or more mutations per megabase of DNA, indicates eligibility for pembrolizumab across cancer types.
NTRK gene fusions — Very rare, but a positive result indicates eligibility for larotrectinib or entrectinib regardless of where the cancer started.
FGFR2, MET, and other amplifications — Found in a minority of stomach cancers and currently of interest mainly for clinical trials.

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

Pathologic stage (pTNM)

Pathologic stage describes how far a stomach adenocarcinoma 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 stomach. 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. If chemotherapy was given before surgery, the stage is written with a “y” in front, as ypT and ypN.

Tumor stage (pT)

pTis — High-grade dysplasia, also called carcinoma in situ. 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, remaining within the mucosa.
pT1b — The tumor has grown into the submucosa.
pT2 — The tumor has grown into the muscularis propria, the main muscle layer.
pT3 — The tumor has grown through the muscle layer into the subserosal connective tissue, without breaking through the outer surface.
pT4a — The tumor has broken through the serosa, the outer surface of the stomach.
pT4b — The tumor has grown directly into a neighboring organ or structure, such as the spleen, pancreas, colon, liver, diaphragm, or abdominal wall.

Nodal stage (pN)

pN0 — No cancer was found in any lymph nodes examined.
pN1 — Cancer was found in one or two lymph nodes.
pN2 — Cancer was found in three to six lymph nodes.
pN3a — Cancer was found in seven to fifteen lymph nodes.
pN3b — Cancer was found in sixteen or more lymph nodes.
pNX — Lymph nodes were not submitted or could not be assessed.

The pT and pN results are combined into an overall stage group from I to IV. Specimens removed after chemotherapy 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 stomach?

The prognosis for adenocarcinoma of the stomach depends most of all on the pathologic stage, particularly how deeply the tumor grew into the stomach wall and how many lymph nodes contain cancer. In the United States, five-year relative survival is approximately 77% when the cancer is still confined to the stomach, 37% when it has reached nearby structures or lymph nodes, and 8% when it has spread to distant organs, with all stages combined at approximately 38%. Because these figures come from people diagnosed several years ago, they do not yet reflect the newer chemotherapy and immunotherapy regimens now in use. Outcomes are considerably better in countries such as Japan and South Korea, where screening programs find many cancers at an early stage.

Early gastric cancer, meaning a tumor confined to the mucosa or submucosa, has a much better outlook than these overall figures suggest and is often curable, with five-year survival above 90% when lymph nodes are not involved.

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

Deeper invasion into the stomach wall — Outcomes worsen at each step from pT1 through pT4, with breaking through the serosa a particularly important threshold.
A greater number of positive lymph nodes — The strongest predictor of outcome after depth of invasion.
Positive surgical margin — Linked to cancer returning at the surgical site.
Poorly cohesive or signet ring cell type — These tumors tend to be found at a later stage, spread through the wall and into the abdominal lining more readily, and respond less well to chemotherapy than gland-forming tumors.
Lymphovascular or perineural invasion — Both raise the risk of recurrence.
Poor response to neoadjuvant chemotherapy — 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.

Some findings point the other way. Mismatch repair deficient and EBV-positive tumors carry a better outlook stage for stage and open specific treatment options, and HER2-positive and claudin 18.2-positive tumors have targeted treatments that have meaningfully improved survival in advanced disease.

What happens after this diagnosis?

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

For a small early tumor confined to the mucosa, meeting size and grade criteria and with no lymphovascular invasion, removal through the endoscope by endoscopic submucosal dissection may be sufficient, avoiding an operation on the stomach entirely. The resected tissue is examined to confirm the tumor was completely removed and did not extend deeper than expected.

For tumors that have grown deeper or reached lymph nodes but have not spread to distant organs, treatment usually combines chemotherapy with surgery. Chemotherapy given before and after surgery, most often the FLOT regimen, is the standard approach in North America and Europe. Since late 2025 the immunotherapy drug durvalumab has also been approved for use with FLOT before and after surgery in resectable stomach and gastroesophageal junction adenocarcinoma. Surgery removes part or all of the stomach along with the regional lymph nodes.

For cancer that has spread to distant organs, treatment is directed by the biomarker results. 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.

Nutrition is a central part of care after stomach surgery and is often underestimated. Removing part or all of the stomach changes how food is handled, and smaller more frequent meals are usually needed. Iron, vitamin B12, calcium, and vitamin D can all become deficient, and vitamin B12 usually requires lifelong injections after total removal of the stomach. A dietitian is generally involved from the outset. Follow-up includes regular clinical review, blood tests, and periodic imaging, and endoscopy when part of the stomach remains.

Questions to ask your doctor

What histologic type and grade does my pathology report show?
Is my tumor intestinal type or diffuse type, and does that change my treatment?
What is the pathologic stage of my cancer (pT and pN), and what does that mean for me?
How deeply did the tumor grow into the wall of my stomach?
How many lymph nodes were examined, and how many contained cancer?
Were all of the surgical margins negative, and how close was the tumor to the nearest edge?
Was lymphovascular or perineural invasion present?
If I had chemotherapy before surgery, what was my treatment response score?
What were my HER2, PD-L1, mismatch repair, claudin 18.2, and EBV results?
Do any of my biomarker results make me eligible for targeted therapy or immunotherapy?
Should I be referred for genetic counseling, and should my family members be tested?
What additional treatment is recommended, and in what order?
Are there clinical trials open to someone with my stage and biomarker profile?
What changes to my eating should I expect, and will I need vitamin or mineral supplements?
What follow-up tests and imaging will I need, and how often?