A 38-year-old woman with a history of eight neoplasms. Her family history included advanced paternal age (75 years old) at conception and prostate cancer in the father’s eighties. At the time of the patient’s birth, the mother was 23 years old, and she had an unremarkable medical history. There was no history of early-onset cancer in other family members.

The patient’s initial tumor was an osteosarcoma of the right femur, diagnosed at the age of 12. The tumor was treated with neoadjuvant chemotherapy comprising cisplatin-doxorubicin and subsequent surgical resection. Chemotherapy was continued for six months after resection.

At the age of 26, the patient presented with a rapidly growing mass in the right breast, which was diagnosed as synchronous ductal carcinoma (pT2 pN0 MX) with positive estrogen and progesterone receptor expression, negative HER2 status, and high-grade sarcoma of the breast (pT2 pN0 MX). A radical mastectomy was performed, followed by chemotherapy (tamoxifen, goserelin, and ibandronic acid) for five years.

One year later, doxorubicin-induced cardiomyopathy was diagnosed and the patient was admitted. During this hospitalization, a left epitrochlear mass was observed and removed. Pathology reported a high-grade pleomorphic sarcoma (pT1 pN0 M0) with free margins of resection. At this point, LFS was clinically diagnosed with the Chompret Criteria. A comprehensive examination of the patient’s family cancer history revealed that none of the seven paternal half-siblings had a history of cancer (the oldest was 68 years old at this point). The patient’s father had been diagnosed with prostate cancer and died at the age of 82. Neither the patient’s mother nor her only maternal uncle had a history of cancer.

At the age of 28, the patient was found to have another mass in her left breast. The pathology report showed invasive lobular carcinoma (pT2 pN0 MX). Consequently, she underwent a radical left mastectomy. At the age of 30, the patient underwent sequencing for TP53 from a peripheral blood sample which revealed the pathogenic variant c.586 C > T (p.R196X) in exon 6; thus, LFS was confirmed. The patient refused routine surveillance after diagnosis due to personal reasons.

At 35 years of age, an ovarian mass was incidentally detected during routine transvaginal echography. Subsequent evaluation with abdominopelvic contrasted computed tomography revealed a right adnexal mass, peritoneal carcinomatosis, and abdominal adenomegalies. Further examination via upper endoscopy detected an ulcerated mass in the lesser curvature of the stomach, which biopsies confirmed as infiltrating gastric adenocarcinoma (pT2 N0 M1) positive for HER2 and Helicobacter pylori. Colonoscopy showed no abnormal findings. The ovarian tumor was resected, along with a hysterectomy, bilateral salpingo-oophorectomy, appendicectomy, and omentectomy performed laparoscopically. Pathological examination confirmed metastatic signet ring cell adenocarcinoma, likely from a gastrointestinal source. A diagnosis of stage IV diffuse gastric adenocarcinoma with bilateral Krukenberg tumors and lymphatic and peritoneal metastasis was made. One month after surgery, the patient was started on docetaxel-carboplatin-fluorouracil (TPF) and trastuzumab.

During hospitalization for chemotherapy, the patient presented with a right epitrochlear mass that rapidly increased in size. Surgical excision was performed, and the pathology exam revealed a stage II leiomyosarcoma (pT2, pN0, M0) with compromised margins. A positron emission tomography (PET) scan showed a hypermetabolic lesion in the right upper limb region where tumor resection was performed and a nodular hypermetabolic lesion anterior to the left kidney, which was thought to be a peritoneal implant of gastric adenocarcinoma. The medical board opted to continue monitoring these lesions, given the patient’s ongoing chemotherapy treatment.

Five months after the diagnosis of gastric adenocarcinoma the patient completed six cycles of docetaxel + cisplatin + 5-fluorouracil (DCF)-trastuzumab therapy and underwent a complete cytoreduction surgery with Hyperthermic Intraperitoneal Chemotherapy (HIPEC). A follow-up complete body PET scan showed an increased size of the mass previously seen in the left kidney, now compromising the renal vein; other findings included a solitary pulmonary nodule in the right lung and hypermetabolic internal mammary nodules suspicious of metastasis of gastric adenocarcinoma; no hypermetabolic lesions were seen in the gastrointestinal apparatus or limbs. A radical nephrectomy was performed with a pathology reporting a high-grade pleomorphic sarcoma with an invasion of renal sinus, perihilar region, and adjacent fat tissue with compromised margins (pT2b pN0 M0).

Somatic genomic profiling (Foundation Medicine Inc., Cambridge, MA, USA) was performed using a biopsy of high-grade pleomorphic sarcoma of the kidney to assess possible therapeutic targets. The results showed EED rearrangement in exon 6, RB1 rearrangement in intron 17, and TP53 R196*. Biomarker findings exhibited stable microsatellite status and tumor mutational burden 5 Muts/Mb. Other variants with unknown significance found in the patient’s tumor included APH1A amplification, BCOR E1708D, CDKN2C amplification, FGF10 amplification, FGF19 S78C, IL7R amplification, LRP1B V4109I, LRRK2 M379I, and Q1657L, MLL2 L2161H, RICTOR amplification, SETD2 H1284L, SPEN K2065E, TNFRSF11A splice site 730 + 1G > A, and ZNF217 M410V.

Following the patient’s nephrectomy, a medical board convened to discuss treatment options. The patient declined targeted cancer therapy and opted to continue chemotherapy instead. Three months later, the patient developed thrombosis in multiple veins, including the right renal vein, both common iliac veins, and the inferior vena cava, as well as a pulmonary embolism. Despite medical intervention, the patient died at the age of 38.

The summary of each neoplasm is shown in Table 1. All tumors were diagnosed histologically.