Low Red Blood Cell Count Pancreatic Cancer – Platelets are recognized as important players in hemostasis, thrombosis, and cancer. Preclinical and clinical researches prove that tumorigenesis and metastasis can be promoted by platelets through various crosstalks between cancer cells and platelets. Pancreatic cancer is a devastating disease with high morbidity and mortality worldwide. Although the relationship between pancreatic cancer and platelets in clinical diagnosis has been described, the interplay between pancreatic cancer and platelets, the underlying pathological mechanism and pathways remain a matter of intensive study. This review summarizes recent research on the connections between platelets and pancreatic cancer. Current data indicate different underlying mechanisms involved in their complex crosstalk. Usually, the pancreatic tumor accelerates the aggregation of platelets that form thrombosis. In addition, extracellular vesicles released by platelets promote communication with a neoplastic microenvironment and illustrate how these interactions lead to disease progression. We also discuss the advantages of new model organoids in pancreatic cancer research. A deeper understanding of tumor and platelets crosstalk based on organoids and translational therapies may provide potential diagnostic and therapeutic strategies for pancreatic cancer progression.

The important interaction of tumor cells with platelets is a long-standing concept. Preclinical and clinical studies have shown that tumorigenesis, growth, angiogenesis, and metastasis can be promoted by platelets through various crosstalks between platelets and cancer cells. Correlations between high platelet counts and poor prognosis have often been described for lung, colon, breast, kidney, ovarian, and pancreatic cancers. Platelet-based biomarkers as liquid biopsy for cancer patients may be a potential platform for improving diagnosis. The high risk of venous thrombosis and metastasis has a close relationship with platelets in patients with pancreatic cancer (Sylman et al., 2017). However, studies focused on the crosstalk between pancreatic cancer and platelets in different ways have not been fully investigated compared to other tumors. For example, platelet α-granules contain many different bioactive factors such as vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), epidermal growth factor (EGF), endostatin, angiostatin, platelet factor-4 (PF4 ), or thrombospondin, the exact mechanism of granule release and whether it can be selectively manipulated in pancreatic cancer requires further study. In addition, platelet derived-microparticles and RNA profile alteration are prospective directions for pancreatic cancer diagnosis and treatment (Thaler et al., 2012; Best et al., 2015). At the same time, many drugs have been developed to interfere with cancer growth or metastasis by inhibiting the functions of platelets. These drugs are in pre-clinical development or already in clinical treatment, which target platelet receptors, inhibit platelet granule release, or interfere with platelet-related enzymes (Dovizio et al., 2013 ; Elwood et al., 2016; Sun et al., 2019). In this review, we summarize recent discoveries in the field of pancreatic cancer and platelets. Compared to other cancer research with platelets, we discuss the potential of pancreatic cancer exploration. In addition, we propose a suitable research model for pancreatic cancer and platelet investigation, which provides an insight for further study.

Low Red Blood Cell Count Pancreatic Cancer

Pancreatic cancer remains one of the most deadly neoplasms worldwide. There are three histological classifications of pancreatic cancer. Pancreatic ductal adenocarcinoma (PDAC) originates from the duct cells of the exocrine tissue, representing the most common (> 90%) type. There is a subtype that shows both characteristics of adenocarcinoma and squamous carcinoma. These are adenosquamous carcinomas about 1-4% of exocrine malignancies. Other types are acinar and neuroendocrine tumors. According to Globocan’s estimate, there will be more than 495,773 new patients diagnosed and about 466,000 deaths from pancreatic cancer in 2020.

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From preliminary to invasive cancer, there are three well-defined PDAC precursor lesions: Intraductal papillary mucinous neoplasms (IPMNs), mucinous cystic neoplasms (MCNs), and pancreatic intraepithelial neoplasm (PanIN), the latter being the most frequent. precursor lesion further divided. to PanIN-1, 2, and 3 (Hezel et al., 2006; Hruban et al., 2007).

Pancreatic cancer usually does not cause symptoms in the early stages, which makes it difficult to diagnose. Common symptoms include stomach or back pain, weight loss, loss of appetite, diarrhea, constipation, jaundice, blood clots, and fatigue. These symptoms can have many causes, and may not be pancreatic cancer. Therefore, different types of tests are important for diagnosis. Tests used to diagnose pancreatic cancer include 1. Blood tests, such as blood cell count, liver and kidney function, or tumor markers (such as CA19-9, CEA, B72.3); 2. Ultrasound scan of the abdomen. 3. Computerized tomography (CT) scan or Positron emission tomography (PET-CT) scan. 4. Magnetic resonance imaging (MRI) scan or Magnetic resonance cholangio-pancreatography (MRCP). 5. Endoscopic ultrasound scan (EUS) or with/without Biopsy. 6. Endoscopic retrograde cholangio-pancreatography (ERCP) is usually used when the bile duct is blocked. 7. Laparoscopy. According to these tests, information about tumor size, burden, and involvement of local vessels can be obtained that is necessary to determine the TNM stage (Tumor, Nodes, Metastases) (van Roessel et al., 2018).

Currently, the treatments for pancreatic cancer are chemotherapy, surgery, radiation therapy, targeted therapy, and immunotherapy. Only about 20% of people diagnosed with pancreatic cancer qualify for surgical treatment because most are found after the disease has spread. The types of operations performed depend on the purpose of the operation. For example, the Whipple procedure, which is continued if the tumor is located only in the head of the pancreas. However, a Distal pancreatectomy is usually performed when the cancer is in the tail of the pancreas. Often, surgery is combined with systemic therapy or/and radiation therapy. Adjuvant therapy is given after surgery. Sometimes, certain treatments are used to shrink a tumor before surgery, this is called neoadjuvant therapy or pre-operative therapy. Radiation therapy is performed with high-energy x-rays or other particles to destroy cancer cells such as traditional radiation therapy, stereotactic body radiation (SBRT) or cyberknife, proton beam therapy. Often, chemotherapy is combined with radiation therapy at the same time, which is called radiosensitization. Chemotherapy is the main type of systemic therapy and involves an intravenous tube placed in a vein through a needle or orally. A type or combination of different drugs is used by patients. Currently, the drugs approved for pancreatic cancer are: Fluorouracil (5-FU), Capecitabine, Gemcitabine, Erlotinib, Leucovorin, Irinotecan, Nab-paclitaxel, Nanoliposomal irinotecan, and Oxaliplatin. In addition, there are some targeted treatments that target specific cancer genes, proteins, or tissue environments. For example, Erlotinib blocks the epidermal growth factor receptor (EGFR), Olaparib influences a hereditary BRCA mutation, and Larotrectinib can be used for NTRK fusion (Wang et al., 2015; Filippi et al., 2021; Tutt et al., 2021). In addition, Immunotherapy has become popular in recent years. Immune checkpoint inhibitors are an option for the treatment of pancreatic cancer with high microsatellite instability (MSI-H), which includes anti-PD-1 antibodies such as pembrolizumab (Diaz et al., 2017). Different treatment options depend on the stage of the tumor. For example, resected patients’ chemotherapy is gemcitabine or 5-FU based treatment, however, metastatic cancer uses Gemcitabine plus Nab-paclitaxel or a combination of 5-FU, Leucovorin, Irinotecan, and Oxaliplatin called FOLFIRINOX. However, surgery is not the main treatment method. Appropriate therapeutics are referred to the European Society for Medical Oncology (ESMO) guidelines (Ducreux et al., 2015).

Platelets originate from megakaryocytes, which are in circulation for 5-7 days. The size is approximately 2-4 μm and their volume is about 7 μm

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. A normal number of platelets is between 150,000 and 450,000 per microliter of blood. They are removed from the blood vessels by macrophages and neutrophils and, leave the body through the spleen.

The main role of platelets is to maintain hemostasis, by forming a “platelet clot” (Tomaiuolo et al., 2017). After vascular injury, initial platelet tethering is mediated by the interaction between GPIbα of the platelet receptor GPIb-IX-V and the A1 domain of Von Willebrand factor (vWF) deposited in the subendothelial matrix of the injured vessel wall. After platelet tethering, GPVI and αIIβ1 receptors promote platelet adhesion and activation ( Ruggeri and Jackson, 2013 ; Welsh et al., 2014 ). GPVI has a low affinity for collagen. αIIβ1 maintains strong collagen adhesion and strengthens the GPVI-collagen interaction. Subsequent firm adhesion occurs through the binding of fibronectin, αIIbβ3, laminin, and vWF. In addition, platelet adhesion forms a positive feedback to initiate the activation of circulating platelets. The final step is platelet aggregation through the binding of fibrinogen or vWF to αIIbβ3.

Besides hemostasis and thrombosis, platelets also play an important role in immune activities. Platelets are able to recognize and interact with microbial pathogens including bacteria, viruses, and parasites. Platelet bounding shifts fee L. monocytogenes from “fast” clearance to CRIg-dependent “slow” clearance pathways (Broadley et al., 2016). In addition, different platelet receptors have different effects on cancer development (Supplementary Table 1). Platelets express toll-like receptors from TLR1 to TLR9 that recognize molecular motifs called pathogen-associated molecular patterns (PAMPs) (Cognasse et al., 2015). The interaction between platelets and leukocytes, monocytes, and granulocytes has been proven, which is through different receptor-ligands such as P-Selectin, PSGL-1. Platelets are involved in angiogenesis. Their activation facilitates release, which produces strong angiogenic responses. In addition, the release of platelet-derived phospholipids and microparticles are synergistic regulators of angiogenesis (Walsh et al., 2015). However, tumor growth can be exacerbated by uncontrolled angiogenesis. Breast cancer cells secrete luminal

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