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Oncology3 readJuly 20, 2026

A Mass Appeared Along a Biopsy Needle Track. It Wasn't Pancreatic Cancer

Опухоль на пути биопсийной иглы оказалась не раком

Scientific illustration created with AI assistance.

Two years after surgery for pancreatic cancer, a three-centimeter mass appeared in the wall of a 70-year-old woman’s stomach. It sat precisely where a biopsy needle had previously passed. The most concerning explanation seemed obvious: pancreatic cancer cells might have been deposited along the needle track and grown into a new tumor.

This complication is known as needle tract seeding. It can occur when a needle passes through one organ to collect tissue from another. In this case, the pancreatic lesion could not be reached adequately from the duodenum, so the needle was advanced through the stomach wall. Sampling required two procedures and four needle passes in total.

The original pancreatic mass measured about 10 millimeters and was confirmed as adenocarcinoma. After preoperative treatment, the tumor was surgically removed. The patient then underwent CT surveillance every six months for two years.

At the two-year scan, a roughly 30-millimeter mass was visible in the gastric wall along the former needle path. It also showed increased metabolic activity on PET imaging. Three attempts to obtain diagnostic tissue were unsuccessful because the lesion was extremely firm. The needles retrieved only small amounts of fibrous tissue with little cellular atypia.

With needle tract seeding still impossible to exclude, the medical team performed a partial gastrectomy. The resected mass contained dense collagen and bundles of elongated cells. Its cells showed nuclear accumulation of beta-catenin, a feature associated with desmoid fibromatosis.

Genetic testing provided the clearest distinction. The pancreatic cancer carried KRAS and TP53 driver mutations. Neither was present in the gastric mass. The stomach lesion instead carried a CTNNB1 p.T41A mutation characteristic of sporadic desmoid tumors. The two masses therefore had different molecular origins: the gastric lesion was not descended from the pancreatic cancer.

Desmoid fibromatosis arises from connective tissue. It does not metastasize to distant organs, but it can grow into nearby structures and recur after treatment. Sporadic desmoid tumors commonly involve abnormal beta-catenin signaling, which influences cell growth and tissue repair.

Could the original biopsy have triggered the desmoid tumor? Its exact position along the needle track and the two-year interval make localized injury a biologically plausible explanation. The evidence, however, comes from a single patient with no comparison group. The mass could also have been related to the major pancreatic operation, another local injury, or chance. The authors explicitly state that a causal link remains uncertain.

This report does not estimate how often such tumors occur and does not show that pancreatic biopsies generally cause desmoid fibromatosis. It exposes a diagnostic trap: after cancer treatment, the location and timing of a new mass may support a persuasive explanation without establishing where its cells came from.

Neither the pancreatic cancer nor the desmoid tumor had recurred two years after the gastric surgery. In this case, the lesion’s position suggested the diagnosis, but its molecular history corrected it.